miR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasion

Xia, Hongping; Ng, Sophia; Jiang, Siqi; Cheung, William K.C.; Sze, Johnny; Bian, Xiu‐Wu; Kung, Hsiang‐Fu; Lin, Marie C.M.

doi:10.1016/j.bbrc.2009.11.093

Cited by 181 publications

(114 citation statements)

References 19 publications

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“…In addition, miR200a was also reported to be downregulated in NPC samples compared with adjacent normal tissues. 31 In contrast, we now show that miR-200 family miRNAs are upregulated in NPC cell lines. These findings may be due to variations in miRNA expression levels in cancers of different stages and origins, along with other variables.…”

Section: Discussionmentioning

confidence: 76%

MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN

et al. 2017

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Section: Discussionmentioning

confidence: 76%

MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN

et al. 2017

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“…MiR-135 and miR-315 activate b-catenin by inhibiting the negative regulators, APC and axin, respectively. 126,127 MiR-200a has been shown to regulate b-catenin levels either directly 128 or indirectly by modulating ZEB1/2, and this downregulation of miR-200a in HCC has been reported in various studies, 4,65,106,129,130 thereby supporting its role in mediating an increase in nuclear b-catenin levels and the activation of the pathway in cancer cells. MiR-34a has also been shown to be a negative regulator of the Wnt pathway based on its targeting of WNT1.…”

Section: 3mentioning

confidence: 80%

MicroRNAs in liver cancer: a model for investigating pathogenesis and novel therapeutic approaches

et al. 2014

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MicroRNAs (miRNAs) constitute a large class of short RNAs (e.g., 20-24 nucleotides in length), whose main function is to posttranscriptionally regulate the expression of protein-coding genes. Their importance in tumorigenesis has been demonstrated over the past decade, and correspondingly, they have emerged as potential therapeutic molecules and targets. Liver cancer is one of the most common neoplastic diseases worldwide, and it currently has a poor prognosis owing to largely ineffective therapeutic options. Liver cancer is also an excellent model for testing miRNA-based therapy approaches as it can be easily targeted with the systemic delivery of oligonucleotides. In recent years, the role of miRNAs in hepatocellular carcinoma (HCC) has been established with molecular studies and the development of animal models. These studies have also provided the basis for evaluating the therapeutic potential of miRNAs, or anti-miRNAs. In general, the safety of miRNAs has been proven and antitumor activity has been observed. Moreover, because of the absence or presence of mild side effects, the prophylactic use of miRNA-based approaches may be foreseen.

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“…Recently, Saydam et al (2009) showed that miR-200a downregulation in meningioma subtypes of brain tumors promotes tumor growth by increasing Cyclin D1 and b-catenin in vitro and in vivo. Similarly, it was shown that the overexpression of miR-200a inhibits nasopharyngeal carcinoma cell growth, migration and invasion by targeting b-catenin and Smad interacting protein 1, whereas its knockdown stimulates these processes in these cells (Xia et al, 2010). In contrast, it was reported that the human miR-200 family promotes cell growth when transfected into several cancer cell lines.…”

Section: Introductionmentioning

confidence: 99%

miR-200bc/429 cluster targets PLCγ1 and differentially regulates proliferation and EGF-driven invasion than miR-200a/141 in breast cancer

et al. 2010

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The genes encoding microRNAs of the human miR-200 family map to fragile chromosomal regions and are frequently downregulated upon tumor progression. Although having been reported to regulate epithelial-tomesenchymal transition and transforming growth factorbeta-driven cell invasion, the role of the miR-200 family in EGF-driven breast cancer cell invasion, viability, apoptosis and cell cycle progression is still unknown. In particular, there is no study comparing the roles of the two clusters of this miRNA family. In this study, we show for the first time that miR-200 family members differentially regulate EGF-driven invasion, viability, apoptosis and cell cycle progression of breast cancer cells. We showed that, all miR-200 family members regulate EGFdriven invasion, with the miR-200bc/429 cluster showing stronger effects than the miR-200a/141 cluster. Furthermore, expression of the miR-200a/141 cluster results in G1 arrest supported by increased p27/Kip1 and decreased cyclin dependent kinase 6 expression. In contrast, expression of the 200bc/429 cluster decreases G1 population and increases G2/M phase, in line with the observed reduction of p27/Kip1 and upregulation of the inhibitory phosphorylation of Cdc25C, respectively. To test the hypothesis that phenotypical differences observed between the two clusters are caused by differential targeting spectrums, we performed genome-wide microarray profiling in combination with gain-of-function studies. This identified phospholipase C gamma 1 (PLCG1), which was downregulated only by the miR-200bc/429 cluster, as a potential candidate contributing to these phenotypical differences. Luciferase reporter assays validated PLCG1 as a direct functional target of miR-200bc/429 cluster, but not of miR-200a/141 cluster. Finally, loss of PLCG1 in part mimicked the effect of miR-200bc/429 overexpression in viability, apoptosis and EGF-driven cell invasion of breast cancer cells. Our results suggest that the miR-200 family has a tumor-suppressor function by negatively regulating EGF-driven cell invasion, viability and cell cycle progression in breast cancer.

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miR-200a-mediated downregulation of ZEB2 and CTNNB1 differentially inhibits nasopharyngeal carcinoma cell growth, migration and invasion

Cited by 181 publications

References 19 publications

MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN

MicroRNA-200c plays an oncogenic role in nasopharyngeal carcinoma by targeting PTEN

MicroRNAs in liver cancer: a model for investigating pathogenesis and novel therapeutic approaches

miR-200bc/429 cluster targets PLCγ1 and differentially regulates proliferation and EGF-driven invasion than miR-200a/141 in breast cancer

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