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Journal articles on the topic 'Hepatocellular Carcinoma HSC'

Author: Grafiati

Published: 9 March 2023

Last updated: 31 July 2025

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1

Wang, Pei-Wen, Tung-Yi Lin, Pei-Ming Yang, Chau-Ting Yeh, and Tai-Long Pan. "Hepatic Stellate Cell Modulates the Immune Microenvironment in the Progression of Hepatocellular Carcinoma." International Journal of Molecular Sciences 23, no. 18 (2022): 10777. http://dx.doi.org/10.3390/ijms231810777.

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Hepatocellular carcinoma (HCC) is a major cause of increases in the mortality rate due to cancer that usually develops in patients with liver fibrosis and impaired hepatic immunity. Hepatic stellate cells (HSCs) may directly or indirectly crosstalk with various hepatic cells and subsequently modulate extracellular remodeling, cell invasion, macrophage conversion, and cancer deterioration. In this regard, the tumor microenvironment created by activated HSC plays a critical role in mediating pathogenesis and immune escape during HCC progression. Herein, intermediately differentiated human liver

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2

Mailloux, Adam, and Pearlie Epling-Burnette. "Collagen matrix deposition by hepatic stellate cells protects hepatocellular carcinoma from NK-mediated cytotoxicity (P2013)." Journal of Immunology 190, no. 1_Supplement (2013): 53.7. http://dx.doi.org/10.4049/jimmunol.190.supp.53.7.

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Abstract Liver fibrosis (LF), a leading risk factor for hepatocellular carcinoma (HCC), is caused by collagen-producing hepatic stellate cells (HSC) activated during chronic inflammation secondary to hepatitis-C infection, or alcohol liver disease (ALD). NK cells promote disease resolution via RAE1-dependant HSC clearance. A defect in NK function by an ill-defined mechanism contributes to a pro-fibrotic response. Using an engineered bioartifical collagen matrix, the expression of inhibitory leukocyte associated IgG-like receptor-1 (LAIR-1) was increased on dividing NK cells and IL-2-induced NK

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3

Jia, Shu-Qin, Jian-Jun Ren, Pei-De Dong, and Xing-Kai Meng. "Probing the Hepatic Progenitor Cell in Human Hepatocellular Carcinoma." Gastroenterology Research and Practice 2013 (2013): 1–5. http://dx.doi.org/10.1155/2013/145253.

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Objective. The intrahepatic stem cells, also known as hepatic progenitor cells (HPCs), are able to differentiate into hepatocytes and bile duct epithelia. By exposure of different injuries and different hepatocarcinogenic regimens, the mature hepatocytes can no longer effectively regenerate; stem cells are involved in the pathogenesis of hepatocellular carcinoma.Methods. Immunohistochemistry was performed on 107 paraffin-embedded hepatocellular carcinoma specimens with the marker of hepatocyte and hepatocellular carcinoma (HepPar1), biliary differentiation (CK7,CK19), haemopoietic stem cell (H

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4

Xiong, Hao, and Jinsheng Guo. "Targeting Hepatic Stellate Cells for the Prevention and Treatment of Liver Cirrhosis and Hepatocellular Carcinoma: Strategies and Clinical Translation." Pharmaceuticals 18, no. 4 (2025): 507. https://doi.org/10.3390/ph18040507.

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Hepatic stellate cells (HSC) are the major source of myofibroblasts (MFB) in fibrosis and cancer- associated fibroblasts (CAF) in both primary and metastatic liver cancer. Over the past few decades, there has been significant progress in understanding the cellular and molecular mechanisms by which liver fibrosis and HCC occur, as well as the key roles of HSC in their pathogenesis. HSC-targeted approaches using specific surface markers and receptors may enable the selective delivery of drugs, oligonucleotides, and therapeutic peptides that exert optimized anti-fibrotic and anti-HCC effects. Rec

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5

Wu, Mengna, Huajie Miao, Rong Fu, Jie Zhang, and Wenjie Zheng. "Hepatic Stellate Cell: A Potential Target for Hepatocellular Carcinoma." Current Molecular Pharmacology 13, no. 4 (2020): 261–72. http://dx.doi.org/10.2174/1874467213666200224102820.

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: Liver cancer is a leading cause of cancer-related death worldwide, in which hepatocellular carcinoma (HCC) accounts for the majority. Despite the progression in treatment, the prognosis remains extremely poor for HCC patients. The mechanisms of hepatocarcinogenesis are complex, of which fibrosis is acknowledged as the pre-cancerous stage of HCC. Approximately, 80-90% of HCC develops in the fibrotic or cirrhotic livers. Hepatic stellate cells (HSCs), the main effector cells of liver fibrosis, could secret various biological contents to maintain the liver inflammation. By decades, HSCs are inc

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Quiroz Reyes, Adriana G., Sonia A. Lozano Sepulveda, Natalia Martinez-Acuña, et al. "Cancer Stem Cell and Hepatic Stellate Cells in Hepatocellular Carcinoma." Technology in Cancer Research & Treatment 22 (January 2023): 153303382311636. http://dx.doi.org/10.1177/15330338231163677.

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Hepatocellular carcinoma (HCC) is the most common liver cancer. It is highly lethal and has high recurrence. Death among HCC patients occur mainly due to tumor progression, recurrence, metastasis, and chemoresistance. Cancer stem cells (CSCs) are cell subpopulations within the tumor that promote invasion, recurrence, metastasis, and drug resistance. Hepatic stellate cells (HSCs) are important components of the tumor microenvironment (TME) responsible for primary secretory ECM proteins during liver injury and inflammation. These cells promote fibrogenesis, infiltrate the tumor stroma, and contr

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Liu, Man, Jingying Zhou, Xiaoyu Liu, et al. "Targeting monocyte-intrinsic enhancer reprogramming improves immunotherapy efficacy in hepatocellular carcinoma." Gut 69, no. 2 (2019): 365–79. http://dx.doi.org/10.1136/gutjnl-2018-317257.

