SGOL2 promotes prostate cancer progression by inhibiting RAB1A ubiquitination

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.

LncRNA BANCR promotes oral squamous cell carcinoma progression via regulating Rab1A signaling

“…Circulation of active Rabs can be mediated by guanine nucleotide exchange factors and GTPase‐activating proteins 24 . Rab1A can be regulated by miRNAs in colorectal cancer, prostate cancer, and hepatocellular carcinoma, or inhibited ubiquitination by SGOL2 in prostate cancer 25–28 . The oncogenic role of Rab1A via the mTOR signaling pathway has been preliminarily elucidated 29 .…”

“…24 Rab1A can be regulated by miRNAs in colorectal cancer, prostate cancer, and hepatocellular carcinoma, or inhibited ubiquitination by SGOL2 in prostate cancer. [25][26][27][28] The oncogenic role of Rab1A via the mTOR signaling pathway has been preliminarily elucidated. 29 To the best of our knowledge, this is the first study to analyze the functional and mechanistical role of Rab1A in OSCC progression.…”

High SGO2 predicted poor prognosis and high therapeutic value of lung adenocarcinoma and promoted cell proliferation, migration, invasion, and epithelial-to-mesenchymal transformation

“…Initial research focused on the role of SGO2 in protecting centromeric cohesion during mammalian meiosis I, but subsequent studies found that high SGO2 expression is associated with poor prognosis in a variety of cancers, including liver cancer, prostate cancer, and glioma. [15,[30][31][32][33] By using cancer stem cell-associated genes (RAB10, TCOF1, and PSMD14), Liang et al constructed a prognostic model for HCC and identified SGO2 as a potential therapeutic target. [34] Deng et al used bioinformatics to verify the association between high SGO2 expression and poor overall survival and advanced clinicopathological features in HCC.…”

Targeting Prolyl 4-Hydroxylase Subunit Beta (P4HB) in Cancer: New Roads to Travel

“…Furthermore, P4HB also served as a core role in the autophagy regulatory mechanisms of BLCA, warranting further investigation and exploration [19]. As the population ages over the coming decades, PRAD is one of the most common cancers in the urinary system, placing additional strain on the healthcare system [20][21][22][23][24][25][26]. Consistent with our pan-cancer analysis, our previous studies [8,27] found that P4HB expression was higher in tumor samples than in normal samples and P4HB downregulation could significantly inhibit the cell proliferation of six PRAD cell lines, including LNCap, C4-2, C4-2B, PC3, DU145 and 22RV1 cells.…”