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Journal articles on the topic 'PI3K-Akt signaling pathway'

Author: Grafiati

Published: 4 June 2021

Last updated: 27 July 2025

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1

Urasaki, Yasuyo, Cody Beaumont, Jeffery N. Talbot, David K. Hill, and Thuc T. Le. "Akt3 Regulates the Tissue-Specific Response to Copaiba Essential Oil." International Journal of Molecular Sciences 21, no. 8 (2020): 2851. http://dx.doi.org/10.3390/ijms21082851.

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This study reports a relationship between Akt3 expression and tissue-specific regulation of the pI3K/Akt/mTOR signaling pathway by copaiba essential oil. Akt3, a protein kinase B isoform important for the regulation of neuronal development, exhibited differential expression levels in cells of various origins. In neuronal and microglial cells, where Akt3 is present, copaiba essential oil positively regulated the pI3K/Akt/mTOR signaling pathway. In contrast, in liver cells and T lymphocytes, where Akt3 is absent, copaiba essential oil negatively regulated the pI3K/Akt/mTOR signaling pathway. The

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Huang, Shu-ping, Ze-chao Zhang, Yu Chen, Chang-jie Shang, Min Zhu, and Wei-hong Li. "Review of Chinese medicine intervention in PI3K/AKT pathway to regulate fibrosis." Medicine 104, no. 28 (2025): e42957. https://doi.org/10.1097/md.0000000000042957.

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The phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway plays a crucial role in the regulation of fibrosis, a pathological process characterized by excessive deposition of extracellular matrix components leading to tissue scarring and dysfunction. Traditional Chinese medicine (TCM) has been increasingly recognized for its potential therapeutic effects in fibrosis by targeting various signaling pathways, including the PI3K/AKT pathway. This review aims to summarize the recent advancements in TCM interventions targeting the PI3K/AKT signaling pathway for the regulation

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Liu, Jiali, Pangao Xu, Dekun Liu, et al. "TCM Regulates PI3K/Akt Signal Pathway to Intervene Atherosclerotic Cardiovascular Disease." Evidence-Based Complementary and Alternative Medicine 2021 (December 16, 2021): 1–11. http://dx.doi.org/10.1155/2021/4854755.

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Vascular endothelial injury is the initial stage of atherosclerosis (AS). Stimulating and activating the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway can regulate the expression of vascular endothelial cytokines, thus affecting the occurrence and development of AS. In addition, the PI3K/Akt signaling pathway can regulate the polarization and survival of macrophages and the expression of inflammatory factors and platelet function, thus influencing the progression of AS. In recent years, traditional Chinese medicine (TCM) has been widely recognized for its advantages

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Sahu, Rakesh, and Bhaskar Sahu. "Inhibitory potential of Nelumbo nucifera Gaertn extract on the PI3K/AKT/mTOR signaling pathway." Cell Signaling 2, no. 1 (2024): 96–101. http://dx.doi.org/10.46439/signaling.2.037.

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Nelumbo nucifera Gaertn (NNG), commonly known as sacred lotus or Indian lotus, has been extensively used in traditional medicine for its various pharmacological properties. Emerging research has focused on elucidating its potential as a therapeutic agent against cancer and other diseases. The phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin (mTOR) signaling pathway plays a crucial role in regulating cellular processes such as cell growth, proliferation, and survival, and its dysregulation is implicated in various diseases, including cancer. This review exam

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Meng, Xianwei, Jun Cui, and Guibin He. "Bcl-2 Is Involved in Cardiac Hypertrophy through PI3K-Akt Pathway." BioMed Research International 2021 (March 12, 2021): 1–8. http://dx.doi.org/10.1155/2021/6615502.

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Cardiac hypertrophy (CH) is a common cause of sudden cardiac death and heart failure, resulting in a significant medical burden. The present study is aimed at exploring potential CH-related pathways and the key downstream effectors. The gene expression profile of GSE129090 was obtained from the Gene Expression Omnibus database (GEO), and 1325 differentially expressed genes (DEGs) were identified, including 785 upregulated genes and 540 downregulated genes. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Reactome pathway enrichment analysis of DEGs were then performed. Although there were no

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Zhang, Qingling, Qi Hu, Jian Li, and Zhirui Lin. "WTX beyond WNT signaling pathway." Visualized Cancer Medicine 4 (2023): 2. http://dx.doi.org/10.1051/vcm/2022006.

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Gastric cancer (GC) is a major malignancy in many developing countries with low early detection rate. As a tumour suppressor gene, WTX inhibits PI3K/AKT/mTOR pathway activity by inhibiting PI3K phosphorylation. WTX loss of WTX protein associates with tumor metastasis and poor survival of GC patients. During GC progression, an aberrantly elevated miR-20a-5p expression has been found, which inhibits WTX expression and induces PI3K phosphorylation, thereby activating the PI3K/AKT/mTOR pathway and promoting cellular proliferation and migration. A new mechanism in which miR-20a-5p promotes GC progr

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Lin, Kai, Xinghua Wu, Yuying Qi, Kaiyin Wang, Yunzhu Guan, and Tinghui Hu. "Mechanism of Glucose Transporter Protein 1 Mediating Malignant Behavior in Breast Cancer Through the PI3K/Akt Signaling Pathway." Science of Advanced Materials 15, no. 9 (2023): 1218–23. http://dx.doi.org/10.1166/sam.2023.4533.