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ObjectiveHepatocellular carcinoma (HCC), mostly developed in fibrotic/cirrhotic liver, exhibits relatively low responsiveness to immune checkpoint blockade (ICB) therapy. As myeloid-derived suppressor cell (MDSC) is pivotal for immunosuppression, we investigated its role and regulation in the fibrotic microenvironment with an aim of developing mechanism-based combination immunotherapy.DesignFunctional significance of MDSCs was evaluated by flow cytometry using two orthotopic HCC models in fibrotic liver setting via carbon tetrachloride or high-fat high-carbohydrate diet and verified by clinica

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8

Subramanian, Pallavi, Jochen Hampe, Frank Tacke, and Triantafyllos Chavakis. "Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD)." International Journal of Molecular Sciences 23, no. 13 (2022): 6996. http://dx.doi.org/10.3390/ijms23136996.

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The prevalence of nonalcoholic fatty liver disease (NAFLD), recently also re-defined as metabolic dysfunction associated fatty liver disease (MAFLD), is rapidly increasing, affecting ~25% of the world population. MALFD/NAFLD represents a spectrum of liver pathologies including the more benign hepatic steatosis and the more advanced non-alcoholic steatohepatitis (NASH). NASH is associated with enhanced risk for liver fibrosis and progression to cirrhosis and hepatocellular carcinoma. Hepatic stellate cells (HSC) activation underlies NASH-related fibrosis. Here, we discuss the profibrogenic path

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9

Wang, Wen-Hung, Kuo-Yu Hsuan, Ling-Ya Chu, et al. "Anticancer Effects of Salvia miltiorrhiza Alcohol Extract on Oral Squamous Carcinoma Cells." Evidence-Based Complementary and Alternative Medicine 2017 (2017): 1–9. http://dx.doi.org/10.1155/2017/5364010.

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Researchers have reported significant effects from Danshen (Salvia miltiorrhiza) in terms of inhibiting tumor cell proliferation and promoting apoptosis in breast cancer, hepatocellular carcinomas, promyelocytic leukemia, and clear cell ovary carcinomas. Here we report our data indicating that Danshen extracts, especially alcohol extract, significantly inhibited the proliferation of the human oral squamous carcinoma (OSCC) cell lines HSC-3 and OC-2. We also observed that Danshen alcohol extract activated the caspase-3 apoptosis executor by impeding members of the inhibitor of apoptosis (IAP) f

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MAN, LIU, Jingying Zhou, John Wong, Anthony W. H. Chan, Zhiwei Chen, and Alfred S. L. Cheng. "Delineating the epigenetic regulation of myeloid derived suppressor cell generation in hepatocellular carcinoma associated with cirrhosis." Journal of Immunology 198, no. 1_Supplement (2017): 205.14. http://dx.doi.org/10.4049/jimmunol.198.supp.205.14.

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Abstract Hepatocellular carcinoma (HCC) is the most common liver tumor with dismal prognosis. Since most liver tumors arise in a context of chronic inflammation associated with fibrosis, tumor microenvironment plays a critical role in liver carcinogenesis. Myeloid derived suppressor cell (MDSC) is a population of immature myeloid cells that undermine immune surveillance and facilitate tumor immune escape. As a key driver of liver fibrosis, activated hepatic stellate cell (HSC) has been recently shown to induce MDSC generation through cell-cell contact and/or secreted soluble factors. Given the

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Santamato, Angela, Emilia Fransvea, Francesco Dituri, et al. "Hepatic stellate cells stimulate HCC cell migration via laminin-5 production." Clinical Science 121, no. 4 (2011): 159–68. http://dx.doi.org/10.1042/cs20110002.

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Activated HSCs (hepatic stellate cells) are the main source of extracellular matrix proteins present in cirrhotic liver on which HCC (hepatocellular carcinoma) commonly develops. HCC cells behave differently according to differences in the surrounding microenvironment. In the present study, we have investigated a mechanism whereby HSCs modulate the migratory activity of HCC cells. We used primary cultures of human HSCs to investigate their effect on Hep3B, Alexander, HLE and HLF HCC cells. The expression of Ln-5 (laminin-5) was documented at transcript and protein levels both in vitro and in v

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Dhar, Debanjan, Jacopo Baglieri, Tatiana Kisseleva, and David A. Brenner. "Mechanisms of liver fibrosis and its role in liver cancer." Experimental Biology and Medicine 245, no. 2 (2020): 96–108. http://dx.doi.org/10.1177/1535370219898141.

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Hepatic fibrogenesis is a pathophysiological outcome of chronic liver injury hallmarked by excessive accumulation of extracellular matrix proteins. Fibrosis is a dynamic process that involves cross-talk between parenchymal cells (hepatocytes), hepatic stellate cells, sinusoidal endothelial cells and both resident and infiltrating immune cells. In this review, we focus on key cell-types that contribute to liver fibrosis, cytokines, and chemokines influencing this process and what it takes for fibrosis to regress. We discuss how mitochondria and metabolic changes in hepatic stellate cells modula

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13

Jeng, Kuo-Shyang, Ssu-Jung Lu, Chih-Hsuan Wang, and Chiung-Fang Chang. "Liver Fibrosis and Inflammation under the Control of ERK2." International Journal of Molecular Sciences 21, no. 11 (2020): 3796. http://dx.doi.org/10.3390/ijms21113796.

