Activator of G protein signaling 3 modulates prostate tumor development and progression

Adekoya, Timothy O.; Smith, Nicola; Aladeniyi, Temilade; Blumer, Joe B.; Chen, Xiaoxin L.; Richardson, Ricardo M.

doi:10.1093/carcin/bgz076

Cited by 10 publications

(7 citation statements)

References 47 publications

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“…GPSM1 gene has been found to be involved in cell division, reproduction, and differentiation [49][50][51]. Recent studies have identified GPSM1 as a predisposition gene of premature ovarian insufficiency [52], a plausible gene involved in regulation of skeletal muscle in diabetes mellitus [53], and to be overexpressed in prostate adenocarcinoma [12]. In our study, analyses from Oncomine and UALCAN suggested different results: GPSM1 was found to be under-expressed in breast cancer in the former database, while the latter indicated the reverse.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, bioinformatics analysis and in vivo verification have suggested that GPSM2 negatively influenced patient response to paclitaxel, one of the most effective and well-tolerated chemotherapy drugs for breast cancer [10]. Meanwhile, members of the GPSM family are known to be associated with other neoplasms, namely lung [11], prostate [12], and pancreatic cancer [13].…”

Section: Introductionmentioning

confidence: 99%

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Identifying GPSM Family Members as Potential Biomarkers in Breast Cancer: A Comprehensive Bioinformatics Analysis

Dang

Nguyen

et al. 2021

Biomedicines

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G-protein signaling modulators (GPSMs) are a class of proteins involved in the regulation of G protein-coupled receptors, the most abundant family of cell-surface receptors that are crucial in the development of various tumors, including breast cancer. This study aims to identify the potential therapeutic and prognostic roles of GPSMs in breast cancer. Oncomine and UALCAN databases were queried to determine GPSM expression levels in breast cancer tissues compared to normal samples. Survival analysis was conducted to reveal the prognostic significance of GPSMs in individuals with breast cancer. Functional enrichment analysis was performed using cBioPortal and MetaCore platforms. Finally, the association between GPSMs and immune infiltration cells in breast cancer was identified using the TIMER server. The experimental results then showed that all GPSM family members were significantly differentially expressed in breast cancer according to Oncomine and UALCAN data. Their expression levels were also associated with advanced tumor stages, and GPSM2 was found to be related to worse distant metastasis-free survival in patients with breast cancer. Functional enrichment analysis indicated that GPSMs were largely involved in cell division and cell cycle pathways. Finally, GPSM3 expression was correlated with the infiltration of several immune cells. Members of the GPSM class were differentially expressed in breast cancer. In conclusion, expression of GPSM2 was linked with worse distant metastasis-free outcomes, and hence could potentially serve as a prognostic biomarker. Furthermore, GPSM3 has potential to be a possible target for immunotherapy for breast cancer.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Identifying GPSM Family Members as Potential Biomarkers in Breast Cancer: A Comprehensive Bioinformatics Analysis

Dang

Nguyen

et al. 2021

Biomedicines

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“…Leukemia is one of the most prevalent cancers and accounted for 3.2% of cancer-related death worldwide in 2018 ( 27 ). Several studies have shown the association of GPSM1 with the progression of multiple myeloma ( 28 ), prostate cancer ( 29 ) and esophageal squamous cell carcinoma ( 30 ), but the role of GPSM1 in the development of leukemia has not been defined. The analysis of several datasets extracted from the Oncomine database showed that the expression of GPSM1 in B-ALL is significantly higher than that in controls ( Figure 1 ).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of GPSM1 Inhibits the Proliferation and Promotes the Apoptosis of B-Cell Acute Lymphoblastic Leukemia Cells by Suppressing the ADCY6-RAPGEF3-JNK Signaling Pathway

Zhang

Zhou

Sun

et al. 2021

Pathol. Oncol. Res.

