MiR-203 suppresses tumor growth and invasion and down-regulates MiR-21 expression through repressing Ran in esophageal cancer

Zhang, Fang; Yang, Zhiping; Cao, Minjun; Xu, Yinsheng; Li, Jintao; Chen, Xuebin; Gao, Zhi; Jing, Xin; Zhou, Shaomei; Zhou, Zhixiang; Yang, Yanwen; Wang, Sheng; Zeng, Yi

doi:10.1016/j.canlet.2013.08.037

Cited by 83 publications

(59 citation statements)

References 30 publications

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“…In particular, miR-203 is defined as a tumor suppressor for controlling EMT and metastasis in several cancers (Davis et al, 2006;Mega et al, 2005;Moes et al, 2012;Saini et al, 2011;Zhang et al, 2014;Zhang et al, 2011). Additionally, various research groups studying miRNA expression profiles have revealed that miR-203 decreases in esophageal cancer (Feber et al, 2008;Mathé et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

Epidermal growth factor-induced C/EBPbeta participates in EMT by dampening miR-203 in esophageal squamous cell carcinoma

Shan

Xiong

et al. 2014

Journal of Cell Science

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Epithelial-mesenchymal transition (EMT) is a developmental program that is associated with esophageal squamous cell carcinoma (ESCC) progression and metastasis. Recently, C/EBPb has been reported to be an EMT inducer in cancer. However, the detailed molecular mechanisms remain unclear. Here, we report for the first time, that the truncated CCAAT-enhancer-binding protein b (C/EBPb) LIP isoform is abnormally overexpressed and correlated with cancer metastasis in clinical specimens of human ESCC. Furthermore, we demonstrate that C/EBPb LIP mediates epithelial growth factor (EGF)-induced EMT and increases migration and invasion of esophageal cancer cells in a manner that is dependent on miR-203 inactivation. Finally, we identified miR-203 as a direct target of C/EBPb LIP. Disruption of C/EBPb LIP attenuated the EGF-mediated decrease in miR-203, whereas overexpression of C/ EBPb LIP alone markedly suppressed miR-203. In addition, we demonstrated that C/EBPb LIP inhibited miR-203 transcription by directly interacting with a conserved distal regulatory element upstream of the miR-203 locus, and in doing so, orchestrated chromatin remodeling. In conclusion, our results have revealed a new regulatory mechanism that involves C/EBPb-LIP-mediated downregulation of miR-203, which plays a key role in EMT and metastasis.

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Section: Introductionmentioning

confidence: 99%

Epidermal growth factor-induced C/EBPbeta participates in EMT by dampening miR-203 in esophageal squamous cell carcinoma

Shan

Xiong

et al. 2014

Journal of Cell Science

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“…Esophageal cancer contains two histological types, esophageal squamous cell carcinoma (ESCC) and esophageal adenocarcinoma (EAC) [2]. In China, a high incidence of ESCC exceeds 100 cases per 100,000 people per year.…”

Section: Introductionmentioning

confidence: 99%

Down-Regulation of miR-140 Induces EMT and Promotes Invasion by Targeting Slug in Esophageal Cancer

Jiang

Zhou

et al. 2014

Cell Physiol Biochem

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Background/Aims: MicroRNAs (miRNAs) are reported to regulate cell invasion and functions by interfering with the translation of target mRNAs, but the role of miRNAs in esophageal cancer (EC) remains unclear. Methods: RT-PCR and Western blot were used to detect the expression of miRNAs and candidate genes in EC samples (n=89). miR-140 mimics and inhibitor were tansfected in human TE-1 and Eca-109 cells. The transwell assay was used to examine the cell invasive ability. The regulation mechanism was confirmed by luciferase reporter assay. The markers of EMT were detected by using Western blot. Results: miR-140 expression was decreased in the EC tissues compared with the corresponding adjacent tumor tissues. Low expression of miR-140 promotes cell invasion by using transwell assay, while the effect of miR-140 high expression is reverse. Slug, a target gene of miR-140, was examined by luciferase assay and Western blot. Conclusions: miR-140 may regulate the cell invasion of EC via controlling Slug expression.

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“…Down regulation of miR-203 expression was found in several types of cancers, including gastric cancer [8], hepatocellular carcinoma (OS) [9], non-small cell lung cancer (NSCLC) [10], cervical cancer [11], esophageal cancer [12] as well as melanoma [13]. However, studies also showed that miR-203 was up regulated in breast cancer [14], colorectal cancer [15], ovarian cancer [16] and pancreatic adenocarcinoma [17].…”

Section: Introductionmentioning

confidence: 99%

MiR-203 Determines Poor Outcome and Suppresses Tumor Growth by Targeting TBK1 in Osteosarcoma

Liu¹,

Peng²

2015

Cell Physiol Biochem

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Background/Aims: Increasing evidence has shown that miR-203 plays important role in human cancer progression. However, little is known about the function of miR-203 in osteosarcoma (OS). Methods: The expression of miR-203 in OS tissues and cell lines were examined by qRT-PCR. The biological role of miR-20 in OS cell proliferation was examined in vitro and in vivo. The targets of miR-203 were identified by a luciferase reporter gene assay. Results: miR-203 was down regulated in OS tissues and cell lines; decreased miR-203 was associated with a poor overall survival in OS patients. Restoration of miR-203 expression reduced cell growth in vitro and suppressed tumorigenicity in vivo. In contrast, inhibition of miR-203 stimulated OS cell growth both in vitro and in vivo. In addition, TANK binding kinase 1 (TBK1) was identified as a direct target of miR-203; overexpression of TBK1 partly reversed the suppressive effects of miR-203. Furthermore, TBK1 was found up-regulated and inversely correlated with miR-203 in OS tissues. Conclusion: Taken together, these findings suggest that miR-203 acts as a tumor suppressor via regulation of TBK1 expression in OS progression, and miR-203 may be a promising therapeutic target for OS.

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MiR-203 suppresses tumor growth and invasion and down-regulates MiR-21 expression through repressing Ran in esophageal cancer

Cited by 83 publications

References 30 publications

Epidermal growth factor-induced C/EBPbeta participates in EMT by dampening miR-203 in esophageal squamous cell carcinoma

Epidermal growth factor-induced C/EBPbeta participates in EMT by dampening miR-203 in esophageal squamous cell carcinoma

Down-Regulation of miR-140 Induces EMT and Promotes Invasion by Targeting Slug in Esophageal Cancer

MiR-203 Determines Poor Outcome and Suppresses Tumor Growth by Targeting TBK1 in Osteosarcoma

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