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Chronic liver injury could lead the formation of liver fibrosis, eventually some would develop to hepatocellular carcinoma (HCC), one of the leading malignancies worldwide. The aim of the study is to dissect the role of extracellular signal-regulated kinase 2 (ERK2) signaling in liver fibrosis and inflammation. The choline-deficient, ethionine-supplemented (CDE) diet could lead to fatty livers and generate oval cells, activate hepatocyte stellate cell (HSC) and recruit immune cells as the liver fibrosis model mice. WT and ERK2 deficient (ERK2−/−) mice were compared in terms of liver weight/bod

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14

Iwahashi, Shuichi, Mitsuo Shimada, Yuji Morine, et al. "The effect of hepatic stellate cells on hepatocellular carcinoma progression." Journal of Clinical Oncology 37, no. 4_suppl (2019): 265. http://dx.doi.org/10.1200/jco.2019.37.4_suppl.265.

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265 Background: The hepatic stellate cells (HSCs) localize at the space of Disse in the liver and have multiple functions. They are identified as the major contributor to hepatic fibrosis. Some manuscripts mentioned that activated HSCs predicted prognoses of hepatocellular carcinoma. The aim of this study is to investigate the effect of HSCs and the role of IL-6 / Stat3 pathway on HCC progression. Methods: HCC cells (Hep G2 and Huh 7) were co-cultured with HSC (LX2 and Li90). The viability and migration ability of cancer cells were detected. Also, the expression of epithelial–mesenchymal trans

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Cho, Yuri, Min Ji Park, Koeun Kim, et al. "Tumor-Stroma Crosstalk Enhances REG3A Expressions that Drive the Progression of Hepatocellular Carcinoma." International Journal of Molecular Sciences 21, no. 2 (2020): 472. http://dx.doi.org/10.3390/ijms21020472.

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Abstract: Background: Crosstalk between tumors and their microenvironment plays a crucial role in the progression of hepatocellular carcinoma (HCC). However, there is little existing information about the key signaling molecule that modulates tumor-stroma crosstalk. Methods: Complementary DNA (cDNA) microarray analysis was performed to identify the key molecule in tumor-stroma crosstalk. Subcutaneous xenograft in vivo murine model, immunoblotting, immunofluorescence, and real-time polymerase chain reaction using HCC cells and tissues were performed. Results: The key molecule, regenerating gene

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16

Fujii, Hideki, and Norifumi Kawada. "The Role of Insulin Resistance and Diabetes in Nonalcoholic Fatty Liver Disease." International Journal of Molecular Sciences 21, no. 11 (2020): 3863. http://dx.doi.org/10.3390/ijms21113863.

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Nonalcoholic fatty liver disease (NAFLD) consists of the entire spectrum of fatty liver disease in patients without significant alcohol consumption, ranging from nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH) to cirrhosis, with NASH recently shown as an important cause of hepatocellular carcinoma (HCC). There is a close relationship between insulin resistance (IR) and NAFLD, with a five-fold higher prevalence of NAFLD in patients with type 2 diabetes (T2DM) compared to that in patients without T2DM. IR is involved in the progression of disease conditions such as steatos

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Niu, Gengming, Xiaotian Zhang, Runqi Hong та ін. "GJA1 promotes hepatocellular carcinoma progression by mediating TGF-β-induced activation and the epithelial–mesenchymal transition of hepatic stellate cells". Open Medicine 16, № 1 (2021): 1459–71. http://dx.doi.org/10.1515/med-2021-0344.

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Abstract Introduction Gap junction protein, alpha 1 (GJA1), which is correlated with recurrences and unfavorable prognoses in hepatocellular carcinomas (HCCs), is one of the specific proteins expressed by activated hepatic stellate cells (HSCs). Methods Expression of GJA1 was compared between HCCs and nontumor tissues (NTs), between hepatic cirrhosis and NTs, and between primary and metastatic HCCs using transcriptomic datasets from the Gene Expression Omnibus and the Integrative Molecular Database of Hepatocellular Carcinoma. The in vitro activities of GJA1 were investigated in cultured HSCs

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Seo, Hye-Young, So-Hee Lee, Eugene Han, et al. "Evogliptin Directly Inhibits Inflammatory and Fibrotic Signaling in Isolated Liver Cells." International Journal of Molecular Sciences 23, no. 19 (2022): 11636. http://dx.doi.org/10.3390/ijms231911636.

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Chronic liver inflammation can lead to fibrosis, cirrhosis, and hepatocellular carcinoma. Kupffer cells (KC) secrete proinflammatory and fibrogenic cytokines in response to lipopolysaccharide (LPS), and so play an important role in liver inflammation, where they induce hepatocellular damage. LPS also activates hepatic stellate cells and induces extracellular matrix deposition. In this study, we used isolated primary KC, primary hepatocytes, and primary hepatic stellate cells (HSC) to investigate whether evogliptin directly inhibits inflammatory and fibrotic signaling. We found that evogliptin

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19

Suen, Alfred Long-Hin, Kristy Kwan-Shuen Chan, and Regina Cheuk-Lam Lo. "Abstract 3982: Anti-Stanniocalcin 1 antibody as a potential therapeutic strategy for liver fibrosis and hepatocellular carcinoma." Cancer Research 83, no. 7_Supplement (2023): 3982. http://dx.doi.org/10.1158/1538-7445.am2023-3982.

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Abstract Introduction: Hepatocellular carcinoma (HCC) is the sixth most frequently diagnosed cancer and the third leading cause of cancer deaths. Liver fibrosis (LF) is a progressive disease and cirrhosis, the advanced stage of LF, is per se a risk factor for HCC. Moreover, LF persists after the development of HCC. Stanniocalcin 1 (STC1), as a serum biomarker of both HCC and LF as we previously reported, was found to be secreted from HCC cells and hepatic stellate cells (HSCs). STC1 promoted cell migration and invasion of HCC and activation of HSCs, suggesting that STC1 could be an actionable

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20

Liepelt, Anke, and Frank Tacke. "Stromal cell-derived factor-1 (SDF-1) as a target in liver diseases." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 2 (2016): G203—G209. http://dx.doi.org/10.1152/ajpgi.00193.2016.

