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Updated: Sep 12, 2025

miRNA Expression Analyses in Prostate Cancer Clinical Tissues
Published on: September 8, 2015
USP22-mediated PNMA5 deubiquitination promotes proliferation, migration and invasion of prostate cancer cells
Hong Zhi1, Tana1, Nigemutu Bai1
1Department of Integrated Mongolian and Western Medicine and Urology, Affiliated Hospital of Inner Mongolia Minzu University, Tongliao City, Inner Mongolia Autonomous Region, China.
Background:
Prostate cancer (PCa) stands as one of the primary contributors to cancer-related mortality among men globally. It is reported that USP22 functions as an oncogene, while PNMA5 exhibits a significant pro-metastatic effect. This research investigation centered on examining the interplay between USP22 and PNMA5 and their collaborative role in enhancing PCa progression.
Methods:
The expression of USP22 and PNMA5 in tissue was determined by IHC. The differential expression of cellular USP22 and PNMA5 were detected using qPCR and immunoblotting, respectively. Cell viability and proliferation were assessed by MTT and sphere-formation assay. Transwell and wound-healing assay were conducted to evaluate the metastatic ability. The interaction between USP22 and PNMA5 was detected by Co-IP and IP. A tumor-bearing mice model was established for in vivo detection.
Results:
USP22 and PNMA5 were highly expressed in both PCa tumor tissues and cells. Knocking down USP22 or PNMA5 inhibited the migration and invasion of PCa cells. USP22 mediated the deubiquitination of PNMA5. PNMA5 overexpression reversed the decrease in cell viability and proliferation rate, as well as the diminished migration and invasion ability induced by USP22 knockdown.
Conclusion:
USP22 promotes migration and invasion of PCa cells by regulating PNMA5 deubiquitination.
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