miR-200a suppresses cell growth and migration by targeting MACC1 and predicts prognosis in hepatocellular carcinoma

Feng, Ji-Ye; Wang, Jinbo; Chen, Mingliang; Chen, Gun; Wu, Zikang; Ying, Liping; Zhuo, Qifeng; Zhang, Jianlei; Wang, Weilin

doi:10.3892/or.2014.3642

Cited by 42 publications

(28 citation statements)

References 33 publications

(31 reference statements)

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“…Downregulation of miR-200a has been reported in several human cancers, including nasopharyngeal carcinoma [12], meningiomas [25], and breast cancer [26]. Moreover, restoration of miR-200a inhibited cell proliferation, migration, and invasion of hepatocellular carcinoma [13], nasopharyngeal carcinoma [12], prostate cancer [14], and ovarian cancer [15]. Conversely, inhibition of miR-200a promoted cancer cell development [12], suggesting that miR-200a may act as a tumor suppressor in human cancer.…”

Section: Discussionmentioning

confidence: 94%

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Tumor suppressive microRNA-200a inhibits renal cell carcinoma development by directly targeting TGFB2

et al. 2015

Tumor Biol.

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A large body of evidence indicates that microRNAs play a critical role in tumor initiation and progression by negatively regulating oncogenes or tumor suppressor genes. Here, we report that the expression of miR-200a was notably downregulated in 45 renal cell carcinoma (RCC) samples. Restoration of miR-200a suppressed cell proliferation, migration, and invasion in two RCC cell lines. Furthermore, we used an epithelial-to-mesenchymal transition PCR array to explore the putative target genes of miR-200a. By performing quantitative real-time PCR, ELISA, and luciferase reporter assays, transforming growth factor beta2 (TGFB2) was validated as a direct target gene of miR-200a. Moreover, siRNA-mediated knockdown of TGFB2 partially phenocopied the effect of miR-200a overexpression. These results suggest that miR-200a suppresses RCC development via directly targeting TGFB2, indicating that miR-200a may present a novel target for diagnostic and therapeutic strategies in RCC.

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Section: Discussionmentioning

confidence: 94%

“…* Wei Zhang zhangweispace@163.com * Zhendong Yu dongboyaa@163.com miR-200a may function as a tumor suppressor in human cancers [12][13][14][15]. Furthermore, a previous study showed that miR200a was downregulated in clinical RCC specimens compared with normal kidney tissues [16].…”

Section: Introductionmentioning

confidence: 94%

Tumor suppressive microRNA-200a inhibits renal cell carcinoma development by directly targeting TGFB2

et al. 2015

Tumor Biol.

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“…We found that MACC1 knockdown up-regulated the protein expression levels of LC3-II and Beclin-1 and down-regulated the protein expression level of p62/SQSTM1. MACC1 acted as a target gene for miRNAs, and it has been reported that the expression of MACC1 was down-regulated by miR-143 inhibited the cell migration and invasion in colorectal cancer (Zhang et al, 2012) and MACC1 was down-regulated by miR-200a inhibited the hepatocellular carcinoma cell proliferation and migration (Feng et al, 2015). In our study, miR-590-3p overexpression decreased the expression of MACC1, in addition, MACC1 was identified as a putative target of miR-590-3p.…”

Section: Discussionmentioning

confidence: 99%

Combination of Endothelial-Monocyte-Activating Polypeptide-II with Temozolomide Suppress Malignant Biological Behaviors of Human Glioblastoma Stem Cells via miR-590-3p/MACC1 Inhibiting PI3K/AKT/mTOR Signal Pathway

Zhou

Liu

Xue

et al. 2017

Front. Mol. Neurosci.

