N-myc downstream-regulated gene 2 (NDRG2) suppresses the epithelial–mesenchymal transition (EMT) in breast cancer cells via STAT3/Snail signaling

Kim, Myung-Jin; Lim, Jin Hee; Yang, Young; Lee, Myeong‐Sok; Lim, Jong‐Seok

doi:10.1016/j.canlet.2014.06.023

Cited by 61 publications

(61 citation statements)

References 51 publications

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“…Several studies have shown that ING4 and NDRG2 suppress EMT (29–33). To determinate if the gain of the region 22q11.2 was associated with EMT, we analyzed cell morphology and the presence of EMT markers E-cadherin and vimentin by immunofluorescence.…”

Section: Resultsmentioning

confidence: 99%

“…In the aggressive BrC cell line MDA-MB-231, overexpression of NDRG2 results in downregulation of Snail-1 and upregulation of CDH1 (33). TGF-β is perhaps the most used inducer of EMT in in vitro studies, and Shen and collaborators showed that NDRG2 abrogates the TGF-β-induced EMT (31).…”

Section: Discussionmentioning

confidence: 99%

“…miR-650 is often expressed in prostate, colorectal, hepatocellular, skin and gastric cancers (21–25), with evidence that it targets tumor suppressors ING4 and NDRG2 (23,26–28). ING4 and NDRG2 expression is often lost in cancer and different lines of evidence support their participation in EMT (29–33). …”

Section: Introductionmentioning

confidence: 99%

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A 22q11.2 amplification in the region encoding microRNA-650 correlates with the epithelial to mesenchymal transition in breast cancer primary cultures of Mexican patients

Lango-Chavarría

Chimal-Ramírez

Ruiz‐Tachiquín

et al. 2017

International Journal of Oncology

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Breast cancer ranks first in incidence and mortality in working age women. Cancer initiation and progression relies on accumulation of genetic and epigenetic aberrations that alter cellular processes, among them, epithelial to mesenchymal transition (EMT) denotes particularly aggressive neoplasias given its capacity to invade and metastasize. Several microRNAs (miRNA) have been found able to regulate gene expression at the core of EMT. In this study, the Affymetrix CytoScan HD array was used to analyze three different primary tumor cell isolates from Mexican breast cancer patients. We found an amplification in band 22q11.2 shared by the three samples, in the region that encodes miRNA-650. Overexpression of this miRNA has been associated with downregulation of tumor suppressors ING4 and NDRG2, which have been implicated in cancer progression. Using the Pathway Linker platform the ING4 and NDRG2 interaction networks showed a significant association with signaling pathways commonly deregulated in cancer. Also, several studies support their participation in the EMT. Supporting the latter, we found that the three primary isolates were E-cadherin negative, vimentin positive, presented a cancer stem cell-like phenotype CD44+CD24−/low and were invasive in Transwell invasion assays. This evidence suggests that the gain of region 22q11.2 contributes to trigger EMT. This is the first evidence linking miR-650 and breast cancer.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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A 22q11.2 amplification in the region encoding microRNA-650 correlates with the epithelial to mesenchymal transition in breast cancer primary cultures of Mexican patients

Lango-Chavarría

Chimal-Ramírez

Ruiz‐Tachiquín

et al. 2017

International Journal of Oncology

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“…In addition, previous reports have indicated that the transcription factor signal transducer and activator of transcription 3 (STAT3) can induce EMT in cancer cells through activation of TWIST gene expression by cooperating with the EGFR [30]. STAT3 has also been found to be involved in many types of cancers, such as breast and prostate cancers [25,26]. Given all this evidence, we selected vimentin, E-cadherin, Smad4, and STAT3 as markers of the signalling pathway of EMT in the present study.…”

Section: Introductionmentioning

confidence: 99%

“…Neural cadherin (N-cadherin) is thought to mediate growth cone motility in neurons [24]. However, different signalling pathways appear to be involved in EMT [25][26][27]. Unequivocally, transforming growth factor-β (TGF-β) is a major inducer of different subtypes of EMT, including development, fibrosis, and carcinogenesis, in various cells [28].…”

Section: Introductionmentioning

confidence: 99%

TRPP2 Enhances Metastasis by Regulating Epithelial-Mesenchymal Transition in Laryngeal Squamous Cell Carcinoma

