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Letteratura scientifica selezionata sul tema "Forkhead box protein A1"

Autore: Grafiati

Pubblicato: 10 dicembre 2022

Ultima modifica: 28 gennaio 2023

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Articoli di riviste sul tema "Forkhead box protein A1"

1

Jain, Rohit K., Rutika J. Mehta, Harikrishna Nakshatri, Muhammad T. Idrees e Sunil S. Badve. "High-level expression of forkhead-box protein A1 in metastatic prostate cancer". Histopathology 58, n. 5 (14 marzo 2011): 766–72. http://dx.doi.org/10.1111/j.1365-2559.2011.03796.x.

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2

HE, KELI, HUI ZENG, XIANQUN XU, ANLING LI, QING CAI e XINGHUA LONG. "Clinicopathological significance of forkhead box protein A1 in breast cancer: A meta-analysis". Experimental and Therapeutic Medicine 11, n. 6 (6 aprile 2016): 2525–30. http://dx.doi.org/10.3892/etm.2016.3229.

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3

Ma, Wenqi, Jue Jiang, Miao Li, Hua Wang, Hongli Zhang, Xin He, Lili Huang e Qi Zhou. "The clinical significance of forkhead box protein A1 and its role in colorectal cancer". Molecular Medicine Reports 14, n. 3 (1 agosto 2016): 2625–31. http://dx.doi.org/10.3892/mmr.2016.5583.

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4

Gayyed, MarianaF, MagdyF Ahmed, MedhatM Soliman e Maram El-Hussieny. "Expression and prognostic significance of caveolin-1 and forkhead box protein A1 in gastric adenocarcinoma". Egyptian Journal of Pathology 40, n. 2 (2020): 162. http://dx.doi.org/10.4103/egjp.egjp_2_21.

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5

Hu, Dong Gui, e Peter I. Mackenzie. "Forkhead Box Protein A1 Regulates UDP-Glucuronosyltransferase 2B15 Gene Transcription in LNCaP Prostate Cancer Cells". Drug Metabolism and Disposition 38, n. 12 (24 agosto 2010): 2105–9. http://dx.doi.org/10.1124/dmd.110.035436.

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6

Song, Lan, Zhaojun Xu, Ling Li, Mei Hu, Lijuan Cheng, Lingli Chen e Bo Zhang. "Forkhead box protein A1 inhibits the expression of uncoupling protein 2 in hydrogen peroxide-induced A549 cell line". Cell Stress and Chaperones 19, n. 1 (28 aprile 2013): 53–60. http://dx.doi.org/10.1007/s12192-013-0433-z.

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7

Ren, Hongyu, Pei Zhang, Yong Tang, Mengping Wu e Weikang Zhang. "Forkhead Box Protein A1 is a Prognostic Predictor and Promotes Tumor Growth of Gastric Cancer [Retraction]". OncoTargets and Therapy Volume 15 (luglio 2022): 829–30. http://dx.doi.org/10.2147/ott.s383786.

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8

Liu, Jian, Bohua Chen, Bin Yue e Junde Yang. "MicroRNA-212 suppresses the proliferation and migration of osteosarcoma cells by targeting forkhead box protein A1". Experimental and Therapeutic Medicine 12, n. 6 (7 novembre 2016): 4135–41. http://dx.doi.org/10.3892/etm.2016.3880.

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9

Wang, Shixiong, Sachin Singh, Madhumohan Katika, Sandra Lopez-Aviles e Antoni Hurtado. "High Throughput Chemical Screening Reveals Multiple Regulatory Proteins on FOXA1 in Breast Cancer Cell Lines". International Journal of Molecular Sciences 19, n. 12 (19 dicembre 2018): 4123. http://dx.doi.org/10.3390/ijms19124123.

