Cyclin-dependent kinase 7 gene silencing or knockout represses proliferation of ovarian cancer cells and the mechanism research / 肿瘤

ABSTRACT

Objective: To investigate the role of cyclin-dependent kinase 7 (CDK7) in the proliferation of ovarian cancer cells. Methods: The ovarian cancer cell lines OVCA433, TOV-112D and IGROVl were transfected with specific siRNA to downregulate the expression of CDK7 gene, then the cell proliferation viability was detected by CCK-8 method. The CDK7 gene in ovarian cancer HEY, OVCA420, OVCA433 and IGROVl cells was knocked out by clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR-associated endonuclease 9 (Cas9) system, then the clone formation ability was detected by plate clone formation assay. The ovarian cancer TOV-112D, IGROV1, OVCA433, OVCAR8, OV90, SKOV3 and COV413B cells were treated with CDK7-inhibitor THZl, then the cell proliferation viability and clone formation ability were detected by CCK-8 method and clone formation assay, respectively. Furthermore, the expression level of CDK7 protein and the phosphorylation level of RNA polymerase n (RNAPolE) in IGROV1, OVCA433, SKOV3 and COV41 3B cells treated with THZl were analyzed by Western blotting. Results: The proliferation and clone formation abilities of various ovarian cancer cells were significantly decreased after CDK7 gene was silenced or knocked out (all P < 0.05). THZ1 repressed the proliferation and clon e formation of ovarian cancer cells, an d downregulated the expression of CDK7 and the phosphorylation of RNAPoln (all P < 0.05). Conclusion: CDK7 may promote the proliferation of ovarian cancer cells by regulating the phosphorylation of RNAPoln.