Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2022 May 19;15(5):626. doi: 10.3390/ph15050626

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

PMC Copyright notice

Molecular effects of metformin in cancer cells. Metformin directly inhibits complex I of the electron transport chain in the mitochondria resulting in decreased ATP/AMP ratio and activation of AMPK. AMPK activation inhibits mTOR and activates P53 to impact subsequent cellular processes. Metformin also inhibits mTOR in an AMPK-independent manner, through Rag GTPases and REDD1. Reduced insulin availability through metformin’s systemic effects indirectly modulates the proliferative pathway, PI3K/AKT. AMP: Adenosine Monophosphate; AMPK: AMP-Activated Protein Kinase; ATP: Adenosine Triphosphate; IGF: Insulin-like Growth Factors; IGF-R: Insulin-like Growth Factor Receptor; mTOR: Mammalian Target of Rapamycin; OTC: Organic Cation Transporter; PI3K: Phosphoinositide 3-kinase; REDD1: Regulated in Development and DNA damage responses 1; SLC: Solute Carrier Transporter; TSC2: Tuberous Sclerosis Complex 2. Created in BioRender.