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Effects of metformin on cancers in experimental and clinical studies: Focusing on autophagy and AMPK/mTOR Signaling Pathways
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  • Mohammad Yassin Zamanian,
  • Maryam Golmohammadi,
  • Alexey Yumashev,
  • Ahmed Hjazi,
  • Mariam Alaa Toama,
  • Mervat Ahmed AbdRabou,
  • Anita Gehlot,
  • Enas R. Alwaily,
  • Niyousha Shirsalimi,
  • Pankaj Kumar Yadav,
  • Gervason Moriasi
Mohammad Yassin Zamanian
Hamadan University of Medical Sciences Medical School
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Maryam Golmohammadi
Shahid Beheshti University of Medical Sciences School of Medicine
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Alexey Yumashev
Pervyj Moskovskij gosudarstvennyj medicinskij universitet imeni I M Secenova
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Ahmed Hjazi
Prince Sattam bin Abdulaziz University College of Applied Medical Sciences
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Mariam Alaa Toama
Directorate General of Education in Dhi Qar
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Mervat Ahmed AbdRabou
Al-Jouf University College of Science
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Anita Gehlot
Uttaranchal University Institute of Management
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Enas R. Alwaily
Thi Qar University College of Engineering
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Niyousha Shirsalimi
Hamadan University of Medical Sciences Medical School
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Pankaj Kumar Yadav
Sam Higginbottom University of Agriculture Technology and Sciences
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Gervason Moriasi
Mount Kenya University College of Health Sciences

Corresponding Author:[email protected]

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Metformin (MET) is a preferred drug for the treatment of type 2 diabetes mellitus. Recent studies show that apart from its blood glucose-lowering effects, it also inhibits the development of various tumours, by inducing autophagy. Further, various studies have confirmed the inhibitory effects of MET on cancer cell lines’ propagation, migration, and invasion. However, despite the many publications on the anticancer potential of MET, there is no existing comprehensive review and account of its autophagy-associated anticancer activity, this review. This review noted that MET exerts its anticancer effects by regulating key signalling pathways such as phosphoinositide 3-kinase (PI3K), LC3-I and LC3-II, Beclin-1, p53, and the autophagy-related gene (ATG), inhibiting the mTOR protein, downregulating the expression of p62/SQSTM1, and blockage of the cell cycle at the G0/G1. Moreover, MET can stimulate autophagy through pathways associated with the 5′ adenosine monophosphate-activated protein kinase (AMPK), thereby inhibiting he development and progression of various human cancers, including hepatocellular carcinoma, prostate cancer, pancreatic cancer, osteosarcoma, myeloma, and non-small cell lung cancer. Therefore, this detailed review provides a framework for further investigations that may appraise the autophagy-induced anticancer potential of MET and its repurposing for cancer treatment.