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The chemokine stromal cell-derived factor-1 (SDF-1) or CXCL12 is constitutively expressed in healthy liver. However, its expression increases following acute or chronic liver injury. Liver sinusoidal endothelial cells (LSEC), hepatic stellate cells (HSC), and malignant hepatocytes are important sources of SDF-1/CXCL12 in liver diseases. CXCL12 is able to activate two chemokine receptors with different downstream signaling pathways, CXCR4 and CXCR7. CXCR7 expression is relevant on LSEC, while HSC, mesenchymal stem cells, and tumor cells mainly respond via CXCR4. Here, we summarize recent develo

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Wang, Jun, Kefen Zhang, Xiuming Tang, Yinzhu Chen, and Zhen Ye. "Restricted cubic spline analysis: Age-dependent relationship between MAGEA12 and hepatocellular carcinoma prognosis." Journal of Cancer Research and Therapeutics 21, no. 2 (2025): 457–64. https://doi.org/10.4103/jcrt.jcrt_1690_24.

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ABSTRACT Objectives: Currently, understanding of the nonlinear relationship between age and hepatocellular carcinoma (HCC) prognosis is insufficient. Thus, this study aimed to analyze the relationship between age at HCC diagnosis and overall survival (OS) and identify possible influencing mechanisms. Methods: Clinical data from the TCGA public database were analyzed. Restricted cubic spline and segmented logistic regression were employed to explore the nonlinear relationship between age at diagnosis and mortality risk following hepatectomy. Furthermore, bioinformatics methods were employed to

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Weiskirchen, Ralf, and Frank Tacke. "Relevance of Autophagy in Parenchymal and Non-Parenchymal Liver Cells for Health and Disease." Cells 8, no. 1 (2019): 16. http://dx.doi.org/10.3390/cells8010016.

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Autophagy is a highly conserved intracellular process for the ordered degradation and recycling of cellular components in lysosomes. In the liver, parenchymal cells (i.e., mainly hepatocytes) utilize autophagy to provide amino acids, glucose, and free fatty acids as sources of energy and biosynthesis functions, but also for recycling and controlling organelles such as mitochondria. Non-parenchymal cells of the liver, including endothelial cells, macrophages (Kupffer cells), and hepatic stellate cells (HSC), also employ autophagy, either for maintaining cellular homeostasis (macrophages, endoth

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An, Lingxuan, Ulrich Wirth, Dominik Koch, et al. "Metabolic Role of Autophagy in the Pathogenesis and Development of NAFLD." Metabolites 13, no. 1 (2023): 101. http://dx.doi.org/10.3390/metabo13010101.

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Non-alcoholic fatty liver disease (NAFLD) is a spectrum of liver disease, ranging from simple steatosis to hepatitis, fibrosis, cirrhosis, and hepatocellular carcinoma (HCC). Liver fibrosis, which portends a poor prognosis in NAFLD, is characterized by the excessive accumulation of extracellular matrix (ECM) proteins resulting from abnormal wound repair response and metabolic disorders. Various metabolic factors play crucial roles in the progression of NAFLD, including abnormal lipid, bile acid, and endotoxin metabolism, leading to chronic inflammation and hepatic stellate cell (HSC) activatio

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Sakasai-Sakai, Akiko, Kenji Takeda, and Masayoshi Takeuchi. "Involvement of Intracellular TAGE and the TAGE–RAGE–ROS Axis in the Onset and Progression of NAFLD/NASH." Antioxidants 12, no. 3 (2023): 748. http://dx.doi.org/10.3390/antiox12030748.

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The repeated excessive intake of sugar, a factor that contributes to the onset of nonalcoholic fatty liver disease (NAFLD) and its progression to the chronic form of nonalcoholic steatohepatitis (NASH), markedly increases the hepatocyte content of glyceraldehyde (GA), a glucose/fructose metabolic intermediate. Toxic advanced glycation end-products (toxic AGEs, TAGE) are synthesized by cross-linking reactions between the aldehyde group of GA and the amino group of proteins, and their accumulation has been implicated in the development of NAFLD/NASH and hepatocellular carcinoma (HCC). Our previo

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Ozutsumi, Takahiro, Tadashi Namisaki, Naotaka Shimozato, et al. "Combined Treatment with Sodium-Glucose Cotransporter-2 Inhibitor (Canagliflozin) and Dipeptidyl Peptidase-4 Inhibitor (Teneligliptin) Alleviates NASH Progression in A Non-Diabetic Rat Model of Steatohepatitis." International Journal of Molecular Sciences 21, no. 6 (2020): 2164. http://dx.doi.org/10.3390/ijms21062164.

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Hepatocellular carcinoma (HCC) is the strongest independent predictor of mortality in non-alcoholic steatohepatitis (NASH)-related cirrhosis. The effects and mechanisms of combination of sodium-dependent glucose cotransporter inhibitor and canagliflozin (CA) and dipeptidyl peptidase-4 inhibitor and teneligliptin (TE) on non-diabetic NASH progression were examined. CA and TE suppressed choline-deficient, L-amino acid-defined diet-induced hepatic fibrogenesis and carcinogenesis. CA alone or with TE significantly decreased proinflammatory cytokine expression. CA and TE significantly attenuated he

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Teng, Kun-Yu, Juan M. Barajas, Peng Hu, Samson T. Jacob, and Kalpana Ghoshal. "Role of B Cell Lymphoma 2 in the Regulation of Liver Fibrosis in miR-122 Knockout Mice." Biology 9, no. 7 (2020): 157. http://dx.doi.org/10.3390/biology9070157.

