Modification of cysteine 457 in plakoglobin modulates the proliferation and migration of colorectal cancer cells by altering binding to E-cadherin/catenins

Kim, Suhee; Ahn, Sun Hee; Yang, Hee‐Young; Lee, Jin-Sil; Choi, Hyang-Gi; Lee, Tae‐Hoon

doi:10.1080/13510002.2016.1215120

Cited by 3 publications

(2 citation statements)

References 38 publications

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“…The current results highlight that Sirt7 not only increased N-cadherin expression, but also regulated E-cadherin transcription in an E-box-dependent manner. Notably, although E-cadherin is traditionally considered as a suppressor of cell invasion, the present study observed the inhibitory function of E-cadherin on the cell proliferation, similarly to the findings of Kim et al ( 31 ) and Ji et al ( 32 ) reported in CRC and pancreatic cancer. Although the higher Sirt7 group had a worse overall survival rate, the deaths of the lower Sirt7 group may be due to the complicated tumor metastatic mechanism.…”

Section: Discussionsupporting

confidence: 91%

Sirtuin 7 promotes colorectal carcinoma proliferation and invasion through the inhibition of E-cadherin

et al. 2017

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Sirtuin 7 (Sirt7) is a member of the sirtuin protein family and is implicated in various carcinomas; however, the function of Sirt7 in colorectal carcinoma (CRC) remains unclear. The present study aimed to explore the biological function of Sirt7 in CRC tissues and cell lines, and to investigate the potential underlying mechanism by performing reverse transcription-quantitative polymerase chain reaction analyses, western blot analyses, luciferase reporter assays, cell proliferation and invasion assays. It was demonstrated that Sirt7 presented a higher expression in CRC tissues and cell lines compared with that in normal tissues and cells, and this higher expression was correlated with the tumor size, the tumor, node and metastasis stage and distant metastasis. Knockdown of Sirt7 repressed the proliferation ability of SW620 and HCT116 cells in vitro, while ectopic expression of Sirt7 increased the epithelial-mesenchymal transition and invasion in HT29 and SW480 cells. Notably, these functional effects of Sirt7 were exerted through the repression of E-cadherin. Thus, the data of the present study indicated a novel mechanistic role for Sirt7 as an oncogene in CRC malignancy, and Sirt7 may be a potential therapeutic target.

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Section: Discussionsupporting

confidence: 91%

Sirtuin 7 promotes colorectal carcinoma proliferation and invasion through the inhibition of E-cadherin

et al. 2017

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“…In addition, γ-catenin, known as junction plakoglobin (JUP), interacts with the cytoplasmic domain of cadherins (McEwen et al, 2014 ). In colorectal cancer cells, the C457 modification of γ-catenin results in impaired migration and proliferation of cells by affecting the “cadherin switch” (Conacci-Sorrell et al, 2002 ; Kim et al, 2017 ). However, it is unclear whether the catenin/cadherin complex influences the progression of EMT in lipid nephrotoxicity and therefore warrants confirmation.…”

Section: Introductionmentioning

confidence: 99%

THBS1/CD47 Modulates the Interaction of γ-Catenin With E-Cadherin and Participates in Epithelial–Mesenchymal Transformation in Lipid Nephrotoxicity

Gao

Yang

Zhang

et al. 2021

Front. Cell Dev. Biol.

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Hyperlipidemia, an important risk factor for cardiovascular and end-stage renal diseases, often aggravates renal injury and compromises kidney function. Here, histological analysis of human kidney samples revealed that high lipid levels induced the development of renal fibrosis. To elucidate the mechanism underlying lipid nephrotoxicity, we used two types of mouse models (Apoe−/− and C57BL/6 mice fed a 45 and 60% high-fat diet, respectively). Histological analysis of kidney tissues revealed high-lipid-induced renal fibrosis and inflammation; this was confirmed by examining fibrotic and inflammatory marker expression using Western blotting and real-time polymerase chain reaction. Oxidized low-density lipoprotein (OX-LDL) significantly induced the fibrotic response in HK-2 tubular epithelial cells. RNA-sequencing and Gene Ontology analysis of differentially expressed mRNAs in OX-LDL-treated HK-2 tubular epithelial cells and real-time PCR validation in Apoe−/− mice showed that the expression of thrombospondin-1 (THBS1) in the high-fat group was significantly higher than that of the other top known genes, along with significant overexpression of its receptor CD47. THBS1 knockdown cells verified its relation to OX-LDL-induced fibrosis and inflammation. Liquid chromatography tandem mass spectrometry and STRING functional protein association network analyses predicted that THBS1/CD47 modulated the interaction between γ-catenin and E-cadherin and was involved in epithelial–mesenchymal transition, which was supported by immunoprecipitation and immunohistochemistry. CD47 downregulation following transfection with small-hairpin RNA in OX-LDL-treated tubular epithelial cells and treatment with anti-CD47 antibody restored the expression of E-cadherin and attenuated renal injury, fibrosis, and inflammatory response in OX-LDL-treated cells and in type 2 diabetes mellitus. These findings indicate that CD47 may serve as a potential therapeutic target in long-term lipid-induced kidney injury.

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Early alterations of mitochondrial morphology in dopaminergic neurons from Parkinson's disease-like pathology and time-dependent neuroprotection with D2 receptor activation

2016

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Modification of cysteine 457 in plakoglobin modulates the proliferation and migration of colorectal cancer cells by altering binding to E-cadherin/catenins

Abstract: Pg appears to be redox-sensitive in cancer, and the C457 modification may impair cell migration and proliferation by affecting its interaction with the E-cadherin/catenin axis. Our findings suggest that redox-sensitive cysteines of Pg may be the targets for CRC therapy.

Cited by 3 publications

References 38 publications

Sirtuin 7 promotes colorectal carcinoma proliferation and invasion through the inhibition of E-cadherin

Sirtuin 7 promotes colorectal carcinoma proliferation and invasion through the inhibition of E-cadherin

THBS1/CD47 Modulates the Interaction of γ-Catenin With E-Cadherin and Participates in Epithelial–Mesenchymal Transformation in Lipid Nephrotoxicity

Early alterations of mitochondrial morphology in dopaminergic neurons from Parkinson's disease-like pathology and time-dependent neuroprotection with D2 receptor activation

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