ArticleJournal of Cancer2020
FLRT2 functions as Tumor Suppressor gene inactivated by promoter methylation in Colorectal Cancer.
Article in Journal of Cancer, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
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- Epigenome Reprogramming Through H3K27 and H3K4 Trimethylation as a Resistance Mechanism to DNA Methylation Inhibition in BRAFV600E-Mutated Colorectal Cancer.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
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- Proteogenomic characterization of primary colorectal cancer and metastatic progression identifies proteome-based subtypes and signatures.Cell reports · 2024Article
- The NEDD4/FLRT2 axis regulates NSCLC cell stemness.Frontiers in pharmacology · 2024Article
- Multi-level functional genomics reveals molecular and cellular oncogenicity of patient-based 3' untranslated region mutations.Cell reports · 2023Article
- Fibronectin leucine-rich transmembrane protein 2 drives monocyte differentiation into macrophagesFrontiers in immunology · 2023Article
- Chondroitin Sulfate Proteoglycan 4 as a Marker for Aggressive Squamous Cell Carcinoma.Cancers · 2022Review
- Gaussian graphical models with applications to omics analyses.Statistics in medicine · 2022Article
- Prospective Proteomic Study Identifies Potential Circulating Protein Biomarkers for Colorectal Cancer Risk.Cancers · 2022Article
- Epigenetic Regulation of Intestinal Stem Cells and Disease: A Balancing Act of DNA and Histone Methylation.Gastroenterology · 2021Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal cancer (CRC) is a leading cause of cancer death worldwide. Epigenetic alterations, especially DNA methylation, contribute to the initiation and progression of CRC. To identify novel methylated tumor suppressors in CRC, MethylRAD-Seq screening was performed. As the result, FLRT2 was found to be preferentially methylated. In the present study, we aimed to elucidate the epigenetic regulations and biological functions of FLRT2 in CRC. Significant FLRT2 hypermethylation was initially confirmed in CRC samples and cell lines. Meanwhile, downregulated expression of FLRT2 was observed in CRC, which is probably attributed to promoter methylation of FLRT2. Consistently, the expression of FLRT2 was restored after treatment with DNA demethylating agent 5-AZA. FLRT2 overexpression resulted in impaired cell viability and colony formation. Additionally, FLRT2 overexpression led to a reduction in cell migration and cell invasion. Furthermore, we also observed that FLRT2 induced cell cycle arrest. Mechanistically, these effects were associated with the downregulation of phosphor-AKT, phosphor-ERK, CDK2, Cyclin A, and MMP2, and upregulation of P21. Taken together, these results define a tumor-suppressor role of FLRT2 with epigenetic silencing in the pathogenesis of CRC. Moreover, FLRT2 promoter methylation may be a useful epigenetic biomarker for the prevention and treatment of CRC.
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