Cavin-2 Functions as a Suppressive Regulator in TNF-induced Mesenchymal Stromal Cell Inflammation and Angiogenic Phenotypes

Annabi, Bayader; Zgheib, Alain

doi:10.15283/ijsc16032

Cited by 4 publications

(2 citation statements)

References 39 publications

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“…Codenotti et al [ 48 ] reported that CAVIN2 is a useful marker for discriminating the degree of differentiation in liposarcoma tumors. Annabi et al [ 49 ] highlighted the role of CAVIN2 in the regulation of each inflammatory and angiogenic for TNF-activated MSC. No previous reports are related to the prognosis of cancer outcomes in patients.…”

Section: Discussionmentioning

confidence: 99%

A seven-gene prognostic signature predicts overall survival of patients with lung adenocarcinoma (LUAD)

et al. 2021

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Background Lung adenocarcinoma (LUAD) is one of the most common types in the world with a high mortality rate. Despite advances in treatment strategies, the overall survival (OS) remains short. Our study aims to establish a reliable prognostic signature closely related to the survival of LUAD patients that can better predict prognosis and possibly help with individual monitoring of LUAD patients. Methods Raw RNA-sequencing data were obtained from Fudan University and used as a training group. Differentially expressed genes (DEGs) for the training group were screened. The univariate, least absolute shrinkage and selection operator (LASSO), and multivariate cox regression analysis were conducted to identify the candidate prognostic genes and construct the risk score model. Kaplan–Meier analysis, time-dependent receiver operating characteristic (ROC) curve were used to evaluate the prognostic power and performance of the signature. Moreover, The Cancer Genome Atlas (TCGA-LUAD) dataset was further used to validate the predictive ability of prognostic signature. Results A prognostic signature consisting of seven prognostic-related genes was constructed using the training group. The 7-gene prognostic signature significantly grouped patients in high and low-risk groups in terms of overall survival in the training cohort [hazard ratio, HR = 8.94, 95% confidence interval (95% CI)] [2.041–39.2]; P = 0.0004), and in the validation cohort (HR = 2.41, 95% CI [1.779–3.276]; P < 0.0001). Cox regression analysis (univariate and multivariate) demonstrated that the seven-gene signature is an independent prognostic biomarker for predicting the survival of LUAD patients. ROC curves revealed that the 7-gene prognostic signature achieved a good performance in training and validation groups (AUC = 0.91, AUC = 0.7 respectively) in predicting OS for LUAD patients. Furthermore, the stratified analysis of the signature showed another classification to predict the prognosis. Conclusion Our study suggested a new and reliable prognostic signature that has a significant implication in predicting overall survival for LUAD patients and may help with early diagnosis and making effective clinical decisions regarding potential individual treatment.

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Section: Discussionmentioning

confidence: 99%

A seven-gene prognostic signature predicts overall survival of patients with lung adenocarcinoma (LUAD)

et al. 2021

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“…In addition to the direct effect on ROS production, CAV1 has been proposed as a negative regulator of prostaglandin-endoperoxide synthase (PTGS) 2 (also known as COX2) [ 74 ], which can be up-regulated by ROS and mediates inflammation [ 75 ]. Interestingly, differential regulation of cavin proteins by tumour necrosis factor (TNF), a PTGS2 and inflammation inducer [ 76 ], has been observed in mesenchymal stromal cells [ 77 ]. This study also revealed a role for Cavin2 as a suppressor of TNF signalling.…”

Section: Caveolae and The Oxidative Stress Responsementioning

confidence: 99%

Caveolae and the oxidative stress response

Lim

Parton

2023

Biochemical Society Transactions

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Oxidative stress is a feature of many disease conditions. Oxidative stress can activate a number of cellular pathways leading to cell death, including a distinct iron-dependent pathway involving lipid peroxidation, termed ferroptosis, but cells have evolved complex mechanisms to respond to these stresses. Here, we briefly summarise current evidence linking caveolae to the cellular oxidative stress response. We discuss recent studies in cultured cells and in an in vivo model suggesting that lipid peroxidation driven by oxidative stress causes disassembly of caveolae to release caveola proteins into the cell where they regulate the master transcriptional redox controller, nuclear factor erythroid 2-related factor 2. These studies suggest that caveolae maintain cellular susceptibility to oxidative stress-induced cell death and suggest a crucial role in cellular homeostasis and the response to wounding.

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Serum deprivation protein response intervenes in the proliferation, motility, and extracellular matrix production in keloid fibroblasts by blocking the amplification of TGF-β1/SMAD signal cascade via ERK1/2

Li,

Han,

Wang

et al. 2024

Toxicology and Applied Pharmacology

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Cavin-2 Functions as a Suppressive Regulator in TNF-induced Mesenchymal Stromal Cell Inflammation and Angiogenic Phenotypes

Cited by 4 publications

References 39 publications

A seven-gene prognostic signature predicts overall survival of patients with lung adenocarcinoma (LUAD)

A seven-gene prognostic signature predicts overall survival of patients with lung adenocarcinoma (LUAD)

Caveolae and the oxidative stress response

Serum deprivation protein response intervenes in the proliferation, motility, and extracellular matrix production in keloid fibroblasts by blocking the amplification of TGF-β1/SMAD signal cascade via ERK1/2

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