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Abstract (sommario):

Forkhead box A1 (FOXA1) belongs to the forkhead class transcription factor family, playing pioneering function for hormone receptors in breast and prostate cancers, and mediating activation of linage specific enhancers. Interplay between FOXA1 and breast cancer specific signaling pathways has been reported previously, indicating a regulation network on FOXA1 in breast cancer cells. Here in this study, we aimed to identify which are the proteins that could potentially control FOXA1 function in breast cancer cell lines expressing different molecular markers. We first established a luciferase reporter system reflecting FOXA1 binding to DNA. Then, we applied high throughput chemical screening of multiple protein targets and mass spectrometry in breast cancer cell lines expressing different molecular markers: ER positive/HER2 negative (MCF-7), ER positive/HER2 positive (BT474), and ER negative/HER2 positive (MDA-MB-453). Regardless of estrogen receptor status, HER2 (human epidermal growth factor receptor 2) enriched cell lines showed similar response to kinase inhibitors, indicating the control of FOXA1 by cell signaling kinases. Among these kinases, we identified additional receptor tyrosine kinases and cyclin-dependent kinases as regulators of FOXA1. Furthermore, we performed proteomics experiments from FOXA1 inmunoprecipitated protein complex to identify that FOXA1 interacts with several proteins. Among all the targets, we identified cyclin-dependent kinase 1 (CDK1) as a positive factor to interact with FOXA1 in BT474 cell line. In silico analyses confirmed that cyclin-dependent kinases might be the kinases responsible for FOXA1 phosphorylation at the Forkhead domain and the transactivation domain. These results reveal that FOXA1 is potentially regulated by multiple kinases. The cell cycle control kinase CDK1 might control directly FOXA1 by phosphorylation and other kinases indirectly by means of regulating other proteins.

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Wang, Li-Li, Yin-Ling Xiu, Xi Chen, Kai-Xuan Sun, Shuo Chen, Dan-Dan Wu, Bo-Liang Liu e Yang Zhao. "The transcription factor FOXA1 induces epithelial ovarian cancer tumorigenesis and progression". Tumor Biology 39, n. 5 (maggio 2017): 101042831770621. http://dx.doi.org/10.1177/1010428317706210.

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FOXA1 (forkhead box A1), a member of the FOXA transcription factor superfamily, plays an important role in tumor occurrence and development. However, the relationship between FOXA1 and ovarian cancer has not been reported. We examined normal ovarian tissue and ovarian cancer tissue and found increased FOXA1 expression in the cancer tissue. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and flow cytometry assays demonstrated that transfection with small interfering RNA to silence FOXA1 (si-FOXA1) in ovarian cancer cell lines decreased cell proliferation and induced apoptosis and S-phase arrest. In addition, si-FOXA1 transfection inhibited cell migration and invasion. Western blotting showed that si-FOXA1 transfection decreased the levels of YY1-associated protein 1, cyclin-dependent kinase 1, cyclin D1, phosphatidylinositol-3 kinase, E2F transcription factor 1, B-cell lymphoma 2, and vascular endothelial growth factor A protein. Based on these results, we suggest that FOXA1 plays a catalytic role in ovarian cancer pathogenesis and development by affecting the expression of the above-mentioned proteins.

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Più fonti

Tesi sul tema "Forkhead box protein A1"

1

Tong, Ho-kwan. "Functional regulation of the forkhead box M1 transcription factor by Raf/MEK/MAPK signaling". Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B37654597.

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Tong, Ho-kwan, e 湯皓鈞. "Functional regulation of the forkhead box M1 transcription factor by Raf/MEK/MAPK signaling". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37654597.

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Ricci, Anamaria Ritti. "FOXO3a em leiomioma e leiomiossarcoma uterinos: avaliação de seu potencial para terapia alvo in vitro". Universidade de São Paulo, 2018. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-27022019-123144/.

