Unveiling the Role of PNMA2 in Endometriosis: From Proliferation and Apoptosis to Immunomodulation

Endometriosis is a chronic disease that jeopardises the quality of life of about 10% of women. The aim of this study was to investigate the expression, function, regulatory mechanism, and relationship with immune cell infiltration of PNMA2 in endometriosis. This study investigates the potential involvement and regulatory mechanisms of PNMA2 in the development of endometriosis through the integration of public data, machine learning, clinical sample transcriptome sequencing, and in vitro cell experiments. Cytological in vitro experiments were conducted to validate the impact of PNMA2 on the modulation of proliferation, migration, apoptosis, and autophagy in 12z cells. Rescue experiments were performed based on the autophagy activator (RAPA) to clarify the regulatory details of PNMA2, apoptosis, and autophagy. The Ciberort algorithm was employed to discern the association between PNMA2 gene expression and more than 20 distinct immune cell infiltration types in endometriosis. The expression of PNMA2 exhibited a notable increase in individuals with endometriosis. Knockdown of PNMA2 inhibited the proliferation and migration of 12z cells. Knockdown of PNMA2 could directly promote apoptosis and could also inhibit autophagy and indirectly promote apoptosis. PNMA2 displayed associations with immune cell infiltration and immunomodulation. The present study demonstrated that the up-regulation of PNMA2 was associated with malignant growth, anti-apoptosis, and immunoregulation of human endometriotic cells. Therefore, PNMA2 may serve as a new diagnostic biomarker and a promising therapeutic target.