C21orf2 as a potential regulator of JAK2/STAT3 signaling in prostate cancer cell proliferation and apoptosis: an exploratory study

Abstract Background Prostate cancer (PCa) is a major health concern for men worldwide, and its incidence is rising rapidly, so identifying key molecules that regulate the malignant biological behavior of PCa is crucial for early diagnosis and targeted therapy. This study aimed to elucidate the regulatory role of chromosome 21 open reading frame 2 (C21orf2) in the biological functions of prostate cancer cells and further explore the molecular mechanisms by which C21orf2 regulates cell proliferation and apoptosis via the JAK2/STAT3 signaling pathway. Materials and methods In vitro, C21orf2’s effects on cell proliferation, migration, invasion, and apoptosis were tested using CCK-8, scratch assays, Transwell assays, TUNEL staining, and electron microscopy. Western blotting assessed the impact of C21orf2 on JAK2/STAT3 proteins and related markers. Co-immunoprecipitation and immunofluorescence explored interactions with downstream targets. In vivo, a subcutaneous xenograft model in nude mice validated C21orf2’s role in tumor growth and apoptosis. Results C21orf2 was upregulated in prostate cancer tissues and regulated the malignant biological behavior of prostate cancer cells, and C21orf2 showed a negative correlation with KCTD5. High expression of C21orf2 promoted the activation of the JAK2/STAT3 signaling pathway and upregulated its downstream target genes, including c-MYC, Cyclin A1, Bcl-2, and Cleaved caspase-3, thereby promoting cell proliferation and inhibiting apoptosis. Conclusions Our study indicates that C21orf2 is a potential biomarker for the diagnosis and treatment of prostate cancer and highlights its potential as a therapeutic target through the JAK2/STAT3 signaling pathway in prostate cancer.