ArticleAmerican journal of translational research2024
WTAP knockdown inhibits cell migration through regulating SNAIL1 expression in colorectal cancer.
Article in American journal of translational research, 2024. 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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Who cites it
2 citing papers in PubMed.
- The mechanistic role of Wilms tumor 1-associated protein in cancer pathogenesis, immunity, immunotherapy, and therapy resistance.Investigational new drugs · 2026Review
- Targeting RNA adenosine editing and modification enzymes for RNA therapeutics.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Review
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4 authors.
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Abstract
objectiveN6-methyladenosine (m6A) modification is the most prevalent mRNA modification in carcinogenesis and it plays a crucial role. WTAP, an m6A RNA methyltransferase, is functionally significant in various cancers; however, the specific role and functional mechanism in colorectal cancer (CRC) remain poorly understood.
methodIn this study, we utilized Gene Expression Profiling Interactive Analysis (GEPIA) to compare WTAP expression in CRC and normal tissues. Functional assays including colony formation assay and transwell assay were conducted to assess the impact of WTAP on cell viability and migration. RNA dot blot and MeRIP-PCR assays were used to investigate WTAP's role in m6A modification.
resultsWTAP expression was elevated in CRC tissues. Colony formation and transwell assays showed that WTAP promoted proliferation and migration of CRC cells in vitro. Mechanistically, MeRIP-PCR analysis demonstrated that WTAP knockdown inhibited SNAI1 expression by reducing m6A modification of SNAI1 in CRC cells. Supporting this, analysis of data from GEPIA and cBioPortal revealed a positive correlation between WTAP and SNAI1 expression.
conclusionWTAP may act as an oncogene in CRC by regulating SNAI1 expression.
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