The role of TMEM59L in colorectal cancer progression and its interaction with the TGF-β/Smad pathway
Yang H., Liu J., Jiang P., Sun Y., Chen L., Zhu S.
Animal Study, published in Front Oncol (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Front Oncol (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41378300
- PMCID
- PMC12685656
- DOI
- 10.3389/fonc.2025.1674849
Abstract (original English)
Objective This study aimed to investigate the role of TMEM59L in colorectal cancer (CRC) and its interaction with the TGF-β/Smad signaling pathway. Methods We analyzed the correlation between TMEM59L expression levels and patient survival, as well as its impact on the TGF-β/Smad signaling pathway, using data from The Cancer Genome Atlas (TCGA). Additionally, transwell, CCK-8, EdU, and colony formation assays were conducted to assess the effects of TMEM59L on CRC cell migration, invasion, and proliferation. Gene silencing and overexpression, along with specific inhibitors/agonists, were used to validate the involvement of TMEM59L in the regulation of the TGF-β/Smad signaling pathway. Results We found that high TMEM59L expression was associated with poor patient survival and TGF-β pathway activation. After si-TMEM59L treatment, the migration and invasion abilities of CRC cells were reduced, while cell proliferation remained affected to a lesser extent. Additionally, the levels of TGF-β protein were decreased, and the phosphorylation of Smad2/3 was reduced. In vivo , TMEM59L knockdown reduced metastatic potential as demonstrated by decreased fluorescence intensity, while overexpression of TMEM59L increased metastatic potential, which was reversed by TGF-β inhibition. Conclusion TMEM59L may promote CRC metastasis by enhancing cell migration and invasion, with minimal impact on cell
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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