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Os tumores de musculatura liso do útero se desenvolvem a partir do miométrio e podem apresentar carcterísticas clínicas malignas e benignas. Dentre eles, o leiomiossarcoma (LMS) é o tumor maligno mais comum, com altas taxas de metástase e recidiva, mesmo sendo diagnosticado em estágios iniciais. Já os leiomiomas (LM) são os tumores benignos mais frequentes em mulheres em idade reprodutiva. Ambos possuem mesma diferenciação celular, porém com comportamentos clínico e biológico bastante distintos, e até o momento não se dispõe de tratamento específico ou curativo. Nesse contexto, a busca por novos alvos moleculares pode contribuir não só para um melhor entendimento dessas neoplasias, como também para a descoberta de novas terapias. Em estudo prévio foi observada a expressão aumentada de FOXO3a nos sarcomas uterinos, em comparação aos LMs e ao miométrio adjacente (MM). Além disso, sua expressão foi crescente de acordo com o potencial de malignidade do tumor. Assim, o objetivo do presente estudo foi avaliar in vitro o efeito de terapia alvo específica para FOXO3a em células de LM e LMS. Para isto, linhagens celulares de MM (ATCC PCS-460-011), LM (THESCs - CRL-4003) e LMS (SK-UT-1 - HTB-114) foram caracterizadas quanto à expressão basal de FOXO3a (gene e proteína) e submetidas a tratamento com Genisteína e Metformina ou inativação do gene por siRNA. Os efeitos dos tratamentos foram avaliados por PCR em tempo real, Western Blot, imunocitoquímica, ensaios de proliferação, migração e apoptose. Nossos resultados mostraram que todos os tratamentos realizados interferiram na capacidade de proliferação e migração das células, com maior inibição após as 48 horas nos LMS e 72h nos LM. O efeito obtido na transfecção com siRNA apresentou maior eficiência após 48 h da transfecção nos LMS e 72h nos LM. Os efeitos da inibição de FOXO3a foram maiores na proliferação e migração dos LM, porém os resultados não foram estatisticamente significativos. Dentre as substâncias testadas, a Metformina apresentou maior efeito sobre a proliferação, migração e viabilidade das linhagens celulares. A Genisteína também apresentou efeito inibitório nas células, porém o controle com veículo também apresentou o mesmo efeito citotóxico. De modo geral, os efeitos obtidos com os fármacos, foram tempo e concentração dependentes. Em conjunto, nossos resultados sugerem um relevante do FOXO3a nos tumores de musculatura lisa uterinos, além de apresentá-lo como potencial alvo para terapia específica
Smooth muscle tumors of the uterus develop from the myometrium and may present benign and malignant clinical features. Among them, leiomyosarcoma (LMS) is the most frequent malignant tumor, with high rates of metastasis and relapse, even when diagnosed in early stages. On the other hand, leiomyomas (LM) are the most frequent benign tumors in women of reproductive age. Both have the same cellular differentiation, but with very different clinical and biological behaviors, and so far no specific or curative treatment is available. In this context, the search for new molecular targets can contribute not only for a better understanding of these neoplasms, but also for the discovery of new therapies. In a previous study, increased expression of FOXO3a in uterine sarcomas was observed, compared to LMs and adjacent myometrium (MM). In addition, its expression was increasing according to the malignancy potential of the tumor. Thus, the aim of the present study was to evaluate in vitro, the effect of specific targeted therapy for FOXO3a on LM and LMS cells. For this, MM (ATCC PCS-460-011), LM (THESCs-CRL-4003) and LMS (SK-UT-1-HTB-114) cell lines were characterized for basal expression of FOXO3a (gene and protein) and subsequently submitted to treatment with metformin and genistein, or silencing of FOXO3a by siRNA. The effects of the treatments were evaluated by real-time PCR, Western Blot, immunocytochemistry, proliferation, migration and apoptosis assays. Our results showed that all treatments interfered in the proliferation and migration capacity of the cells, with greater inhibition after 48 hours for LMS and 72 hours LM. The effect obtained in the transfection with siRNA showed higher efficiency after 48 hours of transfection in LMS and 72 hours in LM. The effects of inhibition of FOXO3a were greater in the proliferation and migration of the LM, but the results were not statistically significant. Among the substances tested, Metformin had a greater effect on proliferation, migration and viability of the cell lines. Genistein also had an inhibitory effect on the cells, but the control with the vehicle also presented the same cytotoxic effect. In general, the effects obtained with the drugs were time and concentration dependent. Together, our results suggest a relevant role of FOXO3a in uterine smooth muscle tumors, in addition to presenting it as a potential target for specific therapy

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Rohini, Rajan Meenu. "Unraveling Mechanisms of Insulin Resistance in Type 2 Diabetes in Human Adipocytes : Role of extracellular signal regulated kinase 1/2 (ERK1/2) and forkhead box protein 01 (FOX01)". Doctoral thesis, Linköpings universitet, Avdelningen för cellbiologi, 2016. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-131421.

