Metformin is an AMP kinase-dependent growth inhibitor for breast cancer cells.

By M. Zakikhani, R. Dowling, I. Fantus, Nahum Sonenberg, Michael Pollak. Cancer Research, 2006

1,090 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Surgery

View Paper: https://www.semanticscholar.org/paper/4f04cd4b5d6baa4de40cf115d1cd0a59c76045db

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

1. Michael Pollak
2. B. Viollet
3. I. Ben-Sahra
4. Gerald I. Shulman
5. Nahum Sonenberg
6. D. Alessi
7. Traci E LaMoia
8. David M. Sabatini

In Oncology

1. Michael Pollak

In Surgery

1. Michael Pollak
2. Traci E LaMoia
3. Gerald I. Shulman
4. D. Alessi
5. B. Viollet
6. G. Steinberg

Citations in the corpus

• Metformin, independent of AMPK, induces mTOR inhibition and cell-cycle arrest through REDD1. (2011, background): “In agreement, AMPK inhibition reverses the anti-proliferative effects of metformin in breast and ovarian cancer cells (7, 8).”
• The antidiabetic drug metformin exerts an antitumoral effect in vitro and in vivo through a decrease of cyclin D1 level (2008, background): “, 2005) and inhibit breast and glial cancer cell proliferation in vitro (Zakikhani et al., 2006).”
• Metformin: from mechanisms of action to therapies. (2014, background): “An early finding supporting a direct action of metformin on cancer cells was the observation that the drug was growth inhibitory in vitro in a manner that was associated with AMPK activation and mTOR inhibition as a consequence of metformin-induced energetic stress (Zakikhani et al., 2006).”
• New Users of Metformin Are at Low Risk of Incident Cancer (2009, background): “Metformin also inhibits growth of human breast cancer cells (5).”
• The influence of glucose-lowering therapies on cancer risk in type 2 diabetes (2009, background): “Our observed lack of effect of metformin treatment on the risk of breast cancer was unexpected in the light of the in vitro observations [20] that provided the rationale for an intervention trial with metformin following surgery for breast cancer [21].”
• Metformin inhibits mammalian target of rapamycin-dependent translation initiation in breast cancer cells. (2007, background): “We recently showed that metformin reduced general protein synthesis in MCF-7 cells (33).”
• Cellular and Molecular Mechanisms of Metformin Action (2020, background): “The cancer field has begun to explore the antitumor effect of metformin as a potential treatment for certain cancers (23, 24), and the first trials of metformin for treating aging in healthy humans are currently underway (25, 26).”
• Cellular and molecular mechanisms of metformin: an overview. (2012, background): “The antineoplastic activity of metformin via AMPK activation is mediated through the inhibition of mTORC1 signaling, leading to inhibition of protein synthesis and cell proliferation [121, 123, 124].”