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Archive > Volume 30 Issue 9 > 2023,30(9):777-783. DOI:10.3872/j.issn.1007-385X.2023.09.005 Prev Next
Basic Research
CDC20 expression in endometrial cancer and its effects on the proliferation and apoptosis of RL95-2 cells
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Abstract:
Objective: To evaluate the cell division cycle 20 gene (CDC20) expression in endometrial cancer (EC), and to explore the role and possible mechanism of CDC20 in regulating cell cycle and apoptosis of EC RL95-2 cells. Methods: The mRNA expression matrix of EC and matched patients' clinical information were acquired from The Cancer Genome Atlas (TCGA) database. The differential expression of CDC20 mRNA in EC and its correlation with tumor stage were analyzed with R package. Then, CDC20 expression in RL95-2 cells was detected with qPCR and WB assay. sh-CDC20 was transfected into RL95-2 cells to knockdown CDC20 expression. The effects of CDC20 knockdown on the cell proliferative viability, cell cycle distribution and cell apoptosis were measured with CCK-8 assay and flow cytometry, respectively, and its effect on the activity of Mcl-1/p-Chk1 axis was explored with WB assay. RL95-2 cell transplanted tumor model in nude mice was established to evaluate the anti-tumor effect of sh-CDC20 and its effect on apoptosis and Mcl-1/p-Chk1 axis in tumor tissues.Results: CDC20 was highly expressed in EC tissues and RL95-2 cells (P<0.01), and the high expression of CDC20 was strongly associated with EC tumor stage. Knockdown of CDC20 in RL95-2 cells could inhibit cell proliferative viability and cause cell cycle arrest at G1 phase (P<0.05 or P<0.01), promote cell apoptosis (P<0.01) and decrease the protein expressions of Mcl-1 and p-Chk1 in RL95-2 cells (P<0.05 or P<0.01). Knockdown of CDC20 remarkably inhibited the growth of xenografts in mice and reduced the expressions of Mcl-1 and p-Chk1 (all P<0.01), while promoted tumor cells apoptosis (P<0.01). Conclusion: CDC20 is highly expressed in EC tissues and is associated with tumor stage. Knockdown of CDC20 can inhibit the viability of RL95-2 cells and their transplanted tumors in nude mice and promote apoptosis, which may be related to the Mcl-1/p-Chk1 signaling axis.
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