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Type 2 Diabetes is characterized by hyperglycemia primarily caused due to insulin resistance in insulin responsive tissues and insufficient production of insulin by the β-cells. Insulin resistance appears to develop first in the expanding adipose tissue during caloric surplus and affects other tissues like liver and muscle by ectopic fat accumulation. In spite of significant research in field of insulin signaling, very little has been known about the mechanisms that lead to insulin resistance and T2D. We aim for network-wide knowledge of insulin signaling in human adipocytes and to identify mechanisms that can induce insulin resistance in diabetic individuals. We have herein focused on the transcriptional control of insulin via ERK and FOXO1, and have used mathematical modelling to gain a systems-level understanding of insulin signaling network. Through the work in this thesis, we present for the first time a dynamic comprehensive model for insulin signaling for the adipocytes, for both metabolic and transcriptional control, and that can simulate data from both normal and diabetic individuals. We described insulin regulation of ERK phosphorylation and showed that both its insulin sensitivity and maxima response to insulin was curtailed in adipocytes from diabetic individuals (Paper I). Our findings indicate that insulin regulated ERK pathway exerts control on transcription not only through phosphorylation of Elk-1 but also through phosphorylation of FOXO1 and exerts translational control via phosphorylation of ribosomal protein S6 (Paper I, II). Furthermore, we showed that insulin-induced FOXO1 phosphorylation or its insulin sensitivity was not impaired in diabetic individuals, although FOXO1 protein level was reduced by 45% in adipocytes from patients with type 2 diabetes. Comprehensive analysis of the detailed insulin signaling model showed that attenuation of the feedback from mTORC1 to IRS1-Ser307 explained dominant part of the insulin resistance seen in adipocytes from diabetic individuals (Paper II). More interestingly, inhibition of FOXO1 with a dominant negative construct of FOXO1, mimicked the diabetic state in the adipocytes, with the similarity extending to both insulin signaling as well as the reduced protein levels, as seen in the diabetic adipocytes. We also show that mTORC1 and FOXO1 maintain each other’s expression/activity in the human adipocytes (Paper II, III). Our findings thus demonstrate that the interplay between mTORC1 and FOXO1 maintains normal insulin signaling in the human adipocytes.

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Chappert, Pascal. "Homéostasie et mécanisme d'action in vivo des lymphocytes T régulateurs CD4+CD25+Foxp3+ chez la souris". Paris 6, 2007. http://www.theses.fr/2007PA066312.

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Homéostasie et mécanisme d’action in vivo des lymphocytes T régulateurs CD4+CD25+Foxp3+ chez la souris Parmi les différentes sous populations de cellules T, les cellules T régulatrices CD4+CD25+ (Tregs), gouvernées par le facteur de transcription Foxp3, représentent un lignage unique de cellules dédiées au maintien de la tolérance immune au soi. Des travaux préalables au sein du laboratoire avaient pu montrer leur potentialité dans le cadre de protocoles d’induction de tolérance à long terme en thérapie génique ou cellulaire vis-à-vis d’un antigène donné chez la souris. Les travaux présentés ici ont porté sur divers aspects fondamentaux du mécanisme d’action et de l’homéostasie de ces cellules in vivo dans ces modèles murins non lymphopéniques. Dans un premier temps, nous avons pu montrer que l’action de Tregs spécifiques de l’antigène de rejet, dans les deux modèles étudiés, passait par une altération profonde de l’activation de la réponse T CD8+, conduisant à une inhibition presque totale de la prolifération et de la différentiation de ces cellules in vivo. Nous avons ensuite étudié les modes de recrutement possible in vivo de Tregs spécifiques d’un antigène et nous avons pu montrer que la simple injection par voie intraveineuse d’un peptide restreint aux molécules du CMH de classe II suffisait à induire l’activation et l’accumulation sélective de T CD4+ CD25+ spécifiques de cet antigène en périphérie. Enfin, nous avons tiré profit d’un modèle murin de souris Foxp3eGFP, développé en collaboration avec le laboratoire du Dr Bernard MALISSEN (CIML Marseille) et dans lequel la protéine GFP a été insérée en aval du locus foxp3 endogène, pour mettre en évidence pour la première fois un phénomène de conversion périphérique de T naïf en Treg dans un répertoire polyclonal.

