Metformin: Prevention of genomic instability and cancer: A review

Area of Science:

• Biochemistry
• Genetics
• Pharmacology

Background:

• Metformin, a common diabetes medication, exhibits potential anti-cancer properties.
• Its ability to mitigate genotoxicity from various agents is recognized, but mechanisms remain unclear.
• Genomic instability is a hallmark of cancer development and progression.

Purpose of the Study:

• To review the protective effects of metformin against genotoxicity and genomic instability.
• To elucidate the mechanisms by which metformin reduces DNA damage.
• To highlight metformin's potential role in cancer prevention and treatment.

Main Methods:

• Literature review of studies investigating metformin's effects on DNA damage and repair.
• Analysis of metformin's antioxidant and anti-inflammatory properties.
• Examination of metformin's impact on DNA damage response (DDR) pathways.

Main Results:

• Metformin scavenges reactive oxygen species and nitric oxide, reducing DNA damage.
• It enhances antioxidant enzyme activity and inhibits pro-inflammatory enzymes like NADPH oxidase.
• Metformin stimulates key DNA repair pathways: homologous end-joining, homologous recombination, and nucleotide excision repair.

Conclusions:

• Metformin offers significant protection against genotoxic agents through antioxidant and DNA repair-enhancing mechanisms.
• Its ability to maintain genomic stability suggests a role in cancer prevention and potentially as an adjunct cancer therapy.
• Further research is warranted to fully understand and harness metformin's chemoprotective potential.