ArticleCell cycle (Georgetown, Tex.)2017
Cell proliferation downregulated by TGF-β2-triggered G1/S checkpoint in clinical CAFs.
Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
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- The extracellular matrix drives guanylate production and protects pancreatic cancer cells from oxaliplatin-induced DNA damage.Science advances · 2025Article
- Immunotherapy for lung cancer combining the oligodeoxynucleotides of TLR9 agonist and TGF-β2 inhibitor.Cancer immunology, immunotherapy : CII · 2023Article
- Review
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- Cancer-associated fibroblasts enhance tumorTheranostics · 2018Article
- Glutamic Pyruvate Transaminase GPT2 Promotes Tumorigenesis of Breast Cancer Cells by Activating Sonic Hedgehog Signaling.Theranostics · 2017Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The metabolic reprogramming is indispensible for the fast growth of tumor cells. The metabolism of CAFs is reprogrammed to aerobic glycolysis too. However, it is not clear whether this metabolic reprogramming promotes the growth of CAFs themselves. In this study, we found that the proliferation rate of CAFs was slower than NAFs, which was determined by cell counting, BrdU assay and flow cytometry analysis. Moreover, we found TGF-β signaling regulated cell growth of CAF through RNA-sequencing analysis and Western blot, which was further supported by the observation that TGF-β2 was highly expressed in colon cancer tissues. In the end, we demonstrated that CAFs were critical to tumor cell proliferation, which was supported by the evidence of their close localization in clinical tumor tissue and tumor promoting effect in mice. In brief, our data have manifested that the proliferation rate is decreased in CAFs, which enable CAFs generate more intermediate metabolites to support tumor cells growth, suggesting CAFs is an ideal target for tumor therapy.
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