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An integrative multi-omics analysis leveraging Mendelian randomization and subsequent experimental validation prioritizes glutathione S-transferase mu 5 (GSTM5) as a genomic stability-related gene and a therapeutic vulnerability to PLK1 inhibition in breast cancer
Genetic and experimental analysis identifies GSTM5 as a gene linked to DNA stability and a target for PLK1-blocking treatment in breast cancer
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Abstract
Glutathione S-transferase mu 5 (GSTM5) is identified as a candidate gene potentially protective against breast cancer.
- Circadian rhythm disruption may contribute to increased breast cancer risk, although the molecular mechanisms remain unclear.
- GSTM5 was the only gene among a pre-specified set that met stringent criteria for association with breast cancer.
- Lower levels of GSTM5 expression in breast tumors correlated with hypermethylation of its promoter region and signs of genomic instability.
- In breast cancer cells with low GSTM5 expression, sensitivity to Polo-like kinase 1 (PLK1) inhibition was observed.
- GSTM5 depletion compromised the ability to repair DNA damage after irradiation, indicating its role in genomic stability.
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