Knockdown of GSG2 inhibits prostate cancer progression in�vitro and in�vivo

Yu, Feng; Lin, Yuanyuan; Xu, Xinping; Liu, Weipeng; Tang, Dan; Zhou, Xiaochen; Wang, Gongxian; Zheng, Yi; Xie, An

doi:10.3892/ijo.2020.5043

Cited by 12 publications

(10 citation statements)

References 39 publications

(41 reference statements)

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“… 17 Yu et al reported, in prostate cancer cells, the inhibition of proliferation and migration and promotion of apoptosis, suggesting GSG2 as a tumor promotor in prostate cancer. 14 Similar functions could also be observed in pancreatic cancer 16 and gallbladder carcinoma. 16 In this study, our group discerned GSG2 as a novel regulator of ovarian cancer, thus a potential therapeutic target for treatment and prognostic indicator.…”

Section: Discussionsupporting

confidence: 59%

“… 9 Survivin recognizes H3T3ph to bring the CPC (chromosomal passenger complex) to the centromere region, thereby promoting the metaphase arrangement of chromosomes and the cell cycle. 10–12 Although the function of GSG2 has not been clearly illustrated so far, some studies have shown that it plays a role as a cancer-promoting factor in various human tumors 13 such as prostate cancer, 14 gallbladder cancer 15 and pancreatic cancer. 16 Several studies have shown that its small molecule inhibitor CHR-6494 shows anti-proliferative activity in various tumor cell lines.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

GSG2 Promotes Development and Predicts Poor Prognosis of Ovarian Cancer

Huang

Liu

Zhü

et al. 2021

CMAR

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Section: Discussionsupporting

confidence: 59%

Section: Introductionmentioning

confidence: 99%

GSG2 Promotes Development and Predicts Poor Prognosis of Ovarian Cancer

Huang

Liu

Zhü

et al. 2021

CMAR

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“…However, advanced PCa still lacks effective therapeutic strategies 3–5 . Thus, researchers are currently focused on inhibiting tumor progression to explore effective therapeutic strategies for PCa treatment 6,7 …”

Section: Introductionmentioning

confidence: 99%

Proteomics reveals the function reverse of MPSSS‐treated prostate cancer‐associated fibroblasts to suppress PC‐3 cell viability via the FoxO pathway

et al. 2021

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Prostate cancer‐associated fibroblasts (prostate CAFs) are essential components of the tumor microenvironment and can promote tumor progression through their immunosuppressive functions. MPSSS, a novel polysaccharide purified from Lentinus edodes , has been reported to have anti‐tumor activity. MPSSS could also inhibit the immunosuppressive function of prostate CAFs, which has been demonstrated through that the secretome of MPSSS‐treated prostate CAFs could inhibit the proliferation of T cells. However, how the secretome of MPSSS‐treated prostate CAFs influence prostate cancer progression is still unclear. Interestingly, we found that the low molecular weight (3–100kD) secretome of prostate CAFs (lmwCAFS) could promote the growth of PC‐3 cells, while that of MPSSS‐treated prostate CAFs (MT‐lmwCAFS) could inhibit their growth. We carried out comparative secretomic analysis of lmwCAFS and MT‐lmwCAFS to identify functional molecules that inhibit the growth of PC‐3 cells, and proteomic analysis of lmwCAFS‐treated PC‐3 cells and MT‐lmwCAFS‐treated PC‐3 cells to investigate the underlying molecular mechanism. These analyses suggest that TGF‐β3 from MT‐lmwCAFS may inhibit the growth of PC‐3 cells. The validated experiments revealed that TGF‐β3 from MT‐lmwCAFS activated p21 expression in PC‐3 cells by regulating the FoxO pathway thereby inducing G0/G1 cell cycle arrest of PC‐3 cells. Overall, our data demonstrated that MPSSS reversed the ability of prostate CAFs to suppress the cell viability of PC‐3 cells, which might provide a potential therapeutic strategy to prevent prostate cancer progression.

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“…After that, cells were colored using Giemsa Stain Kit (Abcam, ab150670) for 20 mins. Lasly, images of typical colony morphology were photographed and the the number of colonies in each conditions was counted under a Leica AM6000 microscope [41]. The colony formation assay was conducted with three independent assays in the same method.…”

Section: -Ethynyl-2-deoxyuridine (Edu) Incorporation Assaymentioning

confidence: 99%

LINC00893 Inhibits The Progression of Prostate Cancer Through miR-3173-5p/SOCS3/JAK2/STAT3 Pathway

Yu¹,

Fan²,

Liu³

et al. 2021

Preprint

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Background: Prostate cancer (PCa) is one of the most common malignant tumors in the male urinary system. In recent years, the morbidity and mortality of PCa have been increasing due to the limited effects of existing treatment strategies. Long non-coding RNA (lncRNA) LINC00893 inhibits the proliferation and metastasis of papillary thyroid cancer (PTC) cells, but its role in PCa has not been reported. Our study aims to clarify the role and underlying mechanism of LINC00893 in regulating the progression of PCa.Methods: We analyzed LINC00893 expression through TCGA database. We also collected 66 paires of PCa tissues and matched para-cancerous tissues as well as cell lines and assessed LINC00893 expression. Subsequently, we conducted gain-of-function assays to confirm the role of LINC00893 in PCa. CCK-8, EdU, colony information and transwell assays were implemented to detect cell proliferation, colony formation and metastasis abilities, respectively. RT-qPCR and western blot assays were used to quantify the expression of mRNA and protein. Dual-luciferase reporter, RNA-binding protein immunoprecipitation (RIP) and RNA pull down assays were conducted to evaluate the interaction of molecules. Spearman correlation coefficient analysis was conducted to detect the correlation between molecules.Results: We found that the LINC00893 expression in PCa tissues and cell lines was upregulated compared with matched controls, and patients with low expression of LINC00893 suffered a low overall survival rate. Overexpression of LINC00893 hindered the proliferation, epithelial-mesenchymal transition (EMT) as well as metastasis of PCa cells in vitro and in vivo. In terms of mechanism, suppressor of cytokine signaling 3 (SOCS3)/Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway occupied a central position in the regulation of PCa progression by LINC00893. LINC00893 weakened the inhibition role of miR-3173-5p on SOCS3 expression through functioning as a miR-3173-5p sponge, which inhibited the JAK2/STAT3 signaling pathway. Conclusions: LINC00893 suppresses the progression of prostate cancer through miR-3173-5p/SOCS3/JAK2/STAT3 pathway. our data uncovers a novel mechanism by which LINC00893 hinders the progression of PCa, which enriches the molecular network of LINC00893 regulating the PCa progression and laies a theoretical foundation for PCa targeted therapy.

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Knockdown of GSG2 inhibits prostate cancer progression in�vitro and in�vivo

Cited by 12 publications

References 39 publications

GSG2 Promotes Development and Predicts Poor Prognosis of Ovarian Cancer

GSG2 Promotes Development and Predicts Poor Prognosis of Ovarian Cancer

Proteomics reveals the function reverse of MPSSS‐treated prostate cancer‐associated fibroblasts to suppress PC‐3 cell viability via the FoxO pathway

LINC00893 Inhibits The Progression of Prostate Cancer Through miR-3173-5p/SOCS3/JAK2/STAT3 Pathway

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