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To investigate the mechanism of action of GLUT1 in mediating breast cancer development through the PI3K/Akt signaling pathway. Knockdown of breast cancer cell line MDA-MB-231 GLUT1 was achieved by siRNA with the addition of IGF-1, an activator of the PI3K/AKT signaling pathway. The experimental groupings were NC, shGLUT1, shNC+IGF-1, and shGLUT1+IGF-1. The proliferation, invasion, and migration behaviors of breast cancer cells were observed by MTT, Transwell, and scratch-repair assays; Western blot was used to detect the protein expression levels of p-PI3K, p-AKT, and p-mTOR in the PI3K-AKT si

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Li, Xiao, Xu Feng, Chunkang Chang, Qi He, and Wu Lingyun. "Identification of microRNA-Regulated Pathways through a Integration of Mcrorna-mRNA Microarray and Bioinformatics Analysis in CD34+ Cells of Myelodysplastic Syndromes." Blood 124, no. 21 (2014): 3238. http://dx.doi.org/10.1182/blood.v124.21.3238.3238.

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Abstract Background MicroRNAs (miRNAs) are considered to play a key role in the pathogenesis of myelodysplastic syndromes (MDS). However, the effect of miRNA and targeted mRNA on signal transduction is not fully understood in MDS. Objective The objective of this study is to identify the miRNAs-regulated pathways. Methods Affymetrix GeneChip microRNA and PrimeView Array were used to analyze miRNAs and gene expression profile of CD34+ cells in 12 MDS patients and 6 healthy controls. Comprehensive bioinformatics analysis of the coordinate expression of miRNAs and mRNAs including Difference, Go, P

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Pungsrinont, Thanakorn, Julia Kallenbach, and Aria Baniahmad. "Role of PI3K-AKT-mTOR Pathway as a Pro-Survival Signaling and Resistance-Mediating Mechanism to Therapy of Prostate Cancer." International Journal of Molecular Sciences 22, no. 20 (2021): 11088. http://dx.doi.org/10.3390/ijms222011088.

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Androgen deprivation therapy (ADT) and androgen receptor (AR)-targeted therapy are the gold standard options for treating prostate cancer (PCa). These are initially effective, as localized and the early stage of metastatic disease are androgen- and castration-sensitive. The tumor strongly relies on systemic/circulating androgens for activating AR signaling to stimulate growth and progression. However, after a certain point, the tumor will eventually develop a resistant stage, where ADT and AR antagonists are no longer effective. Mechanistically, it seems that the tumor becomes more aggressive

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Savova, Martina, Liliya Mihaylova, Daniel Tews, Martin Wabitsch, and Milen Georgiev. "Targeting PI3K/AKT signaling pathway in obesity." Targeting PI3K/AKT signaling pathway in obesity 159 (January 11, 2023): 114244. https://doi.org/10.1016/j.biopha.2023.114244.

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Obesity is a disorder with an increasing prevalence, which impairs the life quality of patients and intensifies societal health care costs. The development of safe and innovative prevention strategies and therapeutic approaches is thus of great importance. The complex pathophysiology of obesity involves multiple signaling pathways that influence energy metabolism in different tissues. The phosphatidylinositol 3-kinases (PI3K)/ protein kinase B (AKT) pathway is critical for the metabolic homeostasis and its function in insulin-sensitive tissues is described in the context of health, obesity and

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Shorning, Boris Y., Manisha S. Dass, Matthew J. Smalley, and Helen B. Pearson. "The PI3K-AKT-mTOR Pathway and Prostate Cancer: At the Crossroads of AR, MAPK, and WNT Signaling." International Journal of Molecular Sciences 21, no. 12 (2020): 4507. http://dx.doi.org/10.3390/ijms21124507.

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Oncogenic activation of the phosphatidylinositol-3-kinase (PI3K), protein kinase B (PKB/AKT), and mammalian target of rapamycin (mTOR) pathway is a frequent event in prostate cancer that facilitates tumor formation, disease progression and therapeutic resistance. Recent discoveries indicate that the complex crosstalk between the PI3K-AKT-mTOR pathway and multiple interacting cell signaling cascades can further promote prostate cancer progression and influence the sensitivity of prostate cancer cells to PI3K-AKT-mTOR-targeted therapies being explored in the clinic, as well as standard treatment

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Fan, Demin, Qiang Liu, Fei Wu, et al. "Prognostic significance of PI3K/AKT/ mTOR signaling pathway members in clear cell renal cell carcinoma." PeerJ 8 (June 1, 2020): e9261. http://dx.doi.org/10.7717/peerj.9261.

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Background Renal cell carcinoma (RCC) is a fatal disease, in which the PI3K/AKT/mTOR signaling pathway serves an important role in the tumorigenesis. Previous studies have reported the prognostic significance of PI3K/AKT/mTOR signaling pathway members in RCC; however, there is insufficient evidence to date to confirm this. Thus, the present study aimed to systematically investigate the prognostic roles of multiple PI3K/AKT/mTOR signaling proteins in clear cell RCC (ccRCC) using online large-scale databases. Methods The mRNA expression profiles of PI3K/AKT/mTOR signaling pathway proteins PTEN,

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Wiese, Wojciech, Julia Barczuk, Olga Racinska, et al. "PI3K/Akt/mTOR Signaling Pathway in Blood Malignancies—New Therapeutic Possibilities." Cancers 15, no. 21 (2023): 5297. http://dx.doi.org/10.3390/cancers15215297.

