MicroRNA-20b inhibits the proliferation, migration and invasion of bladder cancer EJ cells via the targeting of cell cycle regulation and Sp-1-mediated MMP-2 expression

Park, Sung Lyea; Cho, Tae-Min; Won, Se Yeon; Song, Junhui; Noh, Dae-Hwa; Kim, Wun-Jae; Moon, Sung‐Kwon

doi:10.3892/or.2015.4119

Cited by 31 publications

(30 citation statements)

References 25 publications

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“…34 However, another study has demonstrated that miR-20b exerts tumor-suppressor effects in bladder cancer and inhibits cancer cells proliferation, migration and invasion. 35 In this study, we demonstrated the novel tumor-suppressor roles of miR-17 and miR-20b in the taxol resistance of breast cancer. All these studies suggested miR-17 and miR-20b functioned as both a driver and suppressor of cancers dependent on cellular contexts, and its function was determined by multiple factors.…”

Section: Discussionmentioning

confidence: 69%

Decreased expression of microRNA-17 and microRNA-20b promotes breast cancer resistance to taxol therapy by upregulation of NCOA3

Nie

et al. 2016

Cell Death Dis

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Chemoresistance is a major obstacle to effective breast cancer chemotherapy. However, the underlying molecular mechanisms remain unclear. In this study, nuclear receptor coactivator 3 (NCOA3) was found to be significantly increased in taxol-resistant breast cancer tissues and cells. Moreover, overexpression of NCOA3 enhanced breast cancer cell resistance to taxol, whereas depletion of NCOA3 decreased taxol resistance. Subsequently, we investigated whether NCOA3 expression was regulated by miRNAs in breast cancer. By bioinformatics prediction in combination with the data of previous report, miR-17 and miR-20b were selected as the potential miRNAs targeting NCOA3. By real-time PCR analysis, we found that miR-17 and miR-20b were significantly reduced in taxol-resistant breast cancer tissues and cells. In addition, we provided some experimental evidences that miR-17 and miR-20b attenuated breast cancer resistance to taxol in vitro and in vivo models. Furthermore, by luciferase reporter assays, we further validated that both miR-17 and miR-20b directly binded the 3′-untranslated region of NCOA3 mRNA and inhibited its expression in breast cancer cells. Finally, both miR-17 and miR-20b levels were found to be significantly negatively correlated with NCOA3 mRNA levels in breast cancer tissues. Together, our results indicated that loss of miR-17 and miR-20b enhanced breast cancer resistance to taxol by upregulating NCOA3 levels. Our study suggested miR-17, miR-20b and NCOA3 may serve as some predictive biomarkers and potential therapeutic targets in taxol-resistant breast cancer treatment.

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Section: Discussionmentioning

confidence: 69%

Decreased expression of microRNA-17 and microRNA-20b promotes breast cancer resistance to taxol therapy by upregulation of NCOA3

Nie

et al. 2016

Cell Death Dis

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“…In their study inhibition of miR-20b increased protein levels of VEGF and HIF-1α in normoxic tumor cells, an increase of miR-20b expression in hypoxic tumor cells resulted in reduced protein levels of VEGF and HIF-1α (85). Park et al showed that miR-20b expression was downregulated in bladder cancer and an upregulation of this miRNA type lead to inhibition of proliferation, migration and invasion (61). In gastric cancer, downregulated miR-20b expression was associated with hypoxia-induced chemoresistance.…”

Section: Discussionmentioning

confidence: 99%

Hypoxia- and acidosis-driven aberrations of secreted microRNAs in endometrial cancer in vitro

