Investigating the Impact of DNMT1 Depletion on Triple-Negative Breast Cancer Cell Lines
Triple-negative breast cancer (TNBC) is the subtype of breast cancer with the worst prognosis, accounting for approximately 15% of all the breast cancer subtypes. Due to the lack of relevant receptor markers, the current standard treatment for TNBC patients remains the nonspecific chemotherapy. Therefore, identifying new therapeutic strategies and targets for TNBC patients remains an urgent issue. To explore the impact of DNMT1 depletion on triple-negative breast cancer cell lines, we used CRISPR-Cas9 gene-editing technology to knock out (KO) the DNMT1 gene in the TNBC cell line MDA-MB-231. Through transcriptome sequencing and analysis, we compared the differences between wild-type (WT) MDA-MB-231 and DNMT1-KO MDA-MB-231 cells. We found that the deletion of DNMT1 genes promoted the activation of apoptotic signaling pathways and the expression of numerous tumor suppressor genes. Simultaneously, the Wnt signaling pathway-related genes, angiogenesis signaling pathway-related genes, and multiple oncogenes were downregulated. Our results indicate that DNMT1 depletion inhibits the survival and metastasis of MDA-MB-231 cells. DNMT1 may be a potential therapeutic target for treating TNBC patients.