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Blood malignancies remain a therapeutic challenge despite the development of numerous treatment strategies. The phosphatidylinositol-3 kinase (PI3K)/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway plays a central role in regulating many cellular functions, including cell cycle, proliferation, quiescence, and longevity. Therefore, dysregulation of this pathway is a characteristic feature of carcinogenesis. Increased activation of PI3K/Akt/mTOR signaling enhances proliferation, growth, and resistance to chemo- and immunotherapy in cancer cells. Overactivation of

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Li-Jun, Zhang, Huang Zhi-Li, Wang Yan та Li Qiao-Qiao. "Expression of PI3K/AKT Signaling Pathway in IFN-β-induced Differentiation of Human Mesenchymal Stem Cells into Chondroblasts". International Journal of Sciences Volume 8, № 2019-08 (2019): 23–28. https://doi.org/10.5281/zenodo.3979967.

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Induction of chondrogenic differentiation from MSCs are necessary for qualification as sources of seed cells for cartilage tissue engineering。Our previous research showed IFN-β maybe as a helper of TGF-βto promote chondrogenesis of hMSCs. In this paper, we investigated the expression of PI3K/AKT during the chondrogenic differentiation of hMSCs,hMSCs were divided into Blank control group, TGF-β3 group and TGF-β3+IFN-β1a group and then were induced into cartilage pellets respectively . At day 4,7,14,21, the pellets were collected and qRT-PCR and Western blotting were used to detect the relative

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Nepstad, Ina, Kimberley Joanne Hatfield, Ida Sofie Grønningsæter, and Håkon Reikvam. "The PI3K-Akt-mTOR Signaling Pathway in Human Acute Myeloid Leukemia (AML) Cells." International Journal of Molecular Sciences 21, no. 8 (2020): 2907. http://dx.doi.org/10.3390/ijms21082907.

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Acute myeloid leukemia (AML) is a heterogeneous group of diseases characterized by uncontrolled proliferation of hematopoietic stem cells in the bone marrow. Malignant cell growth is characterized by disruption of normal intracellular signaling, caused by mutations or aberrant external signaling. The phosphoinositide 3-kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR) pathway (PI3K-Akt-mTOR pathway) is among one of the intracellular pathways aberrantly upregulated in cancers including AML. Activation of this pathway seems important in leukemogenesis, and given the central role of this pat

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Smit, Daniel J., Laure Cayrefourcq, Marie-Therese Haider, et al. "High Sensitivity of Circulating Tumor Cells Derived from a Colorectal Cancer Patient for Dual Inhibition with AKT and mTOR Inhibitors." Cells 9, no. 9 (2020): 2129. http://dx.doi.org/10.3390/cells9092129.

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Circulating tumor cells (CTCs) are cells shed from the primary tumor into the bloodstream. While many studies on solid tumor cells exist, data on CTCs are scarce. The mortality of cancer is mostly associated with metastasis and recent research identified CTCs as initiators of metastasis. The PI3K/AKT/mTOR signaling pathway is an intracellular pathway that regulates essential functions including protein biosynthesis, cell growth, cell cycle control, survival and migration. Importantly, activating oncogenic mutations and amplifications in this pathway are frequently observed in a wide variety of

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Xu, Miaomiao, Xiaoguang Liu, Peng Bao, et al. "Skeletal Muscle CSE Deficiency Leads to Insulin Resistance in Mice." Antioxidants 11, no. 11 (2022): 2216. http://dx.doi.org/10.3390/antiox11112216.

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Cystathionine-γ-lyase (CSE) is expressed in various tissues and generates H2S via an alternative desulfuration reaction. We sought to explore the functions of skeletal muscle CSE using skeletal muscle conditional knockout CSE (MCSEKO) mice. It was found that body weight, muscle morphology, and exercise capacity were not altered in MCSEKO mice compared with littermate wild-type mice. RNA-seq-based transcriptome analysis showed that 275 genes were differentially regulated in skeletal muscle and multiple signaling pathways including insulin signaling and mTOR, PI3K-AKT, and cGMP-PKG signaling pat

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Deng, Shuo, Hin Chong Leong, Arpita Datta, Vennila Gopal, Alan Prem Kumar, and Celestial T. Yap. "PI3K/AKT Signaling Tips the Balance of Cytoskeletal Forces for Cancer Progression." Cancers 14, no. 7 (2022): 1652. http://dx.doi.org/10.3390/cancers14071652.

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The PI3K/AKT signaling pathway plays essential roles in multiple cellular processes, which include cell growth, survival, metabolism, and motility. In response to internal and external stimuli, the PI3K/AKT signaling pathway co-opts other signaling pathways, cellular components, and cytoskeletal proteins to reshape individual cells. The cytoskeletal network comprises three main components, which are namely the microfilaments, microtubules, and intermediate filaments. Collectively, they are essential for many fundamental structures and cellular processes. In cancer, aberrant activation of the P

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Narayanankutty, Arunaksharan. "Phytochemicals as PI3K/ Akt/ mTOR Inhibitors and Their Role in Breast Cancer Treatment." Recent Patents on Anti-Cancer Drug Discovery 15, no. 3 (2020): 188–99. http://dx.doi.org/10.2174/1574892815666200910164641.

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Background: Breast cancer is the predominant form of cancer in women; various cellular pathways are involved in the initiation and progression of breast cancer. Among the various types of breast cancer that differ in their growth factor receptor status, PI3K/Akt signaling is a common pathway where all these converge. Thus, the PI3K signaling is of great interest as a target for breast cancer prevention; however, it is less explored. Objective: The present review is aimed to provide a concise outline of the role of PI3K/Akt/mTOR pathway in breast carcinogenesis and its progression events, inclu

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Langhammer, Tina-Susann, Catrin Roolf, Saskia Krohn та ін. "PI3K/Akt Signaling Interacts With Wnt/β-Catenin Signaling But Does Not Induce An Accumulation Of β-Catenin In The Nucleus Of Acute Lymphoblastic Leukemia Cell Lines". Blood 122, № 21 (2013): 4886. http://dx.doi.org/10.1182/blood.v122.21.4886.4886.

