ArticleOncoTargets and therapy2020
Downregulation of OSR1 Promotes Colon Adenocarcinoma Progression via FAK-Mediated Akt and MAPK Signaling.
Article in OncoTargets and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Asxl1 loss in mice leads to microcephaly by regulating neural stem cell survival.Animal cells and systems · 2025Article
- OSR1 downregulation indicates an unfavorable prognosis and activates the NF-κB pathway in ovarian cancer.Discover oncology · 2023Article
- The conserved microRNA-229 family controls low-insulin signaling and dietary restriction induced longevity through interactions with SKN-1/NRF2.Aging cell · 2023Article
- Odd-skipped related 1 plays a tumor suppressor role in ovarian cancer via promoting follistatin-like protein 1 transcription.Human cell · 2022Article
- Comprehensive bioinformatics analysis reveals biomarkers of DNA methylation-related genes in varicose veins.Frontiers in genetics · 2022Article
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2 authors at 1 institution in 1 country.
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Abstract
introductionOdd-skipped related transcription factor 1 (OSR1) is a newly identified tumor suppressor in many tumor types. However, the role and mechanism of OSR1 in colon adenocarcinoma (COAD) remain unknown.
methodsOSR1 expression was detected in COAD tissues and cells. COAD cells with OSR1 overexpression or knockdown were analyzed by in vitro CCK-8, transwell and flow cytometry assays, and by in vivo xenograft model.
resultsOSR1 expression was downregulated in COAD and low expression level of OSR1 was positively correlated with tumor stage and lymph node metastasis. Furthermore, low OSR1 expression was significantly associated with poor overall survival (OS) and distant metastasis-free survival (DMFS). Lentivirus-mediated restoration of OSR1 expression-inhibited proliferation, invasion and migration while induced cell cycle arrest and apoptosis in COAD cells in vitro, and inhibited tumor growth in vivo. In contrast, OSR1 knockdown promoted proliferation, invasion and migration in COAD cells in vitro. Mechanistically, OSR1 exerted anticancer effects by inhibiting FAK-mediated activation of Akt and MAPK pathways.
conclusionOur findings suggest that OSR1 functions as a tumor suppressor in COAD by suppressing FAK-mediated activation of Akt and MAPK pathways.
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