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B-cell acute lymphoblastic leukemia (B-ALL) is the common type of blood cancer. Although the remission rate has increased, the current treatment options for B-ALL are usually related to adverse reactions and recurrence, so it is necessary to find other treatment options. G protein signaling modulator 1 (GPSM1) is one of several factors that affect the basic activity of the G protein signaling system, but its role in B-ALL has not yet been clarified. In this study, we analyzed the expression of GPSM1 in the Oncomine database and found that the GPSM1 levels were higher in B-ALL cells than in peripheral blood mononuclear cells (PBMCs). Analyses of the Gene Expression Profiling Interactive Analysis (GEPIA) demonstrated that patients with high GPSM1 levels had shorter survival times than those with low levels. Additionally, gene set enrichment analysis (GSEA) suggested that GPSM1 was positively correlated with proliferation, G protein-coupled receptor (GPCR) ligand binding, Gαs signaling and calcium signaling pathways. In further experiments, GPSM1 was found to be highly expressed in Acute lymphoblastic leukemia (ALL) cell lines, and downregulation of GPSM1 inhibited proliferation and promoted cell cycle arrest and apoptosis in BALL-1 and Reh cells. Moreover, knockdown of GPSM1 suppressed ADCY6 and RAPGEF3 expression in BALL-1 and Reh cells. Furthermore, we reported that GPSM1 regulated JNK expression via ADCY6-RAPGEF3. The present study demonstrates that GPSM1 promotes tumor growth in BALL-1 and Reh cells by modulating ADCY6-RAPGEF3-JNK signaling.

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“…New guidelines in recent years, however, includes combining ADT with other chemotherapeutic drugs (e.g., Docetaxel) to improve overall patient survival [ 7 , 8 ]. Furthermore, various studies have shown how androgen-dependent and -independent pathways promote prostate tumorigenesis [ 2 , 9 , 10 , 11 , 12 , 13 ]. In spite of the successes attained in treatment of prostate cancer, these achievement milestones have been dampened by resistance to drug treatments and generation of evasive mechanisms by tumor cells.…”

Section: Introductionmentioning

confidence: 99%

Cytokines and Chemokines as Mediators of Prostate Cancer Metastasis

Adekoya

Richardson

2020

IJMS

109

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The consequences of prostate cancer metastasis remain severe, with huge impact on the mortality and overall quality of life of affected patients. Despite the convoluted interplay and cross talk between various cell types and secreted factors in the metastatic process, cytokine and chemokines, along with their receptors and signaling axis, constitute important factors that help drive the sequence of events that lead to metastasis of prostate cancer. These proteins are involved in extracellular matrix remodeling, epithelial-mesenchymal-transition, angiogenesis, tumor invasion, premetastatic niche creation, extravasation, re-establishment of tumor cells in secondary organs as well as the remodeling of the metastatic tumor microenvironment. This review presents an overview of the main cytokines/chemokines, including IL-6, CXCL12, TGFβ, CXCL8, VEGF, RANKL, CCL2, CX3CL1, IL-1, IL-7, CXCL1, and CXCL16, that exert modulatory roles in prostate cancer metastasis. We also provide extensive description of their aberrant expression patterns in both advanced disease states and metastatic sites, as well as their functional involvement in the various stages of the prostate cancer metastatic process.

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Activator of G protein signaling 3 modulates prostate tumor development and progression

Cited by 10 publications

References 47 publications

Identifying GPSM Family Members as Potential Biomarkers in Breast Cancer: A Comprehensive Bioinformatics Analysis

Identifying GPSM Family Members as Potential Biomarkers in Breast Cancer: A Comprehensive Bioinformatics Analysis

Knockdown of GPSM1 Inhibits the Proliferation and Promotes the Apoptosis of B-Cell Acute Lymphoblastic Leukemia Cells by Suppressing the ADCY6-RAPGEF3-JNK Signaling Pathway

Cytokines and Chemokines as Mediators of Prostate Cancer Metastasis

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