ArticleCancer science2012
Transforming growth factor-β-stimulated clone-22 is a negative-feedback regulator of Ras / Raf signaling: Implications for tumorigenesis.
Article in Cancer science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 38 citations in OpenAlex.
- Regulatory factor X 7 limits Myc activity during B cell activation and suppresses Myc-dependent lymphomagenesis.Nature immunology · 2026Article
- Novel Insights into TSC22D Family Genes in Metabolic Diseases and Cancer.Biomolecules · 2026Review
- Epstein-Barr Virus Promotes Gastric Cancer Progression by Modulating m6A-Dependent YTHDF1-TSC22D1 Axis.Microorganisms · 2025Article
- TSC22D1 is a newly identified inhibitor of insulin secretion in pancreatic beta cells.The FEBS journal · 2025Article
- Alternative splicing of bunched confers a dual role in hippo pathway-dependent growth and tumorigenesis.Oncogene · 2025Article
- Genetically Engineered ProbioticCancers · 2024Article
- Comprehensive bioinformatic analysis of the expression and prognostic significance of TSC22D domain family genes in adult acute myeloid leukemia.BMC medical genomics · 2023Article
- Transforming Stimulated Clone 22 (TSC-22) Interacts Directly with Bromodomain-Containing Protein 7 (BRD7) to Enhance the Inhibition of Extracellular Signal-Regulate Kinase (ERK) Pathway in Ovarian Cancer.Development & reproduction · 2022Article
- Diagnosis and staging of HCV associated fibrosis, cirrhosis and hepatocellular carcinoma with target identification for miR-650, 552-3p, 676-3p, 512-5p and 147b.Cancer biomarkers : section A of Disease markers · 2022Article
- Identification of Binding Proteins for TSC22D1 Family Proteins Using Mass Spectrometry.International journal of molecular sciences · 2021Article
- Derangement of Metabolic and Lysosomal Gene Profiles in Response to Dexamethasone Treatment in Sarcoidosis.Frontiers in immunology · 2020Article
- Regulation of c-MYC transcriptional activity by transforming growth factor-beta 1-stimulated clone 22.Cancer science · 2018Article
- The bromodomain inhibitor JQ1 triggers growth arrest and apoptosis in testicular germ cell tumours in vitro and in vivo.Journal of cellular and molecular medicine · 2017Article
- Acute transcriptional up-regulation specific to osteoblasts/osteoclasts in medaka fish immediately after exposure to microgravity.Scientific reports · 2016Article
- Control of diabetic hyperglycaemia and insulin resistance through TSC22D4.Nature communications · 2016Article
- Yeast two-hybrid screening identified WDR77 as a novel interacting partner of TSC22D2.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Article
- Discovery of osmotic sensitive transcription factors in fish intestine via a transcriptomic approach.BMC genomics · 2014Article
- Hepatic transforming growth factor-β 1 stimulated clone-22 D1 controls systemic cholesterol metabolism.Molecular metabolism · 2014Article
- Enhanced effector responses in activated CD8+ T cells deficient in diacylglycerol kinases.Cancer research · 2013Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-β (TGF-β)-stimulated clone-22 (TSC-22), also called TSC22D1-2, is a putative tumor suppressor. We previously identified TSC-22 downstream of an active mutant of fms-like tyrosine kinase-3 (Flt3). Here, we show that TSC-22 works as a tumor suppressor through inhibiting Ras/Raf signaling. Notably, TSC-22 was upregulated by Ras/Raf activation, whereas its upregulation was inhibited by concurrent STAT5 activation. Although TSC-22 was normally retained in the cytoplasm by its nuclear export signal (NES), Ras/Raf activation caused nuclear translocation of TSC-22, but not TSC22D1-1. Unlike glucocorticoid-induced leucine zipper (GILZ/TSC22D3-2) previously characterized as a negative regulator of Ras/Raf signaling, TSC-22 failed to interact physically with Ras/Raf. Importantly, transduction with TSC-22, but not TSC22D1-1, suppressed the growth, transformation and tumorigenesis of NIH3T3 cells expressing oncogenic H-Ras: this suppression was enhanced by transduction with a TSC-22 mutant lacking NES that had accumulated in the nucleus. Collectively, upregulation and nuclear translocation of TSC-22 played an important role in the feedback suppression of Ras/Raf signaling. Consistently, TSC22D1-deficient mice were susceptible to tumorigenesis in a mouse model of chemically-induced liver tumors bearing active mutations of Ras/Raf. Thus, TSC-22 negatively regulated Ras/Raf signaling through a mechanism different from GILZ, implicating TSC-22 as a novel suppressor of oncogenic Ras/Raf-induced tumors.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.