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() Is a SMAD3-Dependent TGF-β Target Gene That Promotes Clonogenicity and Correlates with Poor Prognosis in Breast Cancer.
Cells
September 2024
Division of Cellular Medicine, School of Medicine, University of Dundee, Dundee DD1 4HN, UK.
Transforming Growth Factor-β (TGF-β) can have both tumour-promoting and tumour-suppressing activity in breast cancer. Elucidating the key downstream mediators of pro-tumorigenic TGF-β signalling in this context could potentially give rise to new therapeutic opportunities and/or identify biomarkers for anti-TGF-β directed therapy. Here, we identify (also known as innate immunity activator ) as a novel TGF-β target gene which is induced in a SMAD3-dependent but SMAD2/SMAD4-independent manner in human and murine cell lines.
View Article and Find Full Text PDFAldehyde Dehydrogenase 2 Deficiency Aggravates Lung Fibrosis through Mitochondrial Dysfunction and Aging in Fibroblasts.
Am J Pathol
August 2024
Peking University China-Japan Friendship School of Clinical Medicine, Beijing, China; National Center for Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, China-Japan Friendship Hospital, Beijing, China. Electronic address:
Article Synopsis
- Idiopathic pulmonary fibrosis is a severe lung disease linked to abnormal fibroblast activity and excessive extracellular matrix buildup, yet treatment options are limited due to unclear mechanisms.
- Researchers identified aldehyde dehydrogenase 2 (ALDH2) as a promising therapeutic target; decreased ALDH2 levels were found in patients and mouse models of the disease, leading to increased collagen accumulation and worsening pulmonary fibrosis.
- The study revealed that a feedback loop involving transforming growth factor (TGF)-β1 and ALDH2 depletion worsened fibroblast dysfunction, but boosting ALDH2 levels could potentially reverse established fibrosis, suggesting that therapies aimed at enhancing ALDH2 expression could be beneficial.
ZNF469 is a profibrotic regulator of extracellular matrix in hepatic stellate cells.
J Cell Biochem
July 2024
Department of Biochemistry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand.
Activation of quiescent hepatic stellate cells (HSCs) into proliferative myofibroblasts drives extracellular cellular matrix (ECM) accumulation and liver fibrosis; nevertheless, the transcriptional network that promotes such a process is not completely understood. ZNF469 is a putative C2H2 zinc finger protein that may bind to specific genome sequences. It is found to be upregulated upon HSC activation; however, the molecular function of ZNF469 is completely unknown.
View Article and Find Full Text PDFFibroblast-specific PRMT5 deficiency suppresses cardiac fibrosis and left ventricular dysfunction in male mice.
Nat Commun
March 2024
Division of Molecular Medicine, School of Pharmaceutical Sciences, University of Shizuoka, Shizuoka, Japan.
Protein arginine methyltransferase 5 (PRMT5) is a well-known epigenetic regulatory enzyme. However, the role of PRMT5-mediated arginine methylation in gene transcription related to cardiac fibrosis is unknown. Here we show that fibroblast-specific deletion of PRMT5 significantly reduces pressure overload-induced cardiac fibrosis and improves cardiac dysfunction in male mice.
View Article and Find Full Text PDFAberrant TIMP-1 production in tumor-associated fibroblasts drives the selective benefits of nintedanib in lung adenocarcinoma.
Cancer Sci
May 2024
Department of Biomedicine, School of Medicine and Health Sciences, Unit of Biophysics and Bioengineering, University of Barcelona, Barcelona, Spain.
The fibrotic tumor microenvironment is a pivotal therapeutic target. Nintedanib, a clinically approved multikinase antifibrotic inhibitor, is effective against lung adenocarcinoma (ADC) but not squamous cell carcinoma (SCC). Previous studies have implicated the secretome of tumor-associated fibroblasts (TAFs) in the selective effects of nintedanib in ADC, but the driving factor(s) remained unidentified.
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