<i><scp>NUBPL</scp></i>, a novel metastasis‐related gene, promotes colorectal carcinoma cell motility by inducing epithelial–mesenchymal transition

Wang, Yuhui; Wu, Nan; Sun, Donglin; Sun, Haiming; Tong, Dandan; Liu, Duo; Pang, Bo; Su, Li; Jia, Wei Hua; Dai, Jialin; Liu, Yang; Bai, Jing; Geng, Jingshu; Fu, Songbin; Jin, Yan

doi:10.1111/cas.13243

Cited by 16 publications

(16 citation statements)

References 19 publications

(27 reference statements)

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“…EMT entails profound epigenetic and phenotypic modifications to a cell. Previous studies have reported that epithelial cells express high levels of E-cadherin, whereas mesenchymal cells express high levels of N-cadherin and vimentin ( 21 – 23 ). Therefore, detecting the expression level of E-cadherin, N-cadherin and vimentin has become a prevalent strategy for the verification of EMT in cells.…”

Section: Resultsmentioning

confidence: 99%

PADI4‑mediated epithelial‑mesenchymal transition in lung cancer cells

Qu¹,

Xue

Xing

et al. 2019

Mol Med Report

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Lung cancer is a complex disease involving multiple genetic and phenotypic alterations. As a histone modification enzyme, protein-arginine deiminase type-4 (PADI4) and its downstream signaling have been studied in the progression of a variety of types of human cancer, but data on PADI4-mediated posttranslational modification in lung cancer are lacking. The aim of present study was to evaluate the expression of PADI4 and its associated molecular signaling in lung cancer metastasis. The results of the present study indicated that PADI4 was overexpressed in lung cancer cells, while knockdown of PADI4 could lead to attenuation of the lung cancer cell invasion and migration phenotype, which was further verified by determining the epithelial-mesenchymal transition (EMT) marker proteins. Additionally, it was demonstrated that stable knockdown of PADI4 in A549 lung cancer cells resulted in a striking reduction of the EMT-associated Snail1/mothers against decapentaplegic homolog 3/4 transcriptional complex, which was consistent with alterations in migratory and invasive phenotypes of A549 lung cancer cells. Therefore, PADI4-mediated EMT transition is proposed to represent a novel mechanism underlying the epigenetic and phenotypic alterations in lung cancer cells, and the PADI4 associated signaling pathway may be a therapeutic target for treating lung cancer in a clinical setting.

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Section: Resultsmentioning

confidence: 99%

PADI4‑mediated epithelial‑mesenchymal transition in lung cancer cells

Qu¹,

Xue

Xing

et al. 2019

Mol Med Report

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“…It induces EMT, characterized by downregulation of epithelial marker (E-cadherin) and upregulation of mesenchymal markers (N-cadherin and vimentin). Moreover, it activates ERK signaling, believed to promote EMT and tumor metastasis, as inhibition of ERK suppresses the NUBPL-induced changes in EMT and cell motility [ 107 ].…”

Section: Regulation Of Emt In Colorectal Cancermentioning

confidence: 99%

Regulation of EMT in Colorectal Cancer: A Culprit in Metastasis

Datta

2017

Cancers

399

299

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Epithelial to mesenchymal transition (EMT) is a process during which cells lose their epithelial characteristics, for instance cell polarity and cell–cell contact, and gain mesenchymal properties, such as increased motility. In colorectal cancer (CRC), EMT is associated with an invasive or metastatic phenotype. In this review, we discuss recent studies exploring novel regulation mechanisms of EMT in CRC, including the identification of new CRC EMT regulators. Upregulation of inducers can promote EMT, leading to increased invasiveness and metastasis in CRC. These inducers can downregulate E-cadherin and upregulate N-cadherin and vimentin (VIM) through modulating EMT-related signaling pathways, for instance WNT/β-catenin and TGF-β, and EMT transcription factors, such as zinc finger E-box binding homeobox 1 (ZEB1) and ZEB2. In addition, several microRNAs (miRNAs), including members of the miR-34 and miR-200 families, are found to target mRNAs of EMT-transcription factors, for example ZEB1, ZEB2, or SNAIL. Downregulation of these miRNAs is associated with distant metastasis and advanced stage tumors. Furthermore, the role of EMT in circulating tumor cells (CTCs) is also discussed. Mesenchymal markers on the surface of EMT CTCs were found to be associated with metastasis and could serve as potential biomarkers for metastasis. Altogether, these studies indicate that EMT is orchestrated by a complicated network, involving regulators of different signaling pathways. Further studies are required to understand the mechanisms underlying EMT in CRC.

