ArticleJournal of molecular histology2023
ETV5 transcriptionally activates TGFβ1 and promotes cancer cell invasion and migration of NSCLC.
Article in Journal of molecular histology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- The repressor Capicua is a barrier to lung tumor development driven by Kras/Trp53 mutations.EMBO molecular medicine · 2025Article
- Identification of ETV5 as a prognostic marker related to epigenetic modification in pan-cancer and facilitates tumor progression in hepatocellular carcinoma.Scientific reports · 2024Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
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Abstract
The morbidity and mortality of NSCLC remains high worldwide. However, the molecular mechanisms of NSCLC still largely unclear. Ets variant 5 (ETV5) is a transcription factor that found to be overexpressed in multiple cancers. However, the role of ETV5 in NSCLC remains unknown. We aim to explore the role and mechanisms of ETV5 in NSCLC development. The expression of ETV5 was evaluated in NSCLC tissues and cell lines. ETV5 overexpressing and downregulation cell lines were established according to the endogenous expression of ETV5. Functional studies were performed by transwell assay. The downstream targets of ETV5 were screened by PCR array and were confirmed by luciferase reporter assay. We found that overexpression of ETV5 indicates worse prognosis of NSCLC patients. Elevated ETV5 expression promotes NSCLC cell invasion and migration via transcriptional activates of TGFβ1. Therefore, ETV5/TGFβ signaling may serve as a therapeutic target for NSCLS patients.
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