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Hung, Chien-Min. "mTORC2 Promotes Lipid Storage and Suppresses Thermogenesis in Brown Adipose Tissue in Part Through AKT-Independent Regulation of FoxO1: A Dissertation". eScholarship@UMMS, 2016. https://escholarship.umassmed.edu/gsbs_diss/845.

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Recent studies suggest adipose tissue plays a critical role in regulating whole body energy homeostasis in both animals and humans. In particular, activating brown adipose tissue (BAT) activity is now appreciated as a potential therapeutic strategy against obesity and metabolic disease. However, the signaling circuits that coordinate nutrient uptake and BAT function are poorly understood. Here, I investigated the role of the nutrient-sensing mTOR signaling pathway in BAT by conditionally deleting Rictor, which encodes an essential component of mTOR Complex 2 (mTORC2) either in brown adipocyte precursors or mature brown adipocytes. In general, inhibiting BAT mTORC2 reduces glucose uptake and de novo lipogenesis pathways while increases lipid uptake and oxidation pathways indicating a switch in fuel utilization. Moreover, several key thermogenic factors (Ucp1, Pgc1α, and Irf4) are elevated in Rictor-deficient BAT, resulting in enhanced thermogenesis. Accordingly, mice with mTORC2 loss in BAT are protected from HFD-induced obesity and metabolic disease at thermoneutrality. In vitro culture experiments further suggest that mTORC2 cell-autonomously regulates the BAT thermogenic program, especially Ucp1 expression, which depends on FoxO1 activity. Mechanistically, mTORC2 appears to inhibit FoxO1 by facilitating its lysine-acetylation but not through the canonical AKT-mediated phosphorylation pathway. Finally, I also provide evidence that β-adrenergic signaling which normally triggers thermogenesis also induces FoxO1 deacetylation in BAT. Based on these data, I propose a model in which mTORC2 functions in BAT as a critical signaling hub for coordinating nutrient uptake, fuel utilization, and thermogenic gene expression. These data provide a foundation for future studies into the mTORC2-FoxO1 signaling axis in different metabolic tissues and physiological conditions.

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Hung, Chien-Min. "mTORC2 Promotes Lipid Storage and Suppresses Thermogenesis in Brown Adipose Tissue in Part Through AKT-Independent Regulation of FoxO1: A Dissertation". eScholarship@UMMS, 2010. http://escholarship.umassmed.edu/gsbs_diss/845.

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Recent studies suggest adipose tissue plays a critical role in regulating whole body energy homeostasis in both animals and humans. In particular, activating brown adipose tissue (BAT) activity is now appreciated as a potential therapeutic strategy against obesity and metabolic disease. However, the signaling circuits that coordinate nutrient uptake and BAT function are poorly understood. Here, I investigated the role of the nutrient-sensing mTOR signaling pathway in BAT by conditionally deleting Rictor, which encodes an essential component of mTOR Complex 2 (mTORC2) either in brown adipocyte precursors or mature brown adipocytes. In general, inhibiting BAT mTORC2 reduces glucose uptake and de novo lipogenesis pathways while increases lipid uptake and oxidation pathways indicating a switch in fuel utilization. Moreover, several key thermogenic factors (Ucp1, Pgc1α, and Irf4) are elevated in Rictor-deficient BAT, resulting in enhanced thermogenesis. Accordingly, mice with mTORC2 loss in BAT are protected from HFD-induced obesity and metabolic disease at thermoneutrality. In vitro culture experiments further suggest that mTORC2 cell-autonomously regulates the BAT thermogenic program, especially Ucp1 expression, which depends on FoxO1 activity. Mechanistically, mTORC2 appears to inhibit FoxO1 by facilitating its lysine-acetylation but not through the canonical AKT-mediated phosphorylation pathway. Finally, I also provide evidence that β-adrenergic signaling which normally triggers thermogenesis also induces FoxO1 deacetylation in BAT. Based on these data, I propose a model in which mTORC2 functions in BAT as a critical signaling hub for coordinating nutrient uptake, fuel utilization, and thermogenic gene expression. These data provide a foundation for future studies into the mTORC2-FoxO1 signaling axis in different metabolic tissues and physiological conditions.

