MicroRNA-33b inhibits lung adenocarcinoma cell growth, invasion, and epithelial-mesenchymal transition by suppressing Wnt/β-catenin/ZEB1 signaling

Qu, Jingjing; Li, Min; An, Jian; Zhao, Baotian; Zhong, Wen; Gu, Qing; Cao, Liming; Yang, Huanming; Hu, Chengping

doi:10.3892/ijo.2015.3187

Cited by 76 publications

(68 citation statements)

References 55 publications

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“…44 Meanwhile, it was demonstrated that miR-33b inhibited cells growth, invasion and EMT by suppressing Wnt/β-catenin/ZEB1 signaling in lung adenocarcinoma. 45 In this study, we found that lower expression levels of E-cadherin and higher expression levels of Vimentin were detected in the cells that underwent EMT triggered by miR-218 inhibition. Ectopic expression of miR-218 decreased the invasive capacity of lung cancer cells.…”

Section: Discussionmentioning

confidence: 56%

Downregulation of miR-218 contributes to epithelial–mesenchymal transition and tumor metastasis in lung cancer by targeting Slug/ZEB2 signaling

et al. 2017

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Epithelial–mesenchymal transition (EMT) has been recognized as a key element of cell migration and invasion in lung cancer; however, the underlying mechanisms are not fully elucidated. Recently, emerging evidence suggest that miRNAs have crucial roles in control of EMT and EMT-associated traits such as migration, invasion and chemoresistance. Here, we found that miR-218 expression levels were significantly downregulated in lung cancer tissues compared with adjacent non-cancerous tissues, and the levels of miR-218 were significantly associated with histological grades and lymph node metastasis. Overexpression of miR-218 inhibited cell migration and invasion as well as the EMT process. Of particular importance, miR-218 was involved in the metastatic process of lung cancer cells in vivo by suppressing local invasion and distant colonization. We identified Slug and ZEB2 as direct functional targets of miR-218. Inverse correlations were observed between miR-218 levels and Slug/ZEB2 levels in cancer tissue samples. In addition, overexpression of miR-218 in H1299 increased chemosensitivity of cells to cisplatin treatment through suppression of Slug and ZEB2. These findings highlight an important role of miR-218 in the regulation of EMT-related traits and metastasis of lung cancer in part by modulation of Slug/ZEB2 signaling, and provide a potential therapeutic strategy by targeting miR-218 in NSCLC.

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Section: Discussionmentioning

confidence: 56%

Downregulation of miR-218 contributes to epithelial–mesenchymal transition and tumor metastasis in lung cancer by targeting Slug/ZEB2 signaling

et al. 2017

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“…The Wnt/ β -catenin signaling pathway plays an important role in the development of EMT and cancer metastasis [12]. Thus we further determine the β -catenin protein level in cell nucleus by using western blot.…”

Section: Resultsmentioning

confidence: 99%

“…Recently, it has been reported that overexpression of Wnt signaling pathway is involved in metastasis of lung cancer [12, 20]. Wnt/ β -catenin pathway can control cell proliferation by regulating the expression of cell cycle-related gene including c-Myc and modulate EMT by downregulating E-cadherin and upregulating N-cadherin [21, 22].…”

Section: Discussionmentioning

confidence: 99%

Long Noncoding RNA-LET Suppresses Tumor Growth and EMT in Lung Adenocarcinoma

Liu

Pan

et al. 2016

BioMed Research International

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Recently, many studies showed that long noncoding RNAs (lncRNAs) are involved in tumor progression. It is reported that lncRNA-LET is downregulated and has antitumor effect on several types of cancer. This study focuses on the role of lncRNA-LET on lung adenocarcinoma (LAC) progression. RT-PCR results indicated that frequent downregulation of lncRNA-LET in LAC tissues was related to clinicopathologic factors. lncRNA-LET knockdown significantly promoted LAC cell proliferation, invasion, and migration while lncRNA-LET overexpression obviously inhibited LAC cell proliferation, invasion, and migration, indicating a tumor inhibition of lncRNA-LET in LAC progression. Besides, lncRNA-LET inhibited EMT and negatively regulated Wnt/β-catenin pathway in part. Our study suggests that lncRNA-LET exhibits an important tumor-suppressive effect on LAC progression by inhibiting EMT and Wnt/β-catenin pathway, which provides potential therapeutic targets for LAC.

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“…In other malignant tumors, many reports state that miRNAs can influence tumor invasion and metastasis by participating in the EMT process [22–26]. In ovarian cancer, RhoC overexpression promotes EMT, invasion, and metastasis, and RhoC knockout reverses the promoter role of vascular endothelial growth factor (VEGF) and transforming growth factor (TGF) in EMT [16].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-93 Promotes Epithelial–Mesenchymal Transition of Endometrial Carcinoma Cells

Chen

Sun

et al. 2016

PLoS ONE

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MicroRNA-93, derived from a paralog (miR-106b-25) of the miR-17-92 cluster, is involved in the tumorigenesis and progression of many cancers such as breast, colorectal, hepatocellular, lung, ovarian, and pancreatic cancer. However, the role of miR-93 in endometrial carcinoma and the potential molecular mechanisms involved remain unknown. Our results showed that miR-93 was overexpressed in endometrial carcinoma tissues than normal endometrial tissues. The endometrial carcinoma cell lines HEC-1B and Ishikawa were transfected with miR-93-5P, after which cell migration and invasion ability and the expression of relevant molecules were detected. MiR-93 overexpression promoted cell migration and invasion, and downregulated E-cadherin expression while increasing N-cadherin expression. Dual-luciferase reporter assay showed that miR-93 may directly bind to the 3′ untranslated region of forkhead box A1 (FOXA1); furthermore, miR-93 overexpression downregulated FOXA1 expression while miR-93 inhibitor transfection upregulated FOXA1 expression at both mRNA and protein level. In addition, transfection with the most effective FOXA1 small interfering RNA promoted both endometrial cancer cell migration and invasion, and downregulated E-cadherin expression while upregulating N-cadherin expression. Therefore, we suggest that miR-93 may promote the process of epithelial–mesenchymal transition in endometrial carcinoma cells by targeting FOXA1.

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MicroRNA-33b inhibits lung adenocarcinoma cell growth, invasion, and epithelial-mesenchymal transition by suppressing Wnt/β-catenin/ZEB1 signaling

Cited by 76 publications

References 55 publications

Downregulation of miR-218 contributes to epithelial–mesenchymal transition and tumor metastasis in lung cancer by targeting Slug/ZEB2 signaling

Downregulation of miR-218 contributes to epithelial–mesenchymal transition and tumor metastasis in lung cancer by targeting Slug/ZEB2 signaling

Long Noncoding RNA-LET Suppresses Tumor Growth and EMT in Lung Adenocarcinoma

MicroRNA-93 Promotes Epithelial–Mesenchymal Transition of Endometrial Carcinoma Cells

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