MSP58 Knockdown Inhibits the Proliferation of Esophageal Squamous Cell Carcinoma in Vitro and in Vivo

Xu, Chunsheng; Zheng, Jun; Zhang, Hailong; Zhao, Huadong; Zhang, Jing; Wu, Guoqiang; Wu, Lin; Wang, Qing; Wang, Weizhong; Zhang, Jian

doi:10.7314/apjcp.2012.13.7.3233

Cited by 11 publications

(7 citation statements)

References 33 publications

(40 reference statements)

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“…Conversely, overexpression of NDRG2 has been measured in decreased cancer cell growth (Deng et al, 2003;Choi et al, 2007;Yang et al, 2010). NDRG2 can inhibit MSP58 (a 58-kD nuclear microspherule protein)-induced cell proliferation in glioma cells or colon cancer cells (Xu et al, 2012). Consistent with all the previous results, we observed that NDRG2 expression was decreased in two NB cell lines, SK-N-SH and SH-SY5Y ( Figure 1A).…”

Section: Discussionsupporting

confidence: 80%

Overexpression of NDRG2 Can Inhibit Neuroblastoma Cell Proliferation through Negative Regulation by CYR61

Zhang

Li²,

Feng³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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Several recent studies have showed that the n-myc downstream regulated gene 2 (NDRG2) is a new tumor suppressor gene, and that it plays an important role in tumor suppression in several cancers or cancer cell lines. However, few studies focused on its function in neuroblastoma cells. In the present investigation, we demonstrated that NDRG2 overexpression inhibited their proliferation. Using a cDNA microarray, we found that overexpression of NDRG2 inhibited the expression of cysteine-rich protein 61 (CYR61), a proliferation related gene. From our research, CYR61 may partially hinder NDRG2-mediated inhibition of cell proliferation. Overexpression of NDRG2 resulted in accumulation of cells in the G1 phase, which was accompanied by upregulation of p21 and p27 and downregulation of CDK4 and cyclin D1. Taken together, these data indicate that NDRG2 inhibits the proliferation of neuroblastoma cells partially through suppression of CYR61. Our findings offer novel insights into the physiological roles of NDRG2 in neuroblastoma cell proliferation, and NDRG2 may prove to be effective candidate for the treatment of children with neuroblastoma.

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Section: Discussionsupporting

confidence: 80%

Overexpression of NDRG2 Can Inhibit Neuroblastoma Cell Proliferation through Negative Regulation by CYR61

Zhang

Li²,

Feng³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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“…Drosophila MCRS2 is co-purified with RNA polymerase II complexes and is required for normal levels of cycling gene expression ( 37 ). A previous study revealed that MCRS1 and MCRS2 are involved in cell cycle regulation and carcinogenesis ( 20 , 32 ). Carcinoembryonic antigen (CEA) was first identified in 1965 ( 38 ) and has now become the most widely used antigen for diagnosing and for monitoring the prognostic significance of CRC ( 39 ).…”

Section: Introductionmentioning

confidence: 99%

Expression of MCRS1 and MCRS2 and their correlation with serum carcinoembryonic antigen in colorectal cancer

Chen

Zhao

et al. 2016

Experimental and Therapeutic Medicine

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Cancer-associated genes serve a crucial role in carcinogenesis. The present study aimed to investigate the mRNA expression levels of microspherule protein 1 (MCRS1) and MCRS2 in colorectal cancer (CRC) and their association with clinical variables. The mRNA expression levels of MCRS1 and MCRS2 were assessed by semi-quantitative reverse transcription polymerase chain reaction in the tumor and corresponding non-tumor tissues of 54 newly-diagnosed CRC patients, as well as in the normal colonic mucosa tissue of 19 age/gender-matched healthy controls. Immunofluorescence was also employed to identify the expression of MCRS1 in CRC tissues, while the concentration of serum carcinoembryonic antigen (CEA) was determined by an enzyme-linked immunoassay. The results identified a negative correlation between MCRS1 and MCRS2 expression levels (r=−0.3018, P=0.0266). MCRS1 mRNA expression was significantly increased and MCRS2 mRNA expression was decreased in CRC tissues compared with the levels in the corresponding normal tissues (both P<0.001). An increase in MCRS1 expression and a decrease in MCRS2 expression was detected in advanced stage when compared with early stage CRC patients. Immunofluorescence analysis revealed increased expression of MCRS1 in CRC patients. Furthermore, the expression levels of MCRS1 displayed positive correlation, whilst those of MCRS2 displayed negative correlation, with the serum CEA level in patients with CRC. The results suggest that increased MCRS1 and decreased MCRS2 expression appeared to be involved in the pathogenesis of CRC. The present study provides evidence suggesting that MCRS1 and MCRS2 may identify CRC patients at a risk of disease relapse, and thus, may be potential tools for monitoring disease activity and act as novel diagnostic markers in the treatment of CRC.

