Research Paper Volume 14, Issue 24 pp 10050—10066
SGOL2 promotes prostate cancer progression by inhibiting RAB1A ubiquitination
- 1 Department of Immuno-Oncology, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei, P.R. China
- 2 Department of Urinary Surgery, The Fourth Hospital of Hebei Medical University, Shijiazhuang 050011, Hebei, P.R. China
Received: June 9, 2022 Accepted: December 5, 2022 Published: December 23, 2022
https://doi.org/10.18632/aging.204443How to Cite
Copyright: © 2022 Lv et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
Prostate cancer is the most prevalent genitourinary malignant cancer in men worldwide. Patients with prostate cancer who progress to castration-resistant prostate cancer (CRPC) or metastatic CRPC have significantly poorer survival. Advanced prostate cancer is a clinical challenge due to the lack of effective treatment strategies. In the field of oncology, SGOL2 was an emerging and differentially expressed molecule, which enhanced the proliferation of cell populations in vitro in our studies. Mass spectrum and Co-IP validated the interaction of SGOL2 and RAB1A in a protein-protein manner. We further investigated the role of SGOL2 in the regulatory mechanism of RAB1A in prostate cancer cell lines. Furthermore, SGOL2 regulated RAB1A expression by inhibiting its ubiquitination. Rescue Experiments demonstrated that SGOL2 promoted prostate cancer cell proliferation and migration by upregulating RAB1A expression. Finally, we found that SGOL2 and RAB1A may regulate the tumor microenvironment (TME) in prostate cancer. In conclusion, our findings concluded that SGOL2 stabilized RAB1A expression to promote prostate cancer development. Both of them were of great importance in TME modulation.
Abbreviations
CRPC: castration-resistant prostate cancer; mCRPC: metastatic castration-resistant prostate cancer; PPI: protein-protein interaction; MS: mass spectrum; TME: tumor microenvironment; IHC: immunohistochemistry; FBS: fetal bovine serum; RNAi: RNA interference; WB: western blotting; Co-IP: co-immunoprecipitation; MS: mass spectrometry; CHX: cycloheximide.