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MicroRNA-122 (miR-122) has been identified as a marker of various liver injuries, including hepatitis- virus-infection-, alcoholic-, and non-alcoholic steatohepatitis (NASH)-induced liver fibrosis. Here, we report that the extracellular miR-122 from hepatic cells can be delivered to hepatic stellate cells (HSCs) to modulate their proliferation and gene expression. Our published Argonaute crosslinking immunoprecipitation (Ago-CLIP) data identified several pro-fibrotic genes, including Ctgf, as miR-122 targets in mice livers. However, treating Ctgf as a therapeutic target failed to rescue the fi

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Hsieh, Ching-Chuan, Chien-Hui Hung, Meihua Chiang, Yu-Chin Tsai, and Jie-Teng He. "Hepatic Stellate Cells Enhance Liver Cancer Progression by Inducing Myeloid-Derived Suppressor Cells through Interleukin-6 Signaling." International Journal of Molecular Sciences 20, no. 20 (2019): 5079. http://dx.doi.org/10.3390/ijms20205079.

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The tumor microenvironment, which consists of fibroblasts, smooth muscle cells, endothelial cells, immune cells, epithelial cells, and extracellular matrices, plays a crucial role in tumor progression. Hepatic stellate cells (HSCs), a class of unique liver stromal cells, participate in immunomodulatory activities by inducing the apoptosis of effector T-cells, generation of regulatory T-cells, and development of myeloid-derived suppressor cells (MDSCs) to achieve long-term survival of islet allografts. This study provides in vitro and in vivo evidences that HSCs induce the generation of MDSCs t

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Ying, Hanglu, Long Li, Yufen Zhao, and Feng Ni. "Ivermectin Attenuates CCl4-Induced Liver Fibrosis in Mice by Suppressing Hepatic Stellate Cell Activation." International Journal of Molecular Sciences 23, no. 24 (2022): 16043. http://dx.doi.org/10.3390/ijms232416043.

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Liver fibrosis, a common liver dysfunction with high morbidity and mortality rates, is the leading cause of cirrhosis and hepatocellular carcinoma, for which there are no effective therapies. Ivermectin is an antiparasitic drug that also has been showing therapeutic actions in many other diseases, including antiviral and anticancer actions, as well as treating metabolic diseases. Herein, we evaluated the function of ivermectin in regulating liver fibrosis. Firstly, carbon tetrachloride (CCl4)-injected Balb/c mice were used to assess the antifibrosis effects of ivermectin in vivo. Further, CFSC

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Li, Yanchun, Wei Guo, Mengjun Mo, et al. "Multi-omics study of the genomic features and clinical characteristics of hepatic sarcomatoid carcinoma located at different sites." Journal of Clinical Oncology 41, no. 16_suppl (2023): e15153-e15153. http://dx.doi.org/10.1200/jco.2023.41.16_suppl.e15153.

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e15153 Background: Hepatic sarcomatoid carcinoma (HSC) is a rare and highly malignant tumor, which accounts for less than 2% of hepatic carcinoma. HSC can occur in the liver (Sarcomatoid hepatocellular carcinoma, SHCC) or in the intrahepatic bile duct (Sarcomatoid intrahepatic cholangiocarcinoma, SiCCA). We aimed to compare the clinical characteristics and genomic features between SHCC and SiCCA. Methods: In this study, we recruited 20 patients who were pathologically diagnosed with HSC from January 2018 to February 2021 in Hunan Provincial People’s Hospital. Whole exome sequencing and PD-L1 e

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Buakaew, Watunyoo, Sucheewin Krobthong, Yodying Yingchutrakul та ін. "Investigating the Antifibrotic Effects of β-Citronellol on a TGF-β1-Stimulated LX-2 Hepatic Stellate Cell Model". Biomolecules 14, № 7 (2024): 800. http://dx.doi.org/10.3390/biom14070800.

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Liver fibrosis, a consequence of chronic liver damage or inflammation, is characterized by the excessive buildup of extracellular matrix components. This progressive condition significantly raises the risk of severe liver diseases like cirrhosis and hepatocellular carcinoma. The lack of approved therapeutics underscores the urgent need for novel anti-fibrotic drugs. Hepatic stellate cells (HSCs), key players in fibrogenesis, are promising targets for drug discovery. This study investigated the anti-fibrotic potential of Citrus hystrix DC. (KL) and its bioactive compound, β-citronellol (β-CIT),

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Nakhaei-Rad, Saeideh, Silke Pudewell, Amin Mirzaiebadizi, et al. "From Quiescence to Activation: The Reciprocal Regulation of Ras and Rho Signaling in Hepatic Stellate Cells." Cells 14, no. 9 (2025): 674. https://doi.org/10.3390/cells14090674.

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Chronic liver diseases are marked by persistent inflammation and can evolve into liver fibrosis, cirrhosis, and hepatocellular carcinoma. In an affected liver, hepatic stellate cells (HSCs) transition from a quiescent to an activated state and adopt a myofibroblast-like cell phenotype. While these activated cells play a role in supporting liver regeneration, they can also have detrimental effects on liver function as the disease progresses to fibrosis and cirrhosis. These findings highlight the dynamic switching between different signaling pathways involving Ras, Rho GTPases, and Notch signali

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Koyama, Yukinori, Jun Xu, Xiao Liu, and David A. Brenner. "New Developments on the Treatment of Liver Fibrosis." Digestive Diseases 34, no. 5 (2016): 589–96. http://dx.doi.org/10.1159/000445269.