Shen

Jiang

et al. 2016

Cell Physiol Biochem

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Background/Aim: Surgery and chemotherapy treatments of human laryngeal squamous cell carcinoma (HLSCC) may fail due to metastasis, in which epithelial-mesenchymal transition (EMT) plays an important role. TRPP2, a nonselective cation channel, is expressed in various cell types and participates in many biological processes. Here, we show that TRPP2 enhanced metastasis by regulating EMT. Methods: We used immunohistochemistry, western blotting, Ca²⁺ imaging, transwell and wound healing assays to investigate TRPP2 expression levels in HLSCC tissue, and the role of TRPP2 in invasion and metastasis of a human laryngocarcinoma cell line (Hep2 cell). Results: We found that TRPP2 protein expression levels were significantly increased in HLSCC tissue; higher TRPP2 levels were associated with decreased patient survival time and degree of differentiation and advanced clinical stage. Knockdown of TRPP2 by transfection with TRPP2 siRNA markedly suppressed ATP-induced Ca²⁺ release, wound healing, and cell invasion in Hep2 cells. Moreover, TRPP2 siRNA significantly decreased vimentin expression but increased E-cadherin expression in Hep2 cells. In the EMT signalling pathway, TRPP2 siRNA significantly decreased Smad4, STAT3, SNAIL, SLUG and TWIST expression in Hep2 cells. Conclusion: We revealed a previously unknown function of TRPP2 in cancer development and a TRPP2-dependent mechanism underlying laryngocarcinoma cell invasion and metastasis. Our results suggest that TRPP2 may be used as a biomarker for evaluating patient prognosis and as a novel therapeutic target in HLSCC.

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UNC5B‐AS1 promoted ovarian cancer progression by regulating the H3K27me on NDRG2 via EZH2

Wang

Tan

2020

Cell Biology International

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The role of long non‐coding RNAs (lncRNAs) in tumorigenesis and development of ovarian cancer (OC) has caught the attention of scientists. UNC5B antisense RNA 1 (UNC5B‐AS1) is a newly identified carcinogenic lncRNA in thyroid papillary carcinoma, but its role in OC remains unclear. This study is proposed to investigate the function and mechanism of UNC5B‐AS1 in OC. UNC5B‐AS1 expression in OC samples was obtained from gene expression profiling interactive analysis (GEPIA) based on The Cancer Genome Atlas data. Gene expressions were detected by quantitative real‐time polymerase chain reaction (RT‐qPCR) and western blot. Biological functions of UNC5B‐AS1 were assessed by cell counting kit‐8, colony formation, and caspase‐3 analysis. GEPIA revealed the UNC5B‐AS1 upregulation in OC samples. RT‐qPCR assay confirmed the upregulation of UNC5B‐AS1 in OC cells. Functionally, depletion of UCN5B‐AS1 hindered proliferation and prompted apoptosis in OC cells. Mechanistically, we found that UNC5B‐AS1 interacted with zeste 2 polycomb repressive complex 2 subunit (EZH2) to trigger trimethylation of histone H3 at lysine 27 (H3K27me3) on N‐myc downstream regulated gene‐2 (NDRG2) promoter and epigenetically repressed NDRG2. Rescue assay indicated the participation of NDRG2 in the regulation of UNC5B‐AS1 on OC progression. Together, we first illustrated that UNC5B‐AS1 promoted OC progression by regulating the H3K27me on NDRG2 via EZH2, indicating UNC5B‐AS1 as a potential molecular target for OC treatment.

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N-myc downstream-regulated gene 2 (NDRG2) suppresses the epithelial–mesenchymal transition (EMT) in breast cancer cells via STAT3/Snail signaling

Cited by 61 publications

References 51 publications

A 22q11.2 amplification in the region encoding microRNA-650 correlates with the epithelial to mesenchymal transition in breast cancer primary cultures of Mexican patients

A 22q11.2 amplification in the region encoding microRNA-650 correlates with the epithelial to mesenchymal transition in breast cancer primary cultures of Mexican patients

TRPP2 Enhances Metastasis by Regulating Epithelial-Mesenchymal Transition in Laryngeal Squamous Cell Carcinoma

UNC5B‐AS1 promoted ovarian cancer progression by regulating the H3K27me on NDRG2 via EZH2

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