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Rush, Craig M. "Characterization of MAX and FOXA2 mutations unique to endometrial cancer". The Ohio State University, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=osu1542204873523922.

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Swinstead, Erin Elizabeth. "Steroid receptor crosstalk in breast cancer cells". Thesis, 2014. http://hdl.handle.net/2440/90750.

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Breast cancer is the leading cause of cancer related death in women, and approximately 1 in 11 women will develop breast cancer before the age of 75. In 2003, breast cancer was responsible for 16% of cancer related deaths in Australian women. This demonstrates that throughout the life span of the female, this organ has a high risk of developing cancer. The growth and survival of normal breast epithelial cells and breast cancer cells is promoted by estrogens and progesterone and both estrogen receptor (ER) and progesterone receptor (PR) have been shown to play prominent roles in breast cancer progression. It has also been demonstrated that co-treatment of breast cancer cells with corticosteroids and 17β-estadiol (E2) can have opposing effects on the proliferation of breast cancer cells compared with the single treatment. In addition, glucocorticoid receptor (GR) levels have been shown to have clinical implications for breast cancer cell survival. This suggests a possible role for activated GR in breast cancer development. Forkhead box protein 1 (FoxA1), a member of the forkhead class of DNA-binding proteins, has also been shown to be an important factor in breast cancer development. FoxA1 has been shown to dictate ER binding in breast cancer cells and has been deemed responsible for the rapid reprogramming of ER signalling seen in breast cancers with poor outcomes and treatment resistance. However, the effects of ER on the function of FoxA1 have been controversial. The aim of this thesis is to further investigate and characterise GR, ER, and FoxA1 crosstalk in three estrogenic breast cancer cell lines, MCF-7, ZR-75-1, and T-47D cells. It has been determined that the combination of dexamethasone (Dex) and E2 have an altered affect on the cell proliferation of breast cancer cells, compared to the single treatment, suggesting GR can modulate the ER response. In an artificial cell model it has been demonstrated by genome-wide investigations, that activated GR and estrogen receptor (ER) can alter the binding of each other at a subset of sites, by a mechanism termed DynaLoad. In addition, it has been shown that Dex and E2 in combination can regulate a unique subset of genes in breast cancer cells. This provides evidence to indicate that Dex can oppose the growth stimulatory effects of E2 signalling, and further, in combination, Dex and E2, can alter the gene transcriptional prolife of MCF-7 breast cancer cells. To understand how the molecular interplay between GR and ER effect breast cancer progression the genome-wide binding events of activated GR and ER have been investigated. These studies show that a GR and ER DynaLoad mechanism also exists in all three breast cancer cell lines utilised; however, there was very little crossover of binding patterns observed. This suggests that while the mechanisms of DynaLoad are present in all three cell lines, the sites altered are cell specific. Most surprisingly is the discovery of an elevated number of GR sites that are lost upon activation of ER in MCF-7 cells. However, in the other breast cancer cell lines, this finding is not as pronounced. Immunblots show that MCF-7 cells have lower GR protein levels than the other cell lines indicating that steroid receptor (SR) levels play a major role in the effect that the dual hormone treatment has on the cell. This suggests that in a highly estrogenic cell line, ER plays a strong role in modulating GR function, which could have important consequences for disease outcome. Furthermore, and contrary to previous findings, this thesis establishes that activated ER and GR have the ability to alter the genomic response of the well-established pioneer factor FoxA1. Genome-wide analysis of FoxA1 binding, upon treatment of E2 or Dex, shows that both ER and GR can recruit FoxA1 to specific binding sites within the genome through a DynaLoad mechanism. These results indicate that there is not a specific set of pioneer factors which bind to closed chromatin and establish the binding landscape for other transcription factors (TFs). Instead this data suggests that every factor has the potential to affect the binding landscape of other TFs, depending on the chromatin context. Overall, the findings from this thesis have provided novel insight into the crosstalk between GR, ER, and FoxA1, further highlighting the ability of activated SRs to alter the response of one another, and other TFs. In addition, it has also been determined that the outcomes of SR crosstalk is cell-specific and that differing estrogenic breast cancer cells can have altered outcomes, which are dependent on SR levels. This can have potential consequences in breast cancer disease outcomes and progression. In addition, the findings in this thesis have begun to shift our classical understanding of pioneer factors in breast cancer, demonstrating that activated GR and ER have the capabilities to recruit and alter the response of FoxA1. This has provided information on a previously unknown complexity to FoxA1 action in breast cancer cells. The studies in this thesis highlight the signalling complexity of TFs in breast cancer cells and provide the basis for further investigations into GR, ER, and FoxA1 mechanisms and the direct consequences of this on breast cancer outcomes.
Thesis (Ph.D.) -- University of Adelaide, School of Medicine, 2014

