Effect of COL1A1 deletion on proliferation of ovarian cancer ES-2 cells

AIM: To explored the role of collagen type I alpha 1 chain (COL1A1) deletion in proliferation and apoptosis of human ovarian cancer ES-2 cells. METHODS: CRISPR/Cas9-mediated COL1A1 gene knockout vector was constructed and transfected into ES-2 cells, and the ES-2 cells with COL1A1 knockout were obtained by puromycin screening. Genomic sequencing was used to verify the efficiency of knockout. Cell proliferation, colony formation and cell migration were detected in COL1A1 knockout ovarian cancer cells. Cell apoptosis was analyzed by PI-annexin V staining and flow cytometry. Nude mouse model was used to detect the tumorigenic capacity of COL1A1 knockout cells in vivo. RESULTS: COL1A1 deletion inhibited the proliferation and migration of ovarian cancer cells (P < 0.01). COL1A1 deletion blocked the G₂ phase of ovarian cancer cell cycle and promoted apoptosis (P < 0.01). COL1A1 deletion significantly inhibited the expression of osteoblast-specific transcription factor osterix and matrix metalloproteinase-13, and promoted the expression of aggrecanase-1 (P < 0.01). The results of tumor-bearing model in nude mice showed that COL1A1 deletion inhibited the growth rate of tumor. CONCLUSION: COL1A1 deletion inhibits the proliferation and promotes the apoptosis of tumor cells by affecting the expression of a variety of genes, thus reducing the malignant transformation of tumor.