Metformin: A Rising Star to Fight the Epithelial Mesenchymal Transition in Oncology

ISSN: 1875-5992 (Online)
ISSN: 1871-5206 (Print)


Volume 16, 12 Issues, 2016


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Anti-Cancer Agents in Medicinal Chemistry

Formerly: Current Medicinal Chemistry - Anti-Cancer Agents

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Editor-in-Chief:
Michelle Prudhomme
Universite Blaise Pascal - C.N.R.S
Aubiere Cedex
France


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Metformin: A Rising Star to Fight the Epithelial Mesenchymal Transition in Oncology



Anti-Cancer Agents in Medicinal Chemistry, 13(2): 333-340.

Author(s): Guislaine Barriere, Michel Tartary and Michel Rigaud.

Affiliation: Clinical laboratory, Astralab department of specialized Analyses, 7-11 Avenue de Lattre de Tassigny, 87000 Limoges, France.

Abstract

Metformin is a biguanide derivative which is widely prescribed as an oral drug for diabetes mellitus type 2. This old molecule has recently received a new attention because of its therapeutic properties in oncology, that seem to be independent of its action on glycemia homeostasis. The reappraisal of its pharmacological effects was supported by delineation of signaling pathways and more recently clinical trials. Numerous epidemiological studies showed that diabetics have an increased risk of several types of cancer and cancer mortality. Complex relationship between cancer and type 2 diabetes is going to be unraveled and recent observations revealed a significant action of metformin, but not other anti-diabetic agents, on cancer cells. As metformin may act as an anticancer drug through inhibition of mTOR, it might have greater benefice than suggested by insulin lowering alone. This review summarizes major publications on the link between cancer and metformin underscoring new implications of this chemical drug in oncology field. New perspectives about utilization of this molecule in clinical oncological routine, are described, particularly for patients without disturbance of glucose homeostasis. As the epithelial mesenchymal transition (EMT) seems implicated into invasive process and metastasis in cancer, and as metformin is able to inhibit EMT pathways, it is important to highlight cellular mechanisms of metformin.

Keywords:

AKT, AMPK, Cancer, Clinical trials, Dedifferentiated circulating tumor cells, Diabetes, EMT, Epidemiology, Insulin, Metformin, mTOR, Neoadjuvant therapy, S6KB, Stemness.



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Article Details

Volume: 13
Issue Number: 2
First Page: 333
Last Page: 340
Page Count: 8
DOI: 10.2174/1871520611313020018
Price: $58
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