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This study aims to investigate the effect of Endothelial-Monocyte-Activating Polypeptide-II (EMAP-II) combined with temozolomide (TMZ) upon glioblastoma stem cells (GSCs) and its possible molecular mechanisms. In this study, combination of EMAP-II with TMZ inhibited cell viability, migration and invasion in GSCs, and autophagy inhibitor 3-methyl adenine (3-MA) and chloroquine (CQ) partly reverse the anti-proliferative effect of the combination treatment. Autophagic vacuoles were formed in GSCs after the combination therapy, accompanied with the up-regulation of LC3-II and Beclin-1 as well as the down-regulation of p62/SQSTM1. Further, miR-590-3p was up-regulated and Metastasis-associated in colon cancer 1 (MACC1) was down-regulated by the combination treatment in GSCs; MiR-590-3p overexpression and MACC1 knockdown up-regulated LC3-II and Beclin-1 as well as down-regulated p62/SQSTM1 in GSCs; MACC1 was identified as a direct target of miR-590-3p, mediating the effects of miR-590-3p in the combination treatment. Furthermore, the combination treatment and MACC1 knockdown decreased p-PI3K, p-Akt, p-mTOR, p-S6 and p-4EBP in GSCs; PI3K/Akt agonist insulin-like growth factor-1(IGF-1) partly blocked the effect of the combination treatment. Moreover, in vivo xenograft models, the mice given stable overexpressed miR-590-3p cells and treated with EMAP-II and TMZ had the smallest tumor sizes, besides, miR-590-3p + EMAP-II + TMZ up-regulated the expression level of miR-590-3p, LC3-II and Beclin-1 as well as down-regulated p62/SQSTM1. In conclusion, these results elucidated anovel molecular mechanism of EMAP-II in combination with TMZ suppressed malignant biological behaviors of GSCs via miR-590-3p/MACC1 inhibiting PI3K/AKT/mTOR signaling pathway, and might provide potential therapeutic approaches for human GSCs.

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“…miR-200a is able to suppress the epithelial-mesenchymal transition (EMT) process [2–4], which is a critical step in cancer metastasis initiation. In addition, miR-200a has also been shown to suppress cell proliferation and metastasis in several cancers such as pancreatic cancer [5] and hepatocellular carcinoma [6]. More recently, Wu et al reported that miR-200a suppresses pancreatic cancer cell metastasis via the downregulation of DEK, suggesting that miR-200a may constitute a novel target for pancreatic cancer treatment [7].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-9 Promotes Pancreatic Cancer Cells Proliferation and Migration via the miR-200a/Beta-Catenin Axis

Huang

Lei

et al. 2017

BioMed Research International

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Background. Both IL-9 and miR-200a are involved in the pathogenesis of cancers; however, the role of IL-9 in pancreatic cancer and the possible underlying mechanisms remain unknown. The aim of this study was to investigate the effect of IL-9 on pancreatic cancer cells and its interaction with miR-200a. Methods. Pancreatic cancer cells (PANC-1 and AsPC-1) were treated with IL-9 and the expression of miR-200a and β-catenin in pancreatic cancer cells was measured. β-Catenin was examined as a target gene of miR-200a in pancreatic cancer cells. The interaction between IL-9 and miR-200a in pancreatic cancer cells was determined by infecting miR-200a mimics prior to IL-9 treatment and then measuring miR-200a and β-catenin expression. Results. IL-9 significantly promoted the proliferation, invasion, and migration of pancreatic cancer cells; however, the effect on pancreatic cancer cell apoptosis was insignificant. β-Catenin was verified as a target gene of miR-200a in pancreatic cancer cells. Overexpression of miR-200a in pancreatic cancer cells significantly attenuated proliferation and metastasis and reduced β-catenin expression. IL-9 treatment of pancreatic cancer cells decreased miR-200a expression and increased β-catenin expression. The effect of miR-200a on pancreatic cancer cells decreased following IL-9 treatment. Conclusions. IL-9 promotes proliferation and metastasis in pancreatic cancer cells; this effect may partly involve regulation of the miR-200a/β-catenin axis.

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miR-200a suppresses cell growth and migration by targeting MACC1 and predicts prognosis in hepatocellular carcinoma

Cited by 42 publications

References 33 publications

Tumor suppressive microRNA-200a inhibits renal cell carcinoma development by directly targeting TGFB2

Tumor suppressive microRNA-200a inhibits renal cell carcinoma development by directly targeting TGFB2

Combination of Endothelial-Monocyte-Activating Polypeptide-II with Temozolomide Suppress Malignant Biological Behaviors of Human Glioblastoma Stem Cells via miR-590-3p/MACC1 Inhibiting PI3K/AKT/mTOR Signal Pathway

Interleukin-9 Promotes Pancreatic Cancer Cells Proliferation and Migration via the miR-200a/Beta-Catenin Axis

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