Proteasome activator subunit 1/2 promotes the proliferation and invasion of endometrial carcinoma cells by inhibiting the expression of cyclin-dependent kinase 15
Basic research|更新时间:2025-10-22
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Proteasome activator subunit 1/2 promotes the proliferation and invasion of endometrial carcinoma cells by inhibiting the expression of cyclin-dependent kinase 15
Journal of Chongqing Medical UniversityVol. 49, Issue 2, Pages: 158-164(2024)
Zhang Hailin,Li Cong,Xiao Zhenghua,et al.Proteasome activator subunit 1/2 promotes the proliferation and invasion of endometrial carcinoma cells by inhibiting the expression of cyclin-dependent kinase 15[J].Journal of Chongqing Medical University,2024,49(2):158-164.
Zhang Hailin,Li Cong,Xiao Zhenghua,et al.Proteasome activator subunit 1/2 promotes the proliferation and invasion of endometrial carcinoma cells by inhibiting the expression of cyclin-dependent kinase 15[J].Journal of Chongqing Medical University,2024,49(2):158-164. DOI: 10.13406/j.cnki.cyxb.003435.
Proteasome activator subunit 1/2 promotes the proliferation and invasion of endometrial carcinoma cells by inhibiting the expression of cyclin-dependent kinase 15
To investigate the expression level of proteasome activator subunit 1/2(PSME1/2) in endometrial carcinoma and its effect on the proliferation and invasion of endometrial carcinoma cells.
Methods
2
The expression levels of PSME1/2 and cyclin-dependent kinase 15(CDK15) were measured in endometrial cell lines and primary cultured cells,and knock-down strains were used to analyze the correlation between PSME1/2 and CDK15 and the effect of PSME1/2 on tumor proliferation and invasion. The expression levels of PSME1/2 and CDK15 were compared between endometrial carcinoma tissue and paracancerous tissue,and the influence of PSME1/2 and CDK15 on the prognosis of patients with endometrial carcinoma was analyzed.
Results
2
Compared with normal human endometrial cell lines,human endometrial adenocarcinoma HEC1B cells and primary cultured cells had high mRNA and protein expression levels of PMSE1/2 and a reduction in the protein expression of CDK15. Compared with the control group and the double knock-down group,there was an increase in the protein expression level of CDK15 in the HEC1B line with PSME1/2 knock-down,suggesting that CDK15 might be inhibited by PSM
E1/2. There was a high expression level of PMSE1/2 and a low expression level of CDK15 in endometrial carcinoma. There were no significant differences in age,postoperative diagnosis and typing,degree of tumor differentiation,and postoperative stage between the high PSME1/2 expression group and the low PSME1/2 expression group(
P
>
0.05). There was no significant correlation between the expression of PSME1/2 and CDK15 and the poor prognosis of patients with endometrial carcinoma(
P
>
0.05).
Conclusion
2
PSME1/2 can inhibit the expression of CDK15 and promote the proliferation and invasion of endometrial carcinoma cells,and PSME1/2 can also promote endometrial carcinoma.
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Keywords
references
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