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Chen, Yi-Hsuan, e 陳翌萱. "The Effect of Forkhead box protein M1 (FoxM1) Overexpression on Mitochondrial Dynamics". Thesis, 2014. http://ndltd.ncl.edu.tw/handle/08113938961800944220.

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碩士
國立清華大學
生物科技研究所
102
Mitochondria are highly dynamics organelles that are regulated by fission and fusion processes. Mitochondria are responsible for many important functions in cells, such as ATP synthesis, calcium homeostasis, ROS signaling and apoptosis. More and more studies have revealed that mitochondrial dynamics is closely correlated with cellular events. In addition, mitochondrial fusion and fission imbalance has been linked to cancer formation and metastasis. FoxM1 is a transcription factor which is overexpressed in cancer cell and associates with many characteristic features of cancer, such as cell proliferation, metastasis, angiogenesis and apoptosis resistance. The relations between mitochondrial dynamics and FoxM1 have not been explored. We aim to clarify whether FoxM1 plays a role in tumorigenesis through affecting mitochondrial dynamics. In our study, we found that FoxM1 overexpression triggered adjustment of the balance of mitochondrial fusion and fission. In addition, we found FoxM1 overexpression reduced intracellular and mitochondrial superoxide levels. Furthermore, overexpression of FoxM1 aided the mitochondrial respiration activities under induced oxidative stress conditions. Our results indicated that FoxM1 involves in mitochondrial dynamics and adjustments of mitochondrial activities under stress conditions.

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Capitoli di libri sul tema "Forkhead box protein A1"

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Wang, Haitao, Philip Lazarovici e Wenhua Zheng. "Forkhead Box Protein O". In Encyclopedia of Signaling Molecules, 1821–36. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101601.

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Wang, Haitao, Philip Lazarovici e Wenhua Zheng. "Forkhead Box Protein O". In Encyclopedia of Signaling Molecules, 1–16. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101601-1.

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"Forkhead Box Protein O1". In Encyclopedia of Signaling Molecules, 1836. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101305.

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Vicente Dragano, Nathalia Romanelli, e Anne y. Castro Marques. "Native Fruits, Anthocyanins in Nutraceuticals, and the Insulin Receptor/Insulin Receptor Substrate-1/Akt/Forkhead Box Protein Pathway". In Molecular Nutrition and Diabetes, 131–45. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-801585-8.00011-7.

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Atti di convegni sul tema "Forkhead box protein A1"

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Xu, Nuo, Xin Zhang e Chun-xue Bai. "Forkhead Box M1 Confers The Resistance Of Iressa In The SPC-A1 Lung Cancer Cell Line". In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5081.

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Cho, H., GH Han, DB Chay, S. Kim e J.-H. Kim. "EP865 Forkhead box protein O1 and Paired box gene 3 overexpression is associated with poor prognosis in patients with epithelial ovarian cancer". In ESGO Annual Meeting Abstracts. BMJ Publishing Group Ltd, 2019. http://dx.doi.org/10.1136/ijgc-2019-esgo.914.

