Kielin/chordin-like protein, paclitaxel resistance, cervical squamous cell carcinoma, mechanism, functions, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, RC254-282

ObjectiveTo evaluate the mechanism of Kielin/chordin-like protein (KCP) in the resistance of cervical cancer cells to paclitaxel.MethodA cervical squamous carcinoma cell line (SiHa) with KCP knockout was constructed and treated with paclitaxel. Key cell functions were assessed by colony formation assay, measurement of cell proliferation by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and FACS-based detection of apoptosis. The downstream mechanism of KCP-mediated resistance to paclitaxel was then examined using human gene chip detection and IPA bioinformatics analysis, and qPCR analysis was used to validate its downstream genes.Results①Functional studies of SiHa cells showed that KCP knockout (sgRNA) inhibited colony formation and proliferation of SiHa cells in the presence of paclitaxel (p