ArticleCancer medicine2023
MFAP2, upregulated by m1A methylation, promotes colorectal cancer invasiveness via CLK3.
Article in Cancer medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 37 citations in OpenAlex.
- Article
- CLK3 regulates tumor angiogenesis by modulating HIF1α ubiquitination.Cancer gene therapy · 2026Article
- MFAP2 promotes metastasis and drug resistance by regulating epithelial-to-mesenchymal transition through EGFR signaling pathway in colorectal cancer cells.Genes & diseases · 2026Article
- Unveiling the epigenetic landscape: transforming renal cell carcinoma treatment.Clinical epigenetics · 2026Review
- FOXA1-mediated transcription of MFAP2 facilitates cell growth, metastasis and cisplatin resistance in uterine corpus endometrial carcinoma.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Roles of RNA modifications in aging and age-related diseases.BMB reports · 2025Review
- Dynamic modifications of circular RNAs drive oncogenesis.Epigenomics · 2025Review
- Nanoparticle Formulations for Intracellular Delivery in Colorectal Cancer Therapy.AAPS PharmSciTech · 2025Article
- Association between TRMT61B gene polymorphism and Wilms tumor susceptibility in Chinese children.BMC cancer · 2025Article
- m1A-regulated DIAPH3 promotes the invasiveness of colorectal cancer via stabilization of KRT19.Clinical & experimental metastasis · 2025Article
- Cis-regulation analysis of RNA m6A methylation and gene expression in colorectal cancer.Frontiers in genetics · 2025Article
- MFAP2 promotes the progress of esophageal squamous cell carcinoma by enhancing PTGS2 signaling.Journal of Cancer · 2025Article
- Article
- The role of m5C, m1A and m7G modifications in tumors of urinary system.Frontiers in cell and developmental biology · 2025Review
- RNA Modification and Digestive Tract Tumors: A Review.Current medicinal chemistry · 2025Review
- Identification and functional characterization of m1A-related genes in colorectal cancer: implications for prognosis, immune infiltration, and therapeutic strategies.Frontiers in oncology · 2025Article
- CLK3 promotes tumor proliferation by activating MYC signaling.Cell division · 2024Article
- Mechanism insights and therapeutic intervention of tumor metastasis: latest developments and perspectives.Signal transduction and targeted therapy · 2024Review
- Review
- OIP5-AS1/miR-455-3p/microfibril-associated protein 2 axis exacerbates the progression of thyroid carcinoma.Translational cancer research · 2024Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDistant metastasis is the main cause of mortality in colorectal cancer (CRC) patients. N1-methyladenosine (m1A) is a type of epitranscriptome modification. While its regulatory effect on mRNA and its role in CRC metastasis remain unclear.
methodsThe m1A methylation profile of mRNAs in CRC was revealed by m1A methylated RNA immunoprecipitation sequencing. The expression of MFAP2 in tumor tissues was measured by immunohistochemistry and then correlated with the clinical characteristics and prognosