CSN5 promotes renal cell carcinoma metastasis and EMT by inhibiting ZEB1 degradation

Zhang, Shouhua; Zhou, Hong; Chai, Yong; Liu, Zhiqiang; Du, Yunyan; Li, Qiang; Liu, Queling

doi:10.1016/j.bbrc.2017.05.016

Cited by 39 publications

(24 citation statements)

References 27 publications

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“…EMT events have been widely found in the metastasis process of various cancers Ruan et al [45][46][47]. ZEB1 is a critical regulator of the EMT Zhang et al [48,49]. In the current study, we found that miR-142-3p expression was inversely correlated with ZEB1 expression in HCC cells and tissues.…”

Section: Discussionsupporting

confidence: 65%

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

Liu

Jin

et al. 2018

Cell Physiol Biochem

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Background/Aims: MicroRNA-142-3p (miR-142-3p) is dysregulated in many malignancies and may function as a tumor suppressor or oncogene in tumorigenesis and tumor development. However, few studies have investigated the clinical significance and biological function of miR-142-3p in hepatocellular carcinoma (HCC). Methods: The expression levels of taurine upregulated gene 1 (TUG1), miR-142-3p, and zinc finger E-box-binding homeobox 1 (ZEB1) were evaluated in HCC tissues and cell lines by quantitative real-time PCR. MTT and colony formation assays were used to detect cell proliferation ability, transwell assays were used to assess cell migration and invasion, and luciferase reporter assays were used to examine the interaction between the long noncoding RNA TUG1 and miR-142-3p. Tumor formation was evaluated through in vivo experiments. Results: miR-142-3p was significantly downregulated in HCC tissues, but TUG1 was upregulated in HCC tissues. Knockdown of TUG1 and upregulation of miR-142-3p inhibited cell proliferation, cell migration, cell invasion, and the epithelial-mesenchymal transition (EMT). miR-142-3p was found to be a prognostic factor of HCC, and the mechanism by which TUG1 upregulated ZEB1 was via direct binding to miR-142-3p. In vivo assays showed that TUG1 knockdown suppressed cell proliferation and the EMT in nude mice. Conclusion: The results of this study suggest that the TUG1/miR-142-3p/ ZEB1 axis contributes to the formation of malignant behaviors in HCC.

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Section: Discussionsupporting

confidence: 65%

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

Liu

Jin

et al. 2018

Cell Physiol Biochem

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“…P‐Stat3 regulates the progression of nasopharyngeal and breast cancer by activating Jab1 . JAK/Stat3 and Jab1 are implicated in the mechanisms of EMT in different types of human cancer. Data have shown that phosphorylation of Stat3 on Tyr705, not Ser727, drives a transcriptional program that converts an epithelial morphology to a migratory mesenchymal one.…”

Section: Discussionmentioning

confidence: 99%

“…Increasing evidence indicates that Jab1 activity mediates various tumorigenesis‐associated pathways and is a potential target for smoking‐induced lung cancer . P‐Stat3 regulates the progression of nasopharyngeal and breast cancer by activating Jab1, which regulates the expression of ZEB1 and affects the EMT process in renal cancer cells (RCCs) . Notably, the down‐regulation of Jab1 decreases PD‐L1 expression in cancer cells and sensitizes them to anti‐CTLA4 therapy .…”

Section: Introductionmentioning

confidence: 99%

“…22 P-Stat3 regulates the progression of nasopharyngeal and breast cancer by activating Jab1, 23,24 which regulates the expression of ZEB1 and affects the EMT process in renal cancer cells (RCCs). 25 Notably, the down-regulation of Jab1 decreases PD-L1 expression in cancer cells and sensitizes them to anti-CTLA4 therapy. 26,27 Thus, understanding the regulation of α5-nAChR and Jab1 expression has major clinical relevance.…”

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confidence: 99%

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α5‐nAChR contributes to epithelial‐mesenchymal transition and metastasis by regulating Jab1/Csn5 signalling in lung cancer

Chen

Jia

Zhang

et al. 2020

J Cellular Molecular Medi

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Recent studies have showed that α5 nicotinic acetylcholine receptor (α5‐nAChR) is closely associated with nicotine‐related lung cancer. Our previous studies also demonstrated that α5‐nAChR mediates nicotine‐induced lung carcinogenesis. However, the mechanism by which α5‐nAChR functions in lung carcinogenesis remains to be elucidated. Jab1/Csn5 is a key regulatory factor in smoking‐induced lung cancer. In this study, we explored the underlying mechanisms linking the α5‐nAChR‐Jab1/Csn5 axis with lung cancer epithelial‐mesenchymal transition (EMT) and metastasis, which may provide potential therapeutic targets for future lung cancer treatments. Our results demonstrated that the expression of α5‐nAChR was correlated with the expression of Jab1/Csn5 in lung cancer tissues and lung cancer cells. α5‐nAChR expression is associated with Jab1/Csn5 expression in lung tumour xenografts in mice. In vitro, the expression of α5‐nAChR mediated Stat3 and Jab1/Csn5 expression, significantly regulating the expression of the EMT markers, N‐cadherin and Vimentin. In addition, the down‐regulation of α5‐nAChR or/and Stat3 reduced Jab1/Csn5 expression, while the silencing of α5‐nAChR or Jab1/Csn5 inhibited the migration and invasion of NSCLC cells. Mechanistically, α5‐nAChR contributes to EMT and metastasis by regulating Stat3‐Jab1/Csn5 signalling in NSCLC, suggesting that α5‐nAChR may be a potential target in NSCLC diagnosis and immunotherapy.

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“…The migration ability of ESCC cells was tested in a Transwell Boyden Chamber (8 mm pore size; BD Biosciences, San Jose, CA, USA), as previously described . For the cell invasion assay, the polycarbonate membranes of the upper compartment of the chambers were precoated with a matrix gel.…”

Section: Methodsmentioning

confidence: 99%

Capn4 promotes esophageal squamous cell carcinoma metastasis by regulating ZEB1 through the Wnt/β‐catenin signaling pathway

Zhao

et al. 2018

Thoracic Cancer

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BackgroundCapn4 and ZEB1 play important roles in the metastasis of several types of cancer. However, the roles and relationship of Capn4 and ZEB1 in esophageal squamous cell carcinoma (ESCC) remain unclear.MethodsESCC tumor tissues and corresponding normal esophageal epithelial tissues were obtained from 86 patients undergoing resection surgery at the Department of General Surgery, First Affiliated Hospital of Chinese PLA General Hospital from 2012 to 2017. Cell migration and invasion were examined via quantitative real‐time PCR and Western blot assay.ResultsOur results indicate that both Capn4 and ZEB1 are significantly upregulated in ESCC tissues compared to corresponding adjacent tissues, and a positive correlation between expression and associated malignant characteristics was found. Silencing of Capn4 expression markedly inhibited ESCC invasion and metastasis in vitro and in vivo, and was accompanied by decreased ZEB1 expression. Furthermore, the anti‐metastasis role of Capn4 silencing was reversed by ZEB1 overexpression, whereas knockdown of ZEB1 decreased ESCC metastasis driven by the upregulation of Capn4. Mechanistically, Capn4 regulated ZEB1 expression via activation of the Wnt/β‐catenin signaling pathway in ESCC cells.ConclusionOverall, our results show that enhanced Capn4 expression activates the Wnt/β‐catenin signaling pathway, resulting in increased ZEB1 expression and the promotion of ESCC cell metastasis.

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CSN5 promotes renal cell carcinoma metastasis and EMT by inhibiting ZEB1 degradation

Cited by 39 publications

References 27 publications

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

lncRNA TUG1-Mediated Mir-142-3p Downregulation Contributes to Metastasis and the Epithelial-to-Mesenchymal Transition of Hepatocellular Carcinoma by Targeting ZEB1

α5‐nAChR contributes to epithelial‐mesenchymal transition and metastasis by regulating Jab1/Csn5 signalling in lung cancer

Capn4 promotes esophageal squamous cell carcinoma metastasis by regulating ZEB1 through the Wnt/β‐catenin signaling pathway

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