miR-133 is a key negative regulator of CDC42–PAK pathway in gastric cancer

Cheng, Zhenguo; Liu, Funan; Wang, Guanqiao; Li, Yanshu; Zhang, Hongyan; Li, Feng

doi:10.1016/j.cellsig.2014.08.012

Cited by 51 publications

(50 citation statements)

References 45 publications

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“…Among all miRNAs, miR-133 is relatively less studied. Recently, a role of miR-133 in the GC has been acknowledged [9]. However, the molecular mechanisms are largely unknown [10].…”

Section: Introductionmentioning

confidence: 99%

Impairment of growth of gastric carcinoma by miR-133-mediated Her-2 inhibition

Zhang

Xin

et al. 2015

Tumor Biol.

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Gastric carcinoma (GC) is a leading cause of cancer-related death in China. Dysregulation of microRNAs (miRNAs) has been shown to contribute to the development of GC, whereas the role of miR-133 in GC is unknown. Here, we analyzed the levels of miR-133 in GC tissues by reverse and quantitative transcription polymerase chain reaction (RT-qPCR). We overexpressed or inhibited miR-133 in GC cells. Cell growth was analyzed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and cell apoptosis was evaluated by fluorescence-activated cell sorting (FACS) analysis. Targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual-luciferase reporter assay. We detected lower miR-133 levels in GC tissues compared with normal gastric tissue. Moreover, the low miR-133 levels were correlated with low survival rate. Overexpression of miR-133 inhibited cell growth and promoted apoptosis, while depletion of miR-133 increased cell growth and suppressed apoptosis. Moreover, the 3'-untranslated region (3'UTR) of Her-2, the epidermal growth factor receptor (EGFR) that transduces cell growth signals, appeared to be targeted by miR-133. Together, these data suggest that reduced miR-133 levels in GC tissues promote GC growth, which possibly contributes to a low survival rate of GC patients. MiR-133 may target Her-2 to suppress GC cell growth.

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“…Among all miRNAs, miR-133 is relatively less studied. Recently, a role of miR-133 in the GC has been acknowledged [9]. However, the molecular mechanisms are largely unknown [10].…”

Section: Introductionmentioning

confidence: 99%

Impairment of growth of gastric carcinoma by miR-133-mediated Her-2 inhibition

Zhang

Xin

et al. 2015

Tumor Biol.

View full text Add to dashboard Cite

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“…Importantly, 317 the expression levels of miR-142-3p and miR-142-5p were almost ten 318 times higher than the expression level of miR-133a [28]. MiR-133a is 319 known as a negative regulator of the Runt-related transcription factor 320 2 (Runx2) which is essential for the osteoblast differentiation [31] and 321 as a suppressor of the cell division control protein 42 homolog 322 (CDC42), which is involved in various cellular processes such as cell dif-323 ferentiation, cell cycle progression and cytoskeleton organization [32]. MiR-146b was reported to be increased in RA synovial tissue [25,33] 351 and in PBMCs of RA patients [25].…”

mentioning

confidence: 99%

MicroRNAs in rheumatoid arthritis: Altered expression and diagnostic potential

Чуров

Олейник

Knip

2015

Autoimmunity Reviews

197

179

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“…Since its original discovery, CDC42 has been found to influence a variety of signaling events and cellular processes [25,26]. The up-regulation of CDC42 is involved in cell polarity and cell movement [26,27]. Previous studies have also demonstrated that CDC42 played a crucial role in the transforming growth factor (TGF) pathway [28].…”

Section: Discussionmentioning

confidence: 99%

“…It was originally identified in S. cerevisiae as a mediator of cell division [23,24]. Since its original discovery, CDC42 has been found to influence a variety of signaling events and cellular processes [25,26]. The up-regulation of CDC42 is involved in cell polarity and cell movement [26,27].…”

Section: Discussionmentioning

confidence: 99%

Mechanism Analyses for Elucidating the Role of LOXL2 Silencing in Hepatocellular Carcinoma

Wu¹,

Zhang²,

Zhu³

et al. 2015

JAST-A

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Abstract:The paper aimed to study the effect of lysyl oxidase-like 2 (LOXL2) on hepatocellular carcinoma (HCC) and explore the biological mechanisms of tumorigenicity and progression in HCC. The authors used four HCC cell lines to identify LOXL2. A lentiviral vector containing LOXL2-siRNA was constructed to silence the LOXL2 gene in SMMC-7721 cell line, and mRNA of the target gene was detected by real-time polymerase chain reaction (RT-PCR). The effect of LOXL2 silencing on the growth of SMMC-7721 cells was explored with flow cytometry profiling and BrdU labeling. Downstream genes of LOXL2 were selected by microarray and verified by Western Blotting. In the results, LOXL2 expression was significantly up-regulated in four types of HCC cell lines, therefore, SMMC-7721 cell line was selected for further exploration. When SMMC-7721 cell line was infected with LOXL2-siRNA, the expression of LOXL2 mRNA decreased. The silencing of LOXL2 resulted in the cell cycle arrest at the G1-phase, the increased apoptosis and the decreased growth of SMMC-7721 cells on the indicated days by BrdU. Moreover, the MDM2, BIRC3, CDC42, FOS and TGFBR2 genes were selected and verified to be the downstream genes of LOXL2. In conclusion, LOXL2 contributes to the genesis and progression of HCC cells and works by regulating downstream genes of LOXL2 in certain pathways. Therefore, LOXL2 may play an important role in the progression and prognosis of HCC.

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miR-133 is a key negative regulator of CDC42–PAK pathway in gastric cancer

Cited by 51 publications

References 45 publications

Impairment of growth of gastric carcinoma by miR-133-mediated Her-2 inhibition

Impairment of growth of gastric carcinoma by miR-133-mediated Her-2 inhibition

MicroRNAs in rheumatoid arthritis: Altered expression and diagnostic potential

Mechanism Analyses for Elucidating the Role of LOXL2 Silencing in Hepatocellular Carcinoma

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