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Liver fibrosis results from many chronic injuries and often progresses to cirrhosis, liver failure, portal hypertension, and hepatocellular carcinoma. Liver transplantation is the only treatment available for patients with advanced stages of liver fibrosis. Therefore, new strategies for anti-fibrotic therapy are required. Various kinds of hepatocyte damage result in inflammation, which leads to the activation of hepatic stellate cells (HSCs), which are the major source of myofibroblasts in the liver. Myofibroblasts proliferate in response to various kinds of cytokines, chemokines, and growth f

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Stergiou, Ioanna E., Stavros P. Papadakos, Anna Karyda, Ourania E. Tsitsilonis, Meletios-Athanasios Dimopoulos, and Stamatios Theocharis. "EPH/Ephrin Signaling in Normal Hematopoiesis and Hematologic Malignancies: Deciphering Their Intricate Role and Unraveling Possible New Therapeutic Targets." Cancers 15, no. 15 (2023): 3963. http://dx.doi.org/10.3390/cancers15153963.

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Erythropoietin-producing hepatocellular carcinoma receptors (EPHs) represent the largest family of receptor tyrosine kinases (RTKs). EPH interaction with ephrins, their membrane-bound ligands, holds a pivotal role in embryonic development, while, though less active, it is also implicated in various physiological functions during adult life. In normal hematopoiesis, different patterns of EPH/ephrin expression have been correlated with hematopoietic stem cell (HSC) maintenance and lineage-committed hematopoietic progenitor cell (HPC) differentiation, as well as with the functional properties of

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Dewidar, Meyer, Dooley та Meindl-Beinker. "TGF-β in Hepatic Stellate Cell Activation and Liver Fibrogenesis—Updated 2019". Cells 8, № 11 (2019): 1419. http://dx.doi.org/10.3390/cells8111419.

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Liver fibrosis is an advanced liver disease condition, which could progress to cirrhosis and hepatocellular carcinoma. To date, there is no direct approved antifibrotic therapy, and current treatment is mainly the removal of the causative factor. Transforming growth factor (TGF)-β is a master profibrogenic cytokine and a promising target to treat fibrosis. However, TGF-β has broad biological functions and its inhibition induces non-desirable side effects, which override therapeutic benefits. Therefore, understanding the pleiotropic effects of TGF-β and its upstream and downstream regulatory me

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Lai, Chi-Yu, Kun-Yun Yeh, Chiu-Ya Lin та ін. "MicroRNA-21 Plays Multiple Oncometabolic Roles in the Process of NAFLD-Related Hepatocellular Carcinoma via PI3K/AKT, TGF-β, and STAT3 Signaling". Cancers 13, № 5 (2021): 940. http://dx.doi.org/10.3390/cancers13050940.

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MicroRNA-21 (miR-21) is one of the most frequently upregulated miRNAs in liver diseases such as nonalcoholic fatty liver disease (NAFLD) and hepatocellular carcinoma (HCC). However, mechanistic pathways that connect NAFLD and HCC remain elusive. We developed a doxycycline (Dox)-inducible transgenic zebrafish model (LmiR21) which exhibited an upregulation of miR-21 in the liver, which in turn induced the full spectrum of NAFLD, including steatosis, inflammation, fibrosis, and HCC, in the LmiR21 fish. Diethylnitrosamine (DEN) treatment led to accelerated liver tumor formation and exacerbated the

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Wang, Yake, Xiaolong Li, Xiaowen Guan, et al. "The Upregulation of Leucine-Rich Repeat Containing 1 Expression Activates Hepatic Stellate Cells and Promotes Liver Fibrosis by Stabilizing Phosphorylated Smad2/3." International Journal of Molecular Sciences 25, no. 5 (2024): 2735. http://dx.doi.org/10.3390/ijms25052735.

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Liver fibrosis poses a significant global health risk due to its association with hepatocellular carcinoma (HCC) and the lack of effective treatments. Thus, the need to discover additional novel therapeutic targets to attenuate liver diseases is urgent. Leucine-rich repeat containing 1 (LRRC1) reportedly promotes HCC development. Previously, we found that LRRC1 was significantly upregulated in rat fibrotic liver according to the transcriptome sequencing data. Herein, in the current work, we aimed to explore the role of LRRC1 in liver fibrosis and the underlying mechanisms involved. LRRC1 expre

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Orucov, М. Т., E. T. Şamdancı та Ə. B. Həsənov. "ФИБРОЛАМЕЛЛЯРНАЯ ГЕПАТОЦЕЛЛЮЛЯРНАЯ КАРЦИНОМА". Azerbaijan Medical Journal, № 3 (30 вересня 2023): 172–78. http://dx.doi.org/10.34921/amj.2023.3.028.

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Məqalədə müəlliflərin klinik şəraitdə müşahidə etdikləri fibrolamelyar hepatosellulyar karsinomalı (FL-HSK) xəstə haqqında məlumat və bu xəstəlik haqqında ədəbiyyat xülasəsi təqdim edilir. 37 yaşlı kişinin qaraciyərinin sağ payındakı kütlədən alınmış tru-cut biopsiya materialının patohistoloji müayinəsi zamanı lamelyar fibroz daxilində yerləşmiş şiş hüceyrələri aşkar edilmişdir. İmmunhistokimyəvi olaraq şiş hüceyrələri PanCK, sitokeratin 7, CD68, IX karboanhidraza və qlütamin sintetaza əks-cisimləri ilə pozitiv boyanmışdır. Vimentin ilə boyanmadığı halda, CD34 ilə sinusoidal kapilyarizasiya və

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Yoon, Yongdae, Seong Chan Gong, Moon Young Kim, et al. "Generation of Fibrotic Liver Organoids Using Hepatocytes, Primary Liver Sinusoidal Endothelial Cells, Hepatic Stellate Cells, and Macrophages." Cells 12, no. 21 (2023): 2514. http://dx.doi.org/10.3390/cells12212514.