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“…TOJ3 (a quail homolog of MCRS1) behaves as an oncogene during fibroblast transformation, and this transformation activity can be suppressed by the tumor suppressor PTEN [ 8 , 9 ]. MCRS1 overexpression has been documented in a variety of human cancers, and this overexpression was found to induce the proliferation of cancer cells [ 3 , 10 – 12 ]. In the present study, we observed that MCRS1 overexpression promoted the epithelial-mesenchymal transition (EMT) and metastasis in NSCLC cells.…”

Section: Introductionmentioning

confidence: 99%

“…MCRS1 overexpression has been documented in a variety of human tumors [ 3 , 10 – 12 ]; however, the molecular mechanisms underlying MCRS1 alteration remain elusive. In this study, we investigated the mechanisms of MCRS1 regulation in NSCLC cells.…”

Section: Introductionmentioning

confidence: 99%

MCRS1 overexpression, which is specifically inhibited by miR-129*, promotes the epithelial-mesenchymal transition and metastasis in non-small cell lung cancer

2014

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BackgroundAlthough tumor invasion and metastasis are both classical hallmarks of cancer malignancy and the major causes of poor clinical outcomes among cancer patients, the underlying master regulators of invasion and metastasis remain largely unknown. In this study, we observed that an overexpression of microspherule protein 1 (MCRS1) promotes the invasion and metastasis of non-small cell lung cancer (NSCLC) cells. Furthermore, we sought to systematically investigate the pathophysiological functions and related mechanisms of MCRS1.MethodsRetrovirus-mediated RNA interference was employed to knockdown MCRS1 expression in NSCLC cell lines. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot respectively were used to measure levels of mRNA and protein. Further cell permeability assessment, invasion and proliferation assays were conducted to evaluate MCRS1 functions in vitro while nude mice experiments were performed to examine metastatic capability in vivo. Microarray analysis and microRNA (miRNA) sequencing were respectively carried out for mRNA and miRNA expression profiling, while chromatin immunoprecipitation (ChIP), luciferase reporter assay, and miRNA transfection were used to investigate the interaction between MCRS1 and miRNAs.ResultsMCRS1 knockdown induced morphological alterations, increased monolayer integrity, decreased cellular invasion and metastasis, and attenuated stemness and drug resistance among tested NSCLC cells. The levels of MCRS1 expression were likewise correlated with tumor metastasis among NSCLC patients. We identified differentially expressed genes after MCRS1 silencing, which included cell junction molecules, such as ZO-1, Occludin, E-cadherin, and DSG2. However, these differentially expressed genes were not directly recognized by a transcriptional complex containing MCRS1. Furthermore, we found that MCRS1 binds to the miR-155 promoter and regulates its expression, as well as MCRS1 promotes epithelial-mesenchymal transition (EMT), invasion, and metastasis through the up-regulation of miR-155. Systematic investigations ultimately showed that MCRS1 was directly and negatively regulated by the binding of miR-129* to its 3’-UTR, with miR-129* overexpression suppressing the growth and invasion of NSCLC cells.ConclusionsMiR-129* down-regulation induced MCRS1 overexpression, which promotes EMT and invasion/metastasis of NSCLC cells through both the up-regulation of miR-155 and down-regulation of cell junction molecules. This miR-129*/MCRS1/miR-155 axis provides a new angle in understanding the basis for the invasion and metastasis of lung cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/1476-4598-13-245) contains supplementary material, which is available to authorized users.

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MSP58 Knockdown Inhibits the Proliferation of Esophageal Squamous Cell Carcinoma in Vitro and in Vivo

Cited by 11 publications

References 33 publications

Overexpression of NDRG2 Can Inhibit Neuroblastoma Cell Proliferation through Negative Regulation by CYR61

Overexpression of NDRG2 Can Inhibit Neuroblastoma Cell Proliferation through Negative Regulation by CYR61

Expression of MCRS1 and MCRS2 and their correlation with serum carcinoembryonic antigen in colorectal cancer

MCRS1 overexpression, which is specifically inhibited by miR-129*, promotes the epithelial-mesenchymal transition and metastasis in non-small cell lung cancer

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