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Abstract Signaling pathways play essential roles in biological processes as development, cell proliferation and homeostasis. The accurate modulation of signaling pathways, their adapted interaction and their time- and tissue-specific adjusted regulation are required for normal cell development. PI3K/Akt and Wnt/β-Catenin signaling pathways act as key regulators in cell proliferation, differentiation and growth. Both signaling pathways include GSK3β as a common protein, which may mediate an interaction and cross-talk between the pathways. Aberrant activation of PI3K/Akt signaling has been linke

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Li, Xiaojuan, Yunping Tang, Fangmiao Yu, et al. "Inhibition of Prostate Cancer DU-145 Cells Proliferation by Anthopleura anjunae Oligopeptide (YVPGP) via PI3K/AKT/mTOR Signaling Pathway." Marine Drugs 16, no. 9 (2018): 325. http://dx.doi.org/10.3390/md16090325.

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We investigated the antitumor mechanism of Anthopleura anjunae oligopeptide (AAP-H, YVPGP) in prostate cancer DU-145 cells in vitro and in vivo. Results indicated that AAP-H was nontoxic and exhibited antitumor activities. Cell cycle analysis indicated that AAP-H may arrest DU-145 cells in the S phase. The role of the phosphatidylinositol 3-kinase/protein kinase B/mammalian rapamycin target protein (PI3K/AKT/mTOR) signaling pathway in the antitumor mechanism of APP-H was investigated. Results showed that AAP-H treatment led to dose-dependent reduction in the levels of p-AKT (Ser473), p-PI3K (p

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Sicurella, Mariaconcetta, Marica De Chiara, and Luca Maria Neri. "Hedgehog and PI3K/Akt/mTOR Signaling Pathways Involvement in Leukemic Malignancies: Crosstalk and Role in Cell Death." Cells 14, no. 4 (2025): 269. https://doi.org/10.3390/cells14040269.

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The Hedgehog (Hh) and PI3K/Akt/mTOR signaling pathways play a pivotal role in driving the initiation and progression of various cancers, including hematologic malignancies such as acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML), chronic myeloid leukemia (CML), and chronic lymphocytic leukemia (CLL). These pathways are often dysregulated in leukemia cells, leading to increased cell growth, survival, and drug resistance while also impairing mechanisms of cell death. In leukemia, the Hh pathway can be abnormally activated by genetic mutations. Additionally, the PI3K/Akt/mTOR path

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Singh, Sudha B., Cody A. Braun, Amanda Carroll-Portillo, Cristina N. Coffman та Henry C. Lin. "Sulfate-Reducing Bacteria Induce Pro-Inflammatory TNF-α and iNOS via PI3K/Akt Pathway in a TLR 2-Dependent Manner". Microorganisms 12, № 9 (2024): 1833. http://dx.doi.org/10.3390/microorganisms12091833.

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Desulfovibrio, resident gut sulfate-reducing bacteria (SRB), are found to overgrow in diseases such as inflammatory bowel disease and Parkinson’s disease. They activate a pro-inflammatory response, suggesting that Desulfovibrio may play a causal role in inflammation. Class I phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway regulates key events in the inflammatory response to infection. Dysfunctional PI3K/Akt signaling is linked to numerous diseases. Bacterial-induced PI3K/Akt pathway may be activated downstream of toll-like receptor (TLR) signaling. Here, we tested the

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Cohen, Shenhav, Donghoon Lee, Bo Zhai, Steven P. Gygi, and Alfred L. Goldberg. "Trim32 reduces PI3K–Akt–FoxO signaling in muscle atrophy by promoting plakoglobin–PI3K dissociation." Journal of Cell Biology 204, no. 5 (2014): 747–58. http://dx.doi.org/10.1083/jcb.201304167.

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Activation of the PI3K–Akt–FoxO pathway induces cell growth, whereas its inhibition reduces cell survival and, in muscle, causes atrophy. Here, we report a novel mechanism that suppresses PI3K–Akt–FoxO signaling. Although skeletal muscle lacks desmosomes, it contains multiple desmosomal components, including plakoglobin. In normal muscle plakoglobin binds the insulin receptor and PI3K subunit p85 and promotes PI3K–Akt–FoxO signaling. During atrophy, however, its interaction with PI3K–p85 is reduced by the ubiquitin ligase Trim32 (tripartite motif containing protein 32). Inhibition of Trim32 en

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Sanchez, Vanessa, Cydney Nichols, Hye Kim, Eun Gang, and Yong-Mi Kim. "Targeting PI3K Signaling in Acute Lymphoblastic Leukemia." International Journal of Molecular Sciences 20, no. 2 (2019): 412. http://dx.doi.org/10.3390/ijms20020412.

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Adhesion of acute lymphoblastic leukemia (ALL) cells to bone marrow stroma cells triggers intracellular signals regulating cell-adhesion-mediated drug resistance (CAM-DR). Stromal cell protection of ALL cells has been shown to require active AKT. In chronic lymphocytic leukemia (CLL), adhesion-mediated activation of the PI3K/AKT pathway is reported. A novel FDA-approved PI3Kδ inhibitor, CAL-101/idelalisib, leads to downregulation of p-AKT and increased apoptosis of CLL cells. Recently, two additional PI3K inhibitors have received FDA approval. As the PI3K/AKT pathway is also implicated in adhe

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Dunn, Ewan F., Rachel Fearns, and John H. Connor. "Akt Inhibitor Akt-IV Blocks Virus Replication through an Akt-Independent Mechanism." Journal of Virology 83, no. 22 (2009): 11665–72. http://dx.doi.org/10.1128/jvi.01092-09.

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ABSTRACT Many viruses activate the phosphatidylinositol 3′-kinase (PI3k)/Akt intracellular signaling pathway to promote viral replication. We have analyzed whether a rapidly replicating rhabdovirus, vesicular stomatitis virus (VSV), requires the PI3k/Akt signaling pathway for its replication. Through the use of chemical inhibitors of PI3k and Akt, we show that VSV replication and cytopathic effects do not require activation of these kinases. Inhibitors that block the activating phosphorylations of Akt at threonine 308 (Thr308) and serine 473 (Ser473) did not inhibit VSV protein expression or t

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Tuo, Bi-Guang, Guo-Rong Wen, and Ursula Seidler. "Phosphatidylinositol 3-kinase is involved in prostaglandin E2-mediated murine duodenal bicarbonate secretion." American Journal of Physiology-Gastrointestinal and Liver Physiology 293, no. 1 (2007): G279—G287. http://dx.doi.org/10.1152/ajpgi.00488.2006.

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Prostaglandin E2 (PGE2) plays an important role in the regulation of duodenal bicarbonate (HCO3−) secretion, but its signaling pathway(s) are not fully understood. In the present study, we investigated the signaling pathways involved in PGE2-mediated duodenal HCO3− secretion. Murine duodenal mucosal HCO3− secretion was examined in vitro in Ussing chambers by pH-stat titration in the presence of a variety of signal transduction modulators. Phosphatidylinositol 3-kinase (PI3K) activity was measured by immunoprecipitation of PI3K and ELISA, and Akt phosphorylation was measured by Western analysis

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Ling, Mingfa, Lulu Quan, Xumin Lai, et al. "VEGFB Promotes Myoblasts Proliferation and Differentiation through VEGFR1-PI3K/Akt Signaling Pathway." International Journal of Molecular Sciences 22, no. 24 (2021): 13352. http://dx.doi.org/10.3390/ijms222413352.

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It has been demonstrated that vascular endothelial growth factor B (VEGFB) plays a vital role in regulating vascular biological function. However, the role of VEGFB in regulating skeletal muscle cell proliferation and differentiation remains unclear. Thus, this study aimed to investigate the effects of VEGFB on C2C12 myoblast proliferation and differentiation and to explore the underlying mechanism. For proliferation, VEGFB significantly promoted the proliferation of C2C12 myoblasts with the upregulating expression of cyclin D1 and PCNA. Meanwhile, VEGFB enhanced vascular endothelial growth fa

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Mehra, Siddharth, Nilesh Deshpande, and Nagaraj Nagathihalli. "Targeting PI3K Pathway in Pancreatic Ductal Adenocarcinoma: Rationale and Progress." Cancers 13, no. 17 (2021): 4434. http://dx.doi.org/10.3390/cancers13174434.

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Pancreatic ductal adenocarcinoma (PDAC) remains among the deadliest solid tumors that remain treatment-refractory and show a dismal prognosis. More than 90% of PDAC tumors harbor mutations in the K-Ras that exert a strong pro-tumorigenic effect by activating several downstream effector pathways, including phosphatidylinositol-3-kinase (PI3K)-Akt. The role of frequently activated PI3K/Akt pathway in promoting PDAC aggressiveness is well established. Therapeutic approaches targeting PI3K and downstream signaling components in different cellular compartments, including tumor, stromal and immune c

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Su, Yu-Chieh, Wei-Chang Lee, Chih-Chun Wang, Shyh-An Yeh, Wen-Hui Chen, and Po-Jen Chen. "Targeting PI3K/AKT/mTOR Signaling Pathway as a Radiosensitization in Head and Neck Squamous Cell Carcinomas." International Journal of Molecular Sciences 23, no. 24 (2022): 15749. http://dx.doi.org/10.3390/ijms232415749.

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Globally, there are over half a million new patients with head and neck squamous cell carcinomas (HNSCC) every year. The current therapeutic approaches to HNSCC are surgery and adjuvant radiotherapy. These approaches carry a high incidence of metastasis or recurrence from HNSCC cells’ radioresistance. Recent studies have revealed that a combination with radiosensitizers can be used to improve the radioresistance in HNSCC; however, few agents are approved as radiosensitizers. The constitutive activation of phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT)/mammalian target of rapamycin

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Marzec, Michal, Xiaobin Liu, Monika Kasprzycka, et al. "IL-2– and IL-15–induced activation of the rapamycin-sensitive mTORC1 pathway in malignant CD4+ T lymphocytes." Blood 111, no. 4 (2008): 2181–89. http://dx.doi.org/10.1182/blood-2007-06-095182.

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We examined functional status, activation mechanisms, and biologic role of the mTORC1 signaling pathway in malignant CD4+ T cells derived from the cutaneous T-cell lymphoma (CTCL). Whereas the spontaneously growing CTCL-derived cell lines displayed persistent activation of the TORC1 as well as the PI3K/Akt and MEK/ERK pathways, the IL-2–dependent cell lines activated the pathways in response to IL-2 and IL-15 but not IL-21. Activation of mTORC1 and MEK/ERK was nutrient dependent. The mTORC1, PI3K/Akt, and MEK/ERK pathways could also be activated by IL-2 in the primary leukemic, mitogen-preacti

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Singh, Shikha Satendra. "Characterization of a novel regulator of AKT/mTOR signaling in gastric cancer." Journal of Clinical Oncology 34, no. 4_suppl (2016): 68. http://dx.doi.org/10.1200/jco.2016.34.4_suppl.68.