et al. 2017

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Abstract. Due to their post-transcriptional regulatory impact on gene expression, microRNAs (miRNA, miRs) influence decisively cellular processes of differentiation, proliferation and apoptosis. In oncogenic pathways various miRNAs exert either oncogenic or tumor suppressor activities in a stage-specific manner. Dysregulation of miRNA expression pattern has been associated with several human cancers including endometrial cancer (EC). In the present study, expression profile alterations of EC associated secreted miRNAs were determined under the microenvironmental stress situations hypoxia and acidosis occurring in tumor progression and metastasis. The potential influence of hypoxia and acidosis vs. control conditions on the expression levels of 24 EC-relevant miRNA types was quantitatively accessed via real-time PCR in three established EC in vitro models. Expression data were analyzed statistically. In vitro application of hypoxia resulted in downregulation of miR-15a, miR-20a, miR-20b and miR-128-1 in Ishikawa cells (type I EC) and upregulation of miR-21 in EFE-184 cells (type I EC). Acidosis triggered upregulation of tumor promoting miR125b in AN3-CA cell (type II EC), whereas in Ishikawa cells (type I EC) miRNAs with tumor suppressive function were found altered in divergent directions, both up-(let-7a) and down-(miR-22) regulated. Our current findings emphasize the functional importance of secreted miRNAs in the immediate response of EC cells to exogenic stress situations such as the typical tumor epiphenomena hypoxia and acidosis. Focusing on the specific potential of secreted, thus circulating miRNA molecules, alterations in expression levels not only influence intracellular gene expression and signaling cascades, but also transfer the induction of (tumor)biological cellular changes to adjacent cells.

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“…In the present study, we found that miR-20b was downregulated in CC patients and significantly inhibited the proliferation of CC cells in vitro, which is consistent with a previous study that found that miR-20b was downregulated in colon tumors. Furthermore, miR-20b was reported to inhibit the proliferation of melanoma cells by regulating the proteinase-activated receptor-1 (PAR-1), thrombin receptor (27), and to inhibit cell cycle progression by targeting MMP-2 in bladder cancer EJ cells (19).…”

Section: Mir-20b Reduces 5-fu Resistance In the Hct116-r Cellsmentioning

confidence: 99%

“…In recent years, miR-20b has been found to be downregulated in many types of cancer tissues. In addition, miR-20b inhibited the proliferation, migration and invasion of bladder cancer EJ cells via targeting of cell cycle regulation and Sp-1-mediated MMP-2 expression (19). Moreover, miR-20b showed decreased expression in colon tumors relative to normal colon tissue (20).…”

Section: Introductionmentioning

confidence: 96%

miR-20b reduces 5-FU resistance by suppressing the ADAM9/EGFR signaling pathway in colon cancer

Cheng

Zhang

et al. 2016

Oncology Reports

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Chemoresistance is a major obstacle to cancer therapy including that of colon cancer (CC). Although the dysregulation of many miRNAs has been implicated in 5-fluorouracil (5-FU) resistance in CC cells, the specific role of miR-20b in chemoresistance has not been documented. In the present study, we first determined the expression of miR-20b by RT-PCR and the levels of a disintegrin and metalloprotease 9 (ADAM9) and epidermal growth factor receptor (EGFR) by western blotting in CC and adjacent non-cancerous tissues from 5-FU-sensitive or -resistant CC patients. Subsequently, 5-FU-sensitive (HCT116) and -resistant (HCT116-R) cells were obtained, and the levels of miR-20b, ADAM9 and EGFR were detected. Meanwhile, the 5-FU resistance of the cells was examined by assessing cell viability (by MTT assay) and apoptosis (by flow cytometry). After transfection of miR-20b into HCT116-R cells, drug resistance was reexamined. We then confirmed the relationship between miR-20b and ADAM9 by luciferase reporter assay. Finally, 5-FU resistance in HCT116 and HCT116-R cells was compared after transfection with miR-20b. Our results showed that miR-20b was expressed at lower levels in the 5-FU-resistant tissues and cells than in the 5-FU-sensitive tissues and cells. The opposite was the case for expression of ADAM9 and EGFR. In addition, we demonstrated that ADAM9 is a direct target of miR-20b and that miR-20b decreased the 5-FU resistance of HCT116-R cells. Our findings suggest that miR-20b reduces 5-FU resistance to induce apoptosis in vitro by suppressing ADAM9/EGFR in CC cells.

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MicroRNA-20b inhibits the proliferation, migration and invasion of bladder cancer EJ cells via the targeting of cell cycle regulation and Sp-1-mediated MMP-2 expression

Cited by 31 publications

References 25 publications

Decreased expression of microRNA-17 and microRNA-20b promotes breast cancer resistance to taxol therapy by upregulation of NCOA3

Decreased expression of microRNA-17 and microRNA-20b promotes breast cancer resistance to taxol therapy by upregulation of NCOA3

Hypoxia- and acidosis-driven aberrations of secreted microRNAs in endometrial cancer in vitro

miR-20b reduces 5-FU resistance by suppressing the ADAM9/EGFR signaling pathway in colon cancer

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