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- W2463671907 abstract "There is substantial evidence that metformin, an anti-diabetic biguanide, correlates with improved breast cancer response to chemotherapy. The exact mechanism of metformin9s beneficial effect in breast cancer is yet to be fully understood. Metformin inhibits a serine/ threonine kinase called mammalian target of rapamycin (mTOR), which is a central regulator of various intracellular and extracellular stimuli. mTOR transduces signaling from growth factors, such as insulin, to stimulate mRNA translation. Insulin activates mTOR through PI3K-Akt-mediated phosphorylation and consequent activation of protein machinery to promote protein synthesis. Increased protein synthesis in cancer cells contributes to cancer progression. Improved response of breast cancer cells response to chemotherapy following metformin treatment suggests inhibition of mTOR in breast cancer regression. Being a serine / threonine kinase, mTOR may also have a potential role in the regulation of gene transcription via modulating the activity of some transcription factors, particularly, those involved in cell proliferation and differentiation. Kruppel-like factor 4 (KLF-4) is one such transcription factor which is involved in epithelial cells differentiation and proliferation and it is potentially regulated by mTOR. The objective of this study, therefore, was to investigate whether mTOR regulates gene expression by modulating the activity of KLF-4 in breast cancer. Our hypothesis was that mTOR inhibition by metformin results in the upregulation of KLF-4, which functions as a tumor suppressor. Elucidation of the molecular basis of metformin9s effect on KLF-4 could provide the basis for adjuvant therapy in breast cancer. Western blot (WB) studies indicate overexpression of mTOR in some breast cancer cells compared to normal breast epithelial cells. In contrast, WB and Immunohistochemistry studies indicate overexpression of KLF-4 in normal breast cells compared to cancer breast cells. Metformin treatment, with and without insulin, resulted in decreased mTOR level with a concomitant increase in KLF-4 level in breast cancer cells. These results suggest a role of metformin in mediating the inverse relationship between mTOR and KLF-4 in breast cancer. Citation Format: Mohamed Alalem, Alpana Ray, Bimal Ray. Role of mTOR as a transcriptional regulator in breast cancer. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Breast Cancer Research: Genetics, Biology, and Clinical Applications; Oct 3-6, 2013; San Diego, CA. Philadelphia (PA): AACR; Mol Cancer Res 2013;11(10 Suppl):Abstract nr A042." @default.
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- W2463671907 date "2013-10-01" @default.
- W2463671907 modified "2023-09-25" @default.
- W2463671907 title "Abstract A042: Role of mTOR as a transcriptional regulator in breast cancer" @default.
- W2463671907 doi "https://doi.org/10.1158/1557-3125.advbc-a042" @default.
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