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

Area of Science:

• Gynecology
• Oncology
• Molecular Biology

Background:

• Progesterone resistance hinders conservative treatment for endometrial cancer.
• The role of Carboxypeptidase inhibitor (CTMP) in endometrial cancer progression is unclear.
• Effective prediction and reversal of progesterone resistance remain challenging.

Purpose of the Study:

• To investigate the mechanism of CTMP in endometrial cancer.
• To determine CTMP's association with progesterone resistance.
• To explore CTMP's role in the PI3K/AKT signaling pathway.

Main Methods:

• Immunohistochemistry to detect CTMP expression in endometrial tissues.
• Cell culture assays (CCK-8, EDU) for cell growth and proliferation.
• Western blot to analyze CTMP and PI3K/AKT pathway proteins.

Main Results:

• CTMP expression did not differ between sensitive and resistant groups pre-treatment.
• CTMP decreased in progesterone-sensitive tissues post-treatment.
• CTMP knockdown increased sensitivity to medroxyprogesterone acetate (MPA) by inhibiting the PI3K/AKT pathway.

Conclusions:

• CTMP is linked to progestin therapy sensitivity in endometrial atypical hyperplasia and cancer.
• CTMP may promote progesterone resistance via PI3K/AKT pathway activation.
• Targeting CTMP could overcome progesterone resistance in endometrial cancer.