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68 Background: Gastric cancer (GC) is a leading cause of cancer-related death with poor prognosis and “one-size fits all approach”. Dysregulation of PI3K/Akt/mTOR pathway is a common event in GC with PIK3CAmutations reported to correlate with poor prognosis. With prognosis far from satisfactory, we aimed to identify novel surrogate biomarkers. We hypothesize the role of DP103, a DEAD-box RNA helicase, as a novel surrogate biomarker for GC by regulating the PI3K/Akt/mTOR pathway. Additionally, we shed light on high DP103 GC cells responding to Akt/mTOR dual inhibitor treatment, indicating its p

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Zhao, Xingsheng, Yu Ren, Hongkun Ren, et al. "The mechanism of myocardial fibrosis is ameliorated by myocardial infarction-associated transcript through the PI3K/Akt signaling pathway to relieve heart failure." Journal of International Medical Research 49, no. 7 (2021): 030006052110314. http://dx.doi.org/10.1177/03000605211031433.

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Objective This study aimed to investigate the role of long noncoding RNA (LncRNA) myocardial infarction-associated transcript (MIAT) in a heart failure (HF) model in vivo and in vitro by regulating the PI3K/Akt signaling pathway. Methods We established HF models in vivo and in vitro and evaluated the collagen content of these models and other factors. Results We found that when LncRNA MIAT was silenced, vascular endothelial growth factor, phosphorylated protein kinase B (Akt), and phosphorylated phosphoinositide 3-kinase (PI3K) mRNA and protein levels were significantly downregulated, which su

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Wang, Bing-jie, Wang-long Zheng, Nan-nan Feng, et al. "The Effects of Autophagy and PI3K/AKT/m-TOR Signaling Pathway on the Cell-Cycle Arrest of Rats Primary Sertoli Cells Induced by Zearalenone." Toxins 10, no. 10 (2018): 398. http://dx.doi.org/10.3390/toxins10100398.

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A high concentration of Zearalenone (ZEA) will perturb the differentiation of germ cells, and induce a death of germ cells, but the toxic mechanism and molecular mechanism remain unclear. The Sertoli cells (SCs) play an irreplaceable role in spermatogenesis. In order to explore the potential mechanism of ZEA male reproductive toxicity, we studied the effects of ZEA on cell proliferation, cell-cycle distribution, cell-cycle-related proteins and autophagy-related pathway the PI3K/Akt/mTOR signaling in primary cultured rats SCs, and the effects of autophagy and PI3K/AKT/m TOR signaling pathway on

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Bang, Jieun, Mihyeon Jun, Soyun Lee, Hyuk Moon, and Simon Weonsang Ro. "Targeting EGFR/PI3K/AKT/mTOR Signaling in Hepatocellular Carcinoma." Pharmaceutics 15, no. 8 (2023): 2130. http://dx.doi.org/10.3390/pharmaceutics15082130.

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Hepatocellular carcinoma (HCC) poses a significant global health concern, with its incidence steadily increasing. The development of HCC is a multifaceted, multi-step process involving alterations in various signaling cascades. In recent years, significant progress has been made in understanding the molecular signaling pathways that play central roles in hepatocarcinogenesis. In particular, the EGFR/PI3K/AKT/mTOR signaling pathway in HCC has garnered renewed attention from both basic and clinical researchers. Preclinical studies in vitro and in vivo have shown the effectiveness of targeting th

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Showler, Kaye, Mayumi Nishimura, Kazuhiro Daino, et al. "Analysis of genes involved in the PI3K/Akt pathway in radiation- and MNU-induced rat mammary carcinomas." Journal of Radiation Research 58, no. 2 (2016): 183–94. http://dx.doi.org/10.1093/jrr/rrw097.

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Abstract The PI3K/AKT pathway is one of the most important signaling networks in human breast cancer, and since it was potentially implicated in our preliminary investigations of radiation-induced rat mammary carcinomas, our aim here was to verify its role. We included mammary carcinomas induced by the chemical carcinogen 1-methyl-1-nitrosourea to determine whether any changes were radiation-specific. Most carcinomas from both groups showed activation of the PI3K/AKT pathway, but phosphorylation of AKT1 was often heterogeneous and only present in a minority of carcinoma cells. The negative pat

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Wang, Xiao-Mei, Min Yao, Shu-Xia Liu, Jun Hao, Qing-Juan Liu, and Feng Gao. "Interplay between the Notch and PI3K/Akt pathways in high glucose-induced podocyte apoptosis." American Journal of Physiology-Renal Physiology 306, no. 2 (2014): F205—F213. http://dx.doi.org/10.1152/ajprenal.90005.2013.

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Podocyte apoptosis contributes to the pathogenesis of diabetic nephropathy (DN). However, the mechanisms that mediate high glucose (HG)-induced podocyte apoptosis remain poorly understood. Conditionally immortalized mouse podocytes were cultured in HG medium. A chemical inhibitor or a specific short-hairpin RNA (shRNA) vector was used to inhibit the activation of the Notch pathway and the PI3K/Akt pathway in HG-treated podocytes. Western blotting and real-time PCR were used to evaluate the levels of Notch, PI3K/Akt, and apoptotic pathway signaling. The apoptosis rate of HG-treated podocytes wa

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Fresno, Vara Juan Angel, Castro Javier de, and Manuel González-Barón. "PI3K/Akt signalling pathway and cance." Cancer Treatment Reviews 30 (April 1, 2004): 193–204. https://doi.org/10.1016/j.ctrv.2003.07.007.

