ArticleFrontiers in oncology2022
YTHDF2 Inhibits the Migration and Invasion of Lung Adenocarcinoma by Negatively Regulating the FAM83D-TGFβ1-SMAD2/3 Pathway.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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16 citing papers in PubMed, 28 citations in OpenAlex.
- The role of m6A modification in non-small cell lung cancer: functional insights and impact on therapy resistance.Cancer cell international · 2025Review
- The complex role and molecular mechanism of family with sequence similarity genes in cancer: a comprehensive review.Discover oncology · 2025Review
- M6A RNA modification: focusing on non-small cell lung cancer progression, therapeutic strategies and challenges.Frontiers in oncology · 2025Review
- The therapeutic potential of RNA m(6)A in lung cancer.Cell communication and signaling : CCS · 2024Review
- FTO Facilitates Cervical Cancer Malignancy Through Inducing m6A-Demethylation of PIK3R3 mRNA.Cancer medicine · 2024Article
- Targeting RNA modifications with pharmacological agents: New frontiers in cancer therapy.Cancer medicine · 2024Review
- FAM83D acts as an oncogene by regulating cell cycle progression via multiple pathways in synovial sarcoma: a potential novel downstream target oncogene of anlotinib.Discover oncology · 2024Article
- The FBXW7-binding sites on FAM83D are potential targets for cancer therapy.Breast cancer research : BCR · 2024Article
- Cancer metastasis under the magnifying glass of epigenetics and epitranscriptomics.Cancer metastasis reviews · 2023Review
- YTHDF2 exerts tumor-suppressor roles in gastric cancer via up-regulating PPP2CA independently of mBiological procedures online · 2023Article
- Recent Advances in RNA mCancer treatment and research · 2023Article
- N6-methyladenosine reader YTHDF family in biological processes: Structures, roles, and mechanisms.Frontiers in immunology · 2023Review
- METTL3-induced DLGAP1-AS2 promotes non-small cell lung cancer tumorigenesis through mCell cycle (Georgetown, Tex.) · 2022Article
- Methyladenosine Modification in RNAs: From Regulatory Roles to Therapeutic Implications in Cancer.Cancers · 2022Review
- The Potential Value of m6A RNA Methylation in the Development of Cancers Focus on Malignant Glioma.Frontiers in immunology · 2022Review
- Pan-cancer and single-cell analysis revealsFrontiers in genetics · 2022Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveYTH domain family 2 (YTHDF2) is an important N6-methyladenosine (m6A) reader, but its role in lung adenocarcinoma remains elusive. This study assessed its function in lung adenocarcinoma.
methodsYTHDF2 expression in lung adenocarcinoma was explored using public databases, such as The Cancer Genome Atlas (TCGA) and the Clinical Proteomic Tumour Analysis Consortium (CPTAC). The effect of YTHDF2 on a lung adenocarcinoma cell line was explored by performing cytological and molecular experiments. Molecules downstream of YTHDF2 were identified using proteomics, and the related pathways were verified through cytological and molecular biology experiments.
resultsYTHDF2 expression was upregulated in lung adenocarcinoma, and patients with high YTHDF2 expression experienced prolonged overall survival. In two lung cancer cell lines, YTHDF2 knockdown inhibited proliferation but promoted migration, invasion, and the epithelial-mesenchymal transition. The proteomic analysis identified 142 molecules downstream of YTHDF2, and 11 were closely related to survival. Further experiments revealed that YTHDF2 inhibited expression of the family with sequence similarity 83D (FAM83D)-TGFβ1-SMAD2/3 pathway components. This study is the first to show that YTHDF2 regulated the downstream TGFβ1-SMAD2/3 pathway through FAM83D in lung adenocarcinoma.
conclusionYTHDF2 inhibits the migration and invasion of lung adenocarcinoma cells by regulating the FAM83D-TGFβ1-pSMAD2/3 pathway, which may play an important role in lung cancer metastasis.
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