Protein tyrosine phosphatase L1 represses endothelial-mesenchymal transition by inhibiting IL-1β/NF-κB/Snail signaling

Wei, Xiaomin; Wumaier, Gulinuer; Zhu, Ning; Dong, Liang; Li, Chengwei; Xia, Jie; You-zhi, Zhang; Zhang, Peng; Zhang, Xiujuan; Zhang, Yuanyuan; Li, Shengqing

doi:10.1038/s41401-020-0374-x

Cited by 10 publications

(5 citation statements)

References 52 publications

(44 reference statements)

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“…This inhibitory effect of PTPN13 on cell migration and invasion is consistent with the observations in other tumor types (for review, see [24]). PTPN13 overexpression in a hepatocellular carcinoma cell line [14] and PTPN13 inhibition of 15 in lung cancer cells [25] and human umbilical endothelial cells [26] may regulate EMT driver gene expression. In addition, PTPN13 might also inhibit EMT through the stabilization of intercellular junctions via its positive role in desmosome formation [27].…”

Section: Discussionmentioning

confidence: 99%

PTPN13 Participates in the Regulation of Epithelial–Mesenchymal Transition and Platinum Sensitivity in High-Grade Serous Ovarian Carcinoma Cells

Aptecar,

Puech,

Lopez-Crapez

et al. 2023

IJMS

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Epithelial ovarian cancer (EOC) is the leading cause of death from gynecological cancers in Western countries. High-Grade Serous Ovarian Carcinoma (HGSOC) accounts for 60–70% of EOC and is the most aggressive subtype. Reduced PTPN13 expression levels have been previously correlated with worse prognosis in HGSOC. However, PTPN13’s exact role and mechanism of action in these tumors remained to be investigated. To elucidate PTPN13’s role in HGSOC aggressiveness, we used isogenic PTPN13-overexpressing clones of the OVCAR-8 cell line, which poorly expresses PTPN13, and also PTPN13 CRISPR/Cas9-mediated knockout/knockdown clones of the KURAMOCHI cell line, which strongly expresses PTPN13. We investigated their migratory and invasive capacity using a wound healing assay, their mesenchymal-epithelial transition (EMT) status using microscopy and RT-qPCR, and their sensitivity to chemotherapeutic drugs used for HGSOC. We found that (i) PTPN13 knockout/knockdown increased migration and invasion in KURAMOCHI cells that also displayed a more mesenchymal phenotype and increased expression of the SLUG, SNAIL, ZEB-1, and ZEB-2 EMT master genes; and (ii) PTPN13 expression increased the platinum sensitivity of HGSOC cells. These results suggest that PTPN13 might be a predictive marker of response to platinum salts in HGSOC.

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Section: Discussionmentioning

confidence: 99%

PTPN13 Participates in the Regulation of Epithelial–Mesenchymal Transition and Platinum Sensitivity in High-Grade Serous Ovarian Carcinoma Cells

Aptecar,

Puech,

Lopez-Crapez

et al. 2023

IJMS

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“…Bladder carcinoma cell protein extraction was performed according to a previous study [ 37 ]. Briefly, proteins from bladder carcinoma cell lines were extracted using RIPA lysis buffer (Sigma-Aldrich, USA) supplemented with a protease inhibitor cocktail (PIC, Roche, USA).…”

Section: Methodsmentioning

confidence: 99%

Dysregulation and antimetastatic function of circLRIG1 modulated by miR-214-3p/LRIG1 axis in bladder carcinoma