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The article by Fresno Vara et al. is a comprehensive review of the PI3K/Akt signaling pathway and its role in cancer. Although the relevance of this pathway had already been identified in several types of cancer, this study consolidated its importance in cell proliferation, survival, invasion and angiogenesis. In addition, it highlighted how PI3K/Akt dysfunction contributes to treatment resistance and metastasis, key features of malignant tumors. It emphasized that disruption of this pathway favors uncontrolled proliferation and evasion of programmed cell death, which can result in increased r

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Huang, Lu, Qiong Yang, Huihong Chen, Zhenggeng Wang, Qi Liu, and Shuhua Ai. "Tollip promotes hepatocellular carcinoma progression via PI3K/AKT pathway." Open Medicine 17, no. 1 (2022): 626–37. http://dx.doi.org/10.1515/med-2022-0453.

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Abstract The activation of signaling pathways induced by Toll-like receptor (TLR) has been demonstrated to play essential roles in multiple liver diseases. Toll-interacting protein (Tollip) acts as an endogenous negative modulator of TLR signaling and is implicated in various cardio-metabolic diseases. However, the effect of Tollip in hepatocellular carcinoma (HCC) remains elusive. In the current study, enhanced Tollip expression was observed in HCC cells and tissues examined by RT-PCR, western blot, and immunohistochemistry staining. Moreover, the co-immunofluorescence staining demonstrated t

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Darici, Salihanur, Hazem Alkhaldi, Gillian Horne, Heather G. Jørgensen, Sandra Marmiroli, and Xu Huang. "Targeting PI3K/Akt/mTOR in AML: Rationale and Clinical Evidence." Journal of Clinical Medicine 9, no. 9 (2020): 2934. http://dx.doi.org/10.3390/jcm9092934.

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Acute myeloid leukemia (AML) is a highly heterogeneous hematopoietic malignancy characterized by excessive proliferation and accumulation of immature myeloid blasts in the bone marrow. AML has a very poor 5-year survival rate of just 16% in the UK; hence, more efficacious, tolerable, and targeted therapy is required. Persistent leukemia stem cell (LSC) populations underlie patient relapse and development of resistance to therapy. Identification of critical oncogenic signaling pathways in AML LSC may provide new avenues for novel therapeutic strategies. The phosphatidylinositol-3-kinase (PI3K)/

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Li, Jing, Xien Wang, Feng Xu, Yingjie Wu, Feizhen Xia, and Peng Wan. "Molecular Mechanism of Phosphatidylinositol 3-Kinase (PI3K)/Protein Kinase B (AKT) Signaling Pathway-Mediated Autophagy in Gastric Cancer." Journal of Biomaterials and Tissue Engineering 10, no. 2 (2020): 223–27. http://dx.doi.org/10.1166/jbt.2020.2234.

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Gastric cancer seriously threats to the life and health of patient. Abnormal autophagy is related to several diseases, such as aging, neurodegenerative diseases, and gastric cancer. PI3K/Akt signaling mediates multiple biological processes including autophagy. The role of autophagy in gastric cancer and its potential clinical value remains to be further discussed. This study explores the clinical significance of PI3K/Akt signaling in autophagy. Gastric cancer patients received surgeries in our hospital were enrolled as subjects. The tumor tissue and paracarcinoma tissue were extracted. PI3K/Ak

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Liu, Wei, Hongmiao Ren, Jihao Ren, et al. "The Role of EGFR/PI3K/Akt/cyclinD1 Signaling Pathway in Acquired Middle Ear Cholesteatoma." Mediators of Inflammation 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/651207.

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Cholesteatoma is a benign keratinizing and hyper proliferative squamous epithelial lesion of the temporal bone. Epidermal growth factor (EGF) is one of the most important cytokines which has been shown to play a critical role in cholesteatoma. In this investigation, we studied the effects of EGF on the proliferation of keratinocytes and EGF-mediated signaling pathways underlying the pathogenesis of cholesteatoma. We examined the expressions of phosphorylated EGF receptor (p-EGFR), phosphorylated Akt (p-Akt), cyclinD1, and proliferating cell nuclear antigen (PCNA) in 40 cholesteatoma samples an

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Cornejo, Melanie G., Stephen M. Sykes, Cristina Lo Celso, et al. "A Regulatory Network Between Notch and AKT Signaling Pathways Differentially Controls Megakaryocyte Development From Hematopoietic Stem or Committed Progenitor Cells." Blood 114, no. 22 (2009): 384. http://dx.doi.org/10.1182/blood.v114.22.384.384.

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Abstract Abstract 384 The Notch signaling pathway is implicated in a broad range of developmental processes, including cell fate decisions. However, the molecular basis for its role at the different steps of stem cell lineage commitment to a specific lineage is unclear. During hematopoiesis, the Notch signaling pathway is known to play an important role in T cell lineage development. Recently, we demonstrated that the Notch signaling pathway is also a positive regulator of megakaryocyte lineage specification from hematopoietic stem cells (HSC). The importance of a tight regulation of this latt

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Yuan, Yeqin, Huizhi Long, Ziwei Zhou, Yuting Fu, and Binyuan Jiang. "PI3K–AKT-Targeting Breast Cancer Treatments: Natural Products and Synthetic Compounds." Biomolecules 13, no. 1 (2023): 93. http://dx.doi.org/10.3390/biom13010093.