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“…Nucleotide binding protein-like ( NUBPL ), located on ECA1, is required for the assembly of human mitochondrial complex I, which contains 45 evolutionally conserved mitochondrial and nuclear encoded subunits. In addition to its central role for the mitochondrial respiratory chain, overexpression of NUBPL has been documented in melanoma and colorectal cancer tissue [ 34 , 35 ]. Although the effect of this gene on melanoma is still unclear, Wang et al [ 35 ] characterized NUBPL as a metastasis-related gene as they were able to show that the overexpression of NUBPL in colorectal cancer tissue was positively correlated with lymph node metastasis and advanced staging of this form of cancer.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to its central role for the mitochondrial respiratory chain, overexpression of NUBPL has been documented in melanoma and colorectal cancer tissue [ 34 , 35 ]. Although the effect of this gene on melanoma is still unclear, Wang et al [ 35 ] characterized NUBPL as a metastasis-related gene as they were able to show that the overexpression of NUBPL in colorectal cancer tissue was positively correlated with lymph node metastasis and advanced staging of this form of cancer. The authors found that NUBPL induces epithelial–mesenchymal transition through the activation of ERK signaling pathway, a pathway which promotes tumor metastasis.…”

Section: Discussionmentioning

confidence: 99%

Equine vitiligo-like depigmentation in grey horses is related to genes involved in immune response and tumor metastasis

et al. 2021

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Background In horses, the autoimmune disease vitiligo is characterized by the loss of melanocytes and results in patchy depigmentation of the skin around the eyes, muzzle and the perianal region. Vitiligo-like depigmentation occurs predominantly in horses displaying the grey coat colour and is observed at a prevalence level of 26.0–67.0% in grey horses compared with only 0.8–3.5% in non-grey horses. While the polygenetic background of this complex disease is well documented in humans, the underlying candidate genes for this skin disorder in horses remain unknown. In this study we aim to perform a genome-wide association study (GWAS) for identifying putative candidate loci for vitiligo-like depigmentation in horses. Methods In the current study, we performed a GWAS analysis using high-density 670 k single nucleotide polymorphism (SNP) data from 152 Lipizzan and 104 Noriker horses, which were phenotyped for vitiligo-like depigmentation by visual inspection. After quality control 376,219 SNPs remained for analyses, the genome-wide Bonferroni corrected significance level was p < 1.33e-7. Results We identified seven candidate genes on four chromosomes (ECA1, ECA13, ECA17, ECA20) putatively involved in vitiligo pathogenesis in grey horses. The highlighted genes PHF11, SETDB2, CARHSP1 and LITAFD, are associated with the innate immune system, while the genes RCBTB1, LITAFD, NUBPL, PTP4A1, play a role in tumor suppression and metastasis. The antagonistic pathogenesis of vitiligo in relation to cancer specific enhanced cell motility and/or metastasis on typical melanoma predilection sites underlines a plausible involvement of RCBTB1, LITAFD, NUBPL, and PTP4A1. Conclusions The proposed candidate genes for equine vitiligo-like depigmentation, indicate an antagonistic relation between vitiligo and tumor metastasis in a horse population with higher incidence of melanoma. Further replication and expression studies should lead to a better understanding of this skin disorder in horses.

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NUBPL, a novel metastasis‐related gene, promotes colorectal carcinoma cell motility by inducing epithelial–mesenchymal transition

Cited by 16 publications

References 19 publications

PADI4‑mediated epithelial‑mesenchymal transition in lung cancer cells

PADI4‑mediated epithelial‑mesenchymal transition in lung cancer cells

Regulation of EMT in Colorectal Cancer: A Culprit in Metastasis

Equine vitiligo-like depigmentation in grey horses is related to genes involved in immune response and tumor metastasis

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