Cheng,

Li,

Liu

et al. 2024

Biol Direct

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CircLRIG1, a newly discovered circRNA, has yet to have its potential function and biological processes reported. This study explored the role of circLRIG1 in the development and progression of bladder carcinoma and its potential molecular mechanisms. Techniques such as qRT-PCR, Western blot, various cellular assays, and in vivo models were used to investigate mRNA and protein levels, cell behavior, molecular interactions, and tumor growth. The results showed that both circLRIG1 and LRIG1 were significantly reduced in bladder carcinoma tissues and cell lines. Low circLRIG1 expression was associated with poor patient prognosis. Overexpressing circLRIG1 inhibited bladder carcinoma cell growth, migration, and invasion, promoted apoptosis, and decreased tumor growth and metastasis in vivo. Importantly, circLRIG1 was found to sponge miR-214-3p, enhancing LRIG1 expression, and its overexpression also modulated protein levels of E-cadherin, N-cadherin, Vimentin, and LRIG1. Similar effects were observed with LRIG1 overexpression. Notably, a positive correlation was found between circLRIG1 and LRIG1 expression in bladder carcinoma tissues. Additionally, the tumor-suppressing effect of circLRIG1 was reversed by overexpressing miR-214-3p or silencing LRIG1. The study concludes that circLRIG1 suppresses bladder carcinoma progression by enhancing LRIG1 expression via sponging miR-214-3p, providing a potential strategy for early diagnosis and treatment of bladder carcinoma.

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“…Crude proteins were isolated from NSCLC cells following a previously reported protocol (Wei et al 2020 ). Briefly, the cells were first treated with ice-cold RIPA lysis buffer (Sigma, USA) for 15 min and then boiled for 10 min to release proteins.…”

Section: Methodsmentioning

confidence: 99%

EIF4A3-induced circular RNA SCAP facilitates tumorigenesis and progression of non-small-cell lung cancer via miR-7/SMAD2 signaling

Zhang

2023

Environ Sci Pollut Res

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The eukaryotic translation initiation factor 4A (eIF4A) family determines transcription efficiency by directly binding to precursor RNAs. One member, EIF4A3, modulates the expression of circRNAs. Circular RNA SCAP (circSCAP), a newly found circRNA, has been implicated in atherosclerosis. Yet, how circSCAP regulates cancer development and progression remains understudied. Here, we investigated the function of circSCAP and the molecular mechanism in the tumorigenesis and progression of non-small-cell lung cancer (NSCLC). CircSCAP was upregulated in both NSCLC tissues and cell lines and was mainly located in the cytoplasm. CircSCAP expression was promoted by EIF4A3, which was associated with poor prognosis in patients with NSCLC. CircSCAP sponged miR-7 to upregulate small mothers against decapentaplegic 2 (SMAD2). CircSCAP knockdown undermined cell proliferation, migration, and invasion abilities in NSCLC cell lines (SPCA1 and A549), which was rescued by either inhibiting miR-7 or overexpressing SMAD2. Moreover, circSCAP knockdown upregulated E-cadherin, while downregulating N-cadherin, Vimentin, and MMP9 in SPCA1 and A549 cells, which were abolished by either inhibiting miR-7 or overexpressing SMAD2. Additionally, miR-7 was markedly downregulated, whereas SMAD2 was significantly upregulated in NSCLC tissues. MiR-7 expression was inversely correlated with circSCAP and SMAD2 expression in NSCLC tissues. In conclusion, this study demonstrates that circSCAP is significantly upregulated in NSCLC cell lines and tissues and elucidates that circSCAP facilitates NSCLC progression by sponging miR-7 and upregulating SMAD2. The study provides a novel molecular target for early diagnosis and treatment of NSCLC.

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Protein tyrosine phosphatase L1 represses endothelial-mesenchymal transition by inhibiting IL-1β/NF-κB/Snail signaling

Cited by 10 publications

References 52 publications

PTPN13 Participates in the Regulation of Epithelial–Mesenchymal Transition and Platinum Sensitivity in High-Grade Serous Ovarian Carcinoma Cells

PTPN13 Participates in the Regulation of Epithelial–Mesenchymal Transition and Platinum Sensitivity in High-Grade Serous Ovarian Carcinoma Cells

Dysregulation and antimetastatic function of circLRIG1 modulated by miR-214-3p/LRIG1 axis in bladder carcinoma

EIF4A3-induced circular RNA SCAP facilitates tumorigenesis and progression of non-small-cell lung cancer via miR-7/SMAD2 signaling

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