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Breast cancer is the most commonly diagnosed cancer in women. The high incidence of breast cancer, which is continuing to rise, makes treatment a significant challenge. The PI3K–AKT pathway and its downstream targets influence various cellular processes. In recent years, mounting evidence has shown that natural products and synthetic drugs targeting PI3K–AKT signaling have the potential to treat breast cancer. In this review, we discuss the role of the PI3K–AKT signaling pathway in the occurrence and development of breast cancer and highlight PI3K–AKT-targeting natural products and drugs in cl

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Urasaki, Yasuyo, Cody Beaumont, Michelle Workman, Jeffery N. Talbot, David K. Hill, and Thuc T. Le. "Fast-Acting and Receptor-Mediated Regulation of Neuronal Signaling Pathways by Copaiba Essential Oil." International Journal of Molecular Sciences 21, no. 7 (2020): 2259. http://dx.doi.org/10.3390/ijms21072259.

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This study examined the biological activities of copaiba essential oil via measurement of its effects on signaling pathways in the SH-SY5Y neuronal cell line. Nanofluidic proteomic technologies were deployed to measure the phosphorylation of biomarker proteins within the signaling cascades. Interestingly, copaiba essential oil upregulated the pI3K/Akt/mTOR, MAPK, and JAK/STAT signaling pathways in neuronal cells. The effects of copaiba essential oil peaked at 30 min post-treatment, with a half-maximal effective concentration (EC50) of approximately 80 ng/mL. Treatment with cannabinoid receptor

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Das, Margaret, Erica Scappini, Negin P. Martin та ін. "Regulation of Neuron Survival through an Intersectin-Phosphoinositide 3′-Kinase C2β-AKT Pathway". Molecular and Cellular Biology 27, № 22 (2007): 7906–17. http://dx.doi.org/10.1128/mcb.01369-07.

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ABSTRACT While endocytosis attenuates signals from plasma membrane receptors, recent studies suggest that endocytosis also serves as a platform for the compartmentalized activation of cellular signaling pathways. Intersectin (ITSN) is a multidomain scaffolding protein that regulates endocytosis and has the potential to regulate various biochemical pathways through its multiple, modular domains. To address the biological importance of ITSN in regulating cellular signaling pathways versus in endocytosis, we have stably silenced ITSN expression in neuronal cells by using short hairpin RNAs. Decre

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Carón, Rubén W., Adly Yacoub, Xiaoyu Zhu, et al. "H-RAS V12–induced radioresistance in HCT116 colon carcinoma cells is heregulin dependent." Molecular Cancer Therapeutics 4, no. 2 (2005): 243–55. http://dx.doi.org/10.1158/1535-7163.243.4.2.

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Abstract The abilities of mutated active K-RAS and H-RAS proteins, in an isogenic human carcinoma cell system, to modulate the activity of signaling pathways following exposure to ionizing radiation is unknown. Loss of K-RAS D13 expression in HCT116 colorectal carcinoma cells blunted basal extracellular signal-regulated kinase 1/2 (ERK1/2), AKT, and c-Jun NH2-terminal kinase 1/2 activity. Deletion of the allele to express K-RAS D13 also enhanced expression of ERBB1, ERBB3, and heregulin but nearly abolished radiation-induced activation of all signaling pathways. Expression of H-RAS V12 in HCT1

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Jung, Eun-Ju, Jae-Hwan Jo, Claudine Uwamahoro, et al. "Ritonavir Has Reproductive Toxicity Depending on Disrupting PI3K/PDK1/AKT Signaling Pathway." Toxics 12, no. 1 (2024): 73. http://dx.doi.org/10.3390/toxics12010073.

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Ritonavir (RTV) is an antiviral and a component of COVID-19 treatments. Moreover, RTV demonstrates anti-cancer effects by suppressing AKT. However, RTV has cytotoxicity and suppresses sperm functions by altering AKT activity. Although abnormal AKT activity is known for causing detrimental effects on sperm functions, how RTV alters AKT signaling in spermatozoa remains unknown. Therefore, this study aimed to investigate reproductive toxicity of RTV in spermatozoa through phosphoinositide 3-kinase/phosphoinositide-dependent protein kinase-1/protein kinase B (PI3K/PDK1/AKT) signaling. Duroc sperma

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Xiao, Quan, Yun Teng, Changming Xu, et al. "Role of PI3K/AKT Signaling Pathway in Nucleus Pulposus Cells." BioMed Research International 2021 (July 1, 2021): 1–9. http://dx.doi.org/10.1155/2021/9941253.

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Objective. To investigate the role of PI3K/AKT signaling pathway in nucleus pulposus (NP) cells. Methods. Nucleus pulposus (NP) cells were isolated from SD rat, and thereafter, passage three (P3) NP cells were divided into the following experimental groups: control, PI3K/AKT agonist IGF-1 (25 ng/ml, 50 ng/ml, and 100 ng/ml), and PI3K/AKT inhibitor LY294002 (5 μM, 10 μM, and 20 μM). Flow cytometry and BrdU cell proliferation assays were performed to assess apoptosis and the proliferation rate of NP cells. Western blot analysis was performed to examine the protein expression level of Col II, Col

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Alqahtani, Ali, Hazem S. K. Ayesh, and Hafez Halawani. "PIK3CA Gene Mutations in Solid Malignancies: Association with Clinicopathological Parameters and Prognosis." Cancers 12, no. 1 (2019): 93. http://dx.doi.org/10.3390/cancers12010093.

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Phosphoinositide kinases (PIKs) are a group of lipid kinases that are important upstream activators of various significant signaling pathways. Hyperactivation of the PI3K/AKT/mTOR pathways—either via mutations or genomic amplification—confers key oncogenic activity, essential for the development and progression of several solid tumors. Alterations in the PIK3CA gene are associated with poor prognosis of solid malignancies. Although the literature reports contradictory prognostic values of PIK3CA in aggressive cancers, most of the available data highlight the important role of PIK3CA mutation i

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