Down-regulation of BTG3 promotes cell proliferation, migration and invasion and predicts survival in gastric cancer

Ren, Xiaohu; Zhu, Xiaohong; Li, X. M.; Li, Y. L.; Wang, J. M.; Wu, Pingxiang; Lv, Zhenbing; H., W.; Liao, Wenting; Wang, W.; Ding, Yanqing; Li, Liang

doi:10.1007/s00432-014-1826-9

Cited by 34 publications

(39 citation statements)

References 23 publications

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“…4a; Additional file 1: Table S2). Among these, FBXL5 and BTG3 have been reported to regulate EMT and cancer metastasis [24–26]. Data from the microarray analysis was confirmed by qPCR in HeLa cells (Fig.…”

Section: Resultsmentioning

confidence: 65%

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iASPP induces EMT and cisplatin resistance in human cervical cancer through miR-20a-FBXL5/BTG3 signaling

Xiong

Sun

Dong

et al. 2017

J Exp Clin Cancer Res

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BackgroundEpithelial–mesenchymal transition (EMT) and dysregulated microRNAs (miRNAs) have important roles in driving chemoresistance. We previously reported that iASPP is a key EMT inducer and could increase cisplatin resistance in cervical cancer (CC) cells. Herein, we investigate the downstream mechanisms through which iASPP contributes to EMT and cisplatin resistance in CC.MethodsBy using a lentiviral system, we investigated the effects of iASPP knockdown on CC cell growth and chemosensitivity of CC cells to cisplatin in vivo. We examined if miR-20a, which was up-regulated following iASPP overexpression, would influence metastatic phenotypes and cisplatin resistance in CC cells, and explored the possible molecular mechanisms involved.ResultsKnockdown of iASPP suppressed CC cell proliferation and sensitized CC cells to cisplatin in vivo. iASPP promotes miR-20a expression in a p53-dependent manner. Upregulation of miR-20a induced EMT and the recovery of CC cell invasion and cisplatin chemoresistance that was repressed by iASPP knockdown. We identified FBXL5 and BTG3 as two direct miR-20a targets. Silencing of FBXL5 and BTG3 restored cell invasion and cisplatin chemoresistance, which was suppressed by iASPP or miR-20a knockdown. Reduced FBXL5 and BTG3 expression was found in CC samples and associated with poor prognosis in CC patients.ConclusionsiASPP promotes EMT and confers cisplatin resistance in CC via miR-20a-FBXL5/BTG3 signaling.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-017-0520-6) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 65%

“…BTG3 was also shown to suppress proliferation and invasion of gastric and esophageal cancer cells [26, 44]. We demonstrated for the first time that FBXL5 and BTG3 are down-regulated in CC tissues and their downregulation are associated with worse prognosis in CC patients.…”

Section: Discussionmentioning

confidence: 90%

iASPP induces EMT and cisplatin resistance in human cervical cancer through miR-20a-FBXL5/BTG3 signaling

Xiong

Sun

Dong

et al. 2017

J Exp Clin Cancer Res

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“…BTG3 expression was found to positively associate with favorable prognosis of gastric and ovarian cancers [13, 16]. Lv et al [14] found that the hepatocellular cancer patients with lower BTG3 expression had shorter overall survival time than the ones with higher BTG3 expression.…”

Section: Discussionmentioning

confidence: 99%

The suppressing effects of BTG3 expression on aggressive behaviors and phenotypes of colorectal cancer: Anin vitroandvivostudy

Zheng

et al. 2017

Oncotarget

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Here, we found that down-regulated expression of BTG3 might be positively correlated with colorectal carcinogenesis and its overexpression suppressed proliferation, glycolysis, mitochondrial respiration, cell cycle progression, migration, and invasion, and induced apoptosis, senescence and differentiation in SW480 and SW620 cells. After treated with cisplatin, MG132, paclitaxel and SAHA, BTG3 transfectants exhibited lower viability and higher apoptosis than the control in both time- and dose-dependent manners. BTG3 overexpression up- regulated the protein expression of Cyclin E, p16, p27, NF-κB, p38α/β, XIAP, Bcl-2, ATG14 and p53, but down-regulated the mRNA expression of MRP1, BCRP, and mTOR in SW480 and SW620 cells. BTG3 overexpression inhibited tumor growth of SW620 cells by suppressing proliferation and inducing apoptosis. It was suggested that down-regulated BTG3 expression might be considered as a marker for colorectal carcinogenesis. BTG3 overexpression might reverse the aggressive phenotypes and be employed as a potential target for gene therapy of colorectal cancer.

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“…Recent evidence has demonstrated that BTG3 functions as a tumor suppressor in cancer progression. BTG3 expression is downregulated in lung adenocarcinoma, oral squamous cell cancer, or prostate cancer [19][20][21][22]. It was reported that BTG3 was a suppressor in the ESC progression [4].…”

Section: Discussionmentioning

confidence: 98%

Direct Downregulation of B-Cell Translocation Gene 3 by microRNA-93 Is Required for Desensitizing Esophageal Cancer to Radiotherapy

et al. 2017

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Down-regulation of BTG3 promotes cell proliferation, migration and invasion and predicts survival in gastric cancer

Abstract: Down-regulation of BTG3 is closely associated with proliferation, migration and invasion in GC. It may be a novel prognostic biomarker for GC patients.

Cited by 34 publications

References 23 publications

iASPP induces EMT and cisplatin resistance in human cervical cancer through miR-20a-FBXL5/BTG3 signaling

iASPP induces EMT and cisplatin resistance in human cervical cancer through miR-20a-FBXL5/BTG3 signaling

The suppressing effects of BTG3 expression on aggressive behaviors and phenotypes of colorectal cancer: Anin vitroandvivostudy

Direct Downregulation of B-Cell Translocation Gene 3 by microRNA-93 Is Required for Desensitizing Esophageal Cancer to Radiotherapy

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