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Chandra, D., A. Gregory, A. Blumental-Perry, S. Alexander, T. Nyunoya, J. D. Londino, F. C. Sciurba, R. K. Mallampalli e S. D. Shapiro. "Cigarette Smoke Induces Ubiquitination and Degradation of Forkhead Box Protein P1 (FoxP1) Leading to Increased Endoplasmic Reticulum Stress in Lung Epithelial Cells". In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a1216.

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Alexander, S. L., A. Maloy, A. Gregory e D. Chandra. "Cigarette Smoke Causes Forkhead Box Protein P1 (FoxP1) to Be Ubiquitinated and Degraded in Lung Epithelial Cells Resulting in a Dysregulated Endoplasmic Reticulum Stress Response". In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4275.

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Maloy, A., A. Andreas e D. Chandra. "Cigarette Smoke Causes Forkhead Box Protein P1 (FoxP1) to Be Ubiquitinated and Degraded in Lung Epithelial Cells Resulting in a Dysregulated Endoplasmic Reticulum Stress Response". In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a4623.

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Hirani, D. V. B., M. Koch, J. Mohr, K. Dinger, C. Vohlen, C. Klaudt, J. Dötsch e M. A. Alejandre Alcazar. "Kruppel-Like Factor 4 (Klf4) Is a Novel Regulator of Forkhead Box Protein O1 (FOXO1) and of Neonatal Lung Fibroblast Function and Reduced in Hyperoxia-Induced Lung Injury". In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a4444.

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Zheng, Ying, e Wilson S. Meng. "Polycation Coated Polymeric Particles as Vehicles of RNA Delivery Into Immune Cells". In ASME 2010 Conference on Smart Materials, Adaptive Structures and Intelligent Systems. ASMEDC, 2010. http://dx.doi.org/10.1115/smasis2010-3714.

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Abstract (sommario):

The purpose of this work is to develop a carrier system for delivering RNA molecules aimed to downregulate specific functions in T cells. In many forms of cancer, T cells that express the protein Forkhead Box P3 (Foxp3) are associated with cancer progression. These cells can be identified by CD4 and CD25, molecules express on the cell surface. Studies have shown that downregulation of Foxp3 can increase the ability of other immune cells to destroy tumors. A class of RNA molecules, commonly referred to as “siRNA”, bind to and degrade specific messenger RNA (mRNA) in a sequence-dependent manner such that expression of the encoded protein is terminated. Because mRNA molecules are located inside cells, a carrier system is required to facilitate the uptake of siRNA, which does not passively diffuse through the plasma membrane. To this end, nanosized polymeric particles coated with the polycation, ornithinex10-histidinex6 (or O10H6) were used to adsorb siRNA that bind to the mRNA encoding Foxp3. The RNA-loaded particles are spherical and uniform in size (normally distributed, polydispersity index = 0.072). Loading of RNA to the particles was confirmed using gel electrophoresis. RNA complexed with the particles are protected from serum destabilization: 83.1% of RNA were recovered compared to 36.1% in RNA that were not associated with the particles. Association with the particles increased the uptake of the RNA in mouse T cells from 3.2±0.2% (free RNA) to 20.1±3.9%. Specifically, uptake of the RNA in T cells that express CD4 increased from 2.7±0.2% to 27.1±1.3% when particles were employed. These differences are statistically significant in three experiments conducted (p < 0.01). Internalization of the RNA into T cells was confirmed using confocal imaging. Flow cytometric analysis showed that the particle-complexed RNA reduced the percentage of T cells that express both CD4 and CD25 in mice carrying tumors from 24.0% when free RNA molecules were used to 13.5%. In these cells, the level of Foxp3 mRNA was reduced by 30%. In conclusion, the particles facilitate the uptake of siRNA molecules into a population of T cells that is known to promote cancer growth.

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Rapporti di organizzazioni sul tema "Forkhead box protein A1"

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Belaguli, Narasimhaswamy S. Forkhead Box Protein 1 (Foxa1) and the Sumoylation Pathway that Regulates Foxa1 Stability are Potential Targets for Breast Cancer Treatment. Fort Belvoir, VA: Defense Technical Information Center, settembre 2007. http://dx.doi.org/10.21236/ada489768.

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