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Liver organoids generated with single or multiple cell types have been used to investigate liver fibrosis development, toxicity, pathogenesis, and drug screening. However, organoid generation is limited by the availability of cells isolated from primary tissues or differentiated from various stem cells. To ensure cell availability for organoid formation, we investigated whether liver organoids could be generated with cell-line-based Huh-7 hepatocellular carcinoma cells, macrophages differentiated from THP-1 monocytes, and LX-2 hepatic stellate cells (HSCs) and primary liver sinusoidal endothel

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Ding, Ning, Nasun Hah, Ruth T. Yu, et al. "BRD4 is a novel therapeutic target for liver fibrosis." Proceedings of the National Academy of Sciences 112, no. 51 (2015): 15713–18. http://dx.doi.org/10.1073/pnas.1522163112.

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Liver fibrosis is characterized by the persistent deposition of extracellular matrix components by hepatic stellate cell (HSC)-derived myofibroblasts. It is the histological manifestation of progressive, but reversible wound-healing processes. An unabated fibrotic response results in chronic liver disease and cirrhosis, a pathological precursor of hepatocellular carcinoma. We report here that JQ1, a small molecule inhibitor of bromodomain-containing protein 4 (BRD4), a member of bromodomain and extraterminal (BET) proteins, abrogate cytokine-induced activation of HSCs. Cistromic analyses revea

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Akter, Sharmin. "Non-alcoholic Fatty Liver Disease and Steatohepatitis: Risk Factors and Pathophysiology." Middle East Journal of Digestive Diseases 14, no. 2 (2022): 167–81. http://dx.doi.org/10.34172/mejdd.2022.270.

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Non-alcoholic fatty liver disease (NAFLD) and its progressive subtype non-alcoholic steatohepatitis (NASH) are the most prevalent liver diseases, often leading to hepatocellular carcinoma (HCC). This review aims to describe the present knowledge of the risk factors responsible for the development of NAFLD and NASH. I performed a literature review identifying studies focusing on the complex pathogenic pathway and risk factors of NAFLD and steatohepatitis. The relationship between NAFLD and metabolic syndrome is well established and widely recognized. Obesity, dyslipidemia, type 2 diabetes, hype

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Liao, Yi-Jen, Yuan-Hsi Wang, Chao-Lien Liu, Cheng-Chieh Fang, Ming-Hua Hsu та Fat-Moon Suk. "4-Methoxy Sulfonyl Paeonol Inhibits Hepatic Stellate Cell Activation and Liver Fibrosis by Blocking the TGF-β1/Smad, PDGF-BB/MAPK and Akt Signaling Pathways". Applied Sciences 10, № 17 (2020): 5941. http://dx.doi.org/10.3390/app10175941.

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Liver fibrosis initiates the progression of cirrhosis, and, finally, hepatocellular carcinoma (HCC). The increased proliferation and activation of hepatic stellate cells (HSCs) are crucial for hepatic fibrogenesis. Paeonol is the major vigorous component of Cortex Moutan, a traditional herbal medicine widely used for treating various diseases. Here, we identified a novel paeonol derivative (4-methoxy sulfonyl paeonol, 4-MSP) that inhibits TGF-β1-induced Smad2/3 phosphorylation and collagen expression in HSCs. 4-MSP pretreatment suppressed the PDGF-BB–induced phosphorylation of MAPK pathway mem

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Spirk, Marlen, Sebastian Zimny, Maximilian Neumann, Nichole McMullen, Christopher J. Sinal, and Christa Buechler. "Chemerin-156 is the Active Isoform in Human Hepatic Stellate Cells." International Journal of Molecular Sciences 21, no. 20 (2020): 7555. http://dx.doi.org/10.3390/ijms21207555.

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The chemokine chemerin exists as C-terminally processed isoforms whose biological functions are mostly unknown. A highly active human chemerin variant (huChem-157) was protective in experimental hepatocellular carcinoma (HCC) models. Hepatic stellate cells (HSCs) are central mediators of hepatic fibrogenesis and carcinogenesis and express the chemerin receptors chemokine-like receptor 1 (CMKLR1) and G protein-coupled receptor 1 (GPR1). Here we aimed to analyse the effect of chemerin isoforms on the viability, proliferation and secretome of the human HSC cell line LX-2. Therefore, huChem-157, 1

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Claveria-Cabello, Alex, Leticia Colyn, Maria Arechederra, et al. "Epigenetics in Liver Fibrosis: Could HDACs be a Therapeutic Target?" Cells 9, no. 10 (2020): 2321. http://dx.doi.org/10.3390/cells9102321.

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Chronic liver diseases (CLD) represent a worldwide health problem. While CLDs may have diverse etiologies, a common pathogenic denominator is the presence of liver fibrosis. Cirrhosis, the end-stage of CLD, is characterized by extensive fibrosis and is markedly associated with the development of hepatocellular carcinoma. The most important event in hepatic fibrogenesis is the activation of hepatic stellate cells (HSC) following liver injury. Activated HSCs acquire a myofibroblast-like phenotype becoming proliferative, fibrogenic, and contractile cells. While transient activation of HSCs is par

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Lee, Jung Il, Jocelyn H. Wright, Melissa M. Johnson, et al. "Role of Smad3 in platelet-derived growth factor-C-induced liver fibrosis." American Journal of Physiology-Cell Physiology 310, no. 6 (2016): C436—C445. http://dx.doi.org/10.1152/ajpcell.00423.2014.

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Chronic liver injury leads to fibrosis and cirrhosis. Cirrhosis, the end stage of chronic liver disease, is a leading cause of death worldwide and increases the risk of developing hepatocellular carcinoma. Currently, there is a lack of effective antifibrotic therapies to treat fibrosis and cirrhosis. Development of antifibrotic therapies requires an in-depth understanding of the cellular and molecular mechanisms involved in inflammation and fibrosis after hepatic injury. Two growth factor signaling pathways that regulate liver fibrosis are transforming growth factor-β (TGFβ) and platelet-deriv

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Khomich, Olga, Alexander V. Ivanov, and Birke Bartosch. "Metabolic Hallmarks of Hepatic Stellate Cells in Liver Fibrosis." Cells 9, no. 1 (2019): 24. http://dx.doi.org/10.3390/cells9010024.

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Liver fibrosis is a regenerative process that occurs after injury. It is characterized by the deposition of connective tissue by specialized fibroblasts and concomitant proliferative responses. Chronic damage that stimulates fibrogenic processes in the long-term may result in the deposition of excess matrix tissue and impairment of liver functions. End-stage fibrosis is referred to as cirrhosis and predisposes strongly to the loss of liver functions (decompensation) and hepatocellular carcinoma. Liver fibrosis is a pathology common to a number of different chronic liver diseases, including alc

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Gay, Martha, Hong Cao, and Jill P. Smith. "Abstract 6348: Cholecystokinin receptor blockade modulates in vitro fibrosis gene expression." Cancer Research 85, no. 8_Supplement_1 (2025): 6348. https://doi.org/10.1158/1538-7445.am2025-6348.

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Abstract Introduction: Cholecystokinin (CCK) receptors, G-protein coupled receptors, play crucial roles in gastrointestinal physiology, but their overexpression in cancer and fibrosis is implicated in disease progression and therapeutic resistance. Recent evidence suggests that activation of CCK receptors in hepatic stellate cells (HSCs) induces fibrosis-associated gene expression, contributing to liver pathology in conditions like metabolic dysfunction-associated steatohepatitis (MASH) and hepatocellular carcinoma (HCC). We have shown that a diet high in saturated fat induces the expression o

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Shreenivas, Aditya Varnam, Guru Subramanian Guru Murthy, Ben George, et al. "Impact of tumor histology and socioeconomic factors on survival of patients suffering from malignant vascular tumors of liver and hepatocellular carcinomas: A SEER database analysis." Journal of Clinical Oncology 38, no. 15_suppl (2020): e16612-e16612. http://dx.doi.org/10.1200/jco.2020.38.15_suppl.e16612.

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e16612 Background: Primary malignant vascular tumors of the liver are rare, aggressive and poorly understood subtypes of liver cancers. In this analysis, we aim to determine the impact of tumor histology and other socio economic factors on survival of these tumors and hepatocellular carcinomas. Methods: Patients with malignant histopathological diagnoses of hepatocellular carcinoma not otherwise specified (HCC NOS), hepatocellular carcinoma with spindle cell (HCC SP), fibrolamellar (HCC F), clear cell (HCC CL), scirrhous (HCC SC) and pleomorphic variants ( HCC PL), combined hepatocellular carc

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Lopez, Alexis Jared Paz, Brenda Aurora Llanos Salas, Michel Vladimir Alamo Hernandez, et al. "Fibrolamellar Hepatocellular Carcinoma in Young Adult: A Case Report and Literature Review." SAR Journal of Surgery 4, no. 03 (2023): 36–40. http://dx.doi.org/10.36346/sarjs.2023.v04i03.006.

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Fibrolamellar carcinoma (FLC), a truly unique and uncommon variation of hepatocellular carcinoma (HCC), accounting for barely 1%–9% of all HCC cases. Fibrolamellar carcinoma, an unclear malignancy, appears to be more commonly observed in youthful individuals without any preexisting liver conditions. The nomenclature "fibrolamellar" originates from the presence of dense fibrous collagen bands enveloping the neoplastic cells. Contrary to hepatocellular carcinoma (HCC), cirrhosis and viral hepatitis infection do not serve as predisposing factors for fibrolamellar carcinoma (FLC). Additionally, FL

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Rhee Chai, Ming, Padmaan Sankaran, and Lee Ming Yap. "Extrahepatic metastasis of hepatocellular carcinoma: A Malaysian case series." International Journal of Hepatobiliary and Pancreatic Diseases 12, no. 2 (2022): 9–12. http://dx.doi.org/10.5348/100099z04mc2022cs.

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Introduction: Hepatocellular carcinoma (HCC) is a primary malignancy which arises from hepatocytes. It is the sixth most commonly diagnosed cancer and the third leading cause of cancer death worldwide in 2020. It predominantly metastasizes via the hematogenous route. However, there are possibility of distant metastasis via the lymphatic and bone dissemination in a few of HCC cases. Case Series: We report two atypical cases of HCC with distant metastasis to cervical lymph node and bone in Malaysia. The first case reported is a HCC case of extrahepatic metastasis to cervical lymph node and the s

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Pei, Qiying, Qian Yi, and Liling Tang. "Liver Fibrosis Resolution: From Molecular Mechanisms to Therapeutic Opportunities." International Journal of Molecular Sciences 24, no. 11 (2023): 9671. http://dx.doi.org/10.3390/ijms24119671.

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The liver is a critical system for metabolism in human beings, which plays an essential role in an abundance of physiological processes and is vulnerable to endogenous or exogenous injuries. After the damage to the liver, a type of aberrant wound healing response known as liver fibrosis may happen, which can result in an excessive accumulation of extracellular matrix (ECM) and then cause cirrhosis or hepatocellular carcinoma (HCC), seriously endangering human health and causing a great economic burden. However, few effective anti-fibrotic medications are clinically available to treat liver fib

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