Knockdown of CTMP Enhances Progesterone Sensitivity in Endometrial Cancer by Inhibiting the PI3K/AKT Signaling Pathway.

Progesterone resistance is a key factor in the failure of conservative treatment in young endometrial cancer patients, and there is no effective method to predict and reverse progesterone resistance. CTMP is known to be involved in the development and progression of endometrial cancer, but the mechanism is unidentified. In this study, the immunohistochemical method was used to detect the expression of CTMP in the endometrium before and after progesterone treatment. In cell culture experiments, cell growth and proliferation were examined using CCK-8 and EDU incorporation assay. CTMP and PI3K/AKT pathway-related proteins expression were examined using Western blot. The results show that CTMP expression in the progesterone-resistant group of AEH was not significantly different from that in the progestin-sensitive group before treatment. There was no significant change in the expression of CTMP in the AEH progestin-resistant group, whereas there was a significant decrease in the expression of CTMP in the progesterone-sensitive group after treatment. CTMP knockdown enhances the sensitivity of endometrial cancer cells to medroxyprogesterone acetate (MPA) and may act by inhibiting the PI3K/AKT signaling pathway. This study confirms that CTMP may be associated with sensitivity to progestin therapy in endometrial atypical hyperplasia and endometrial cancer. CTMP may induce the development of progesterone resistance in endometrial cancer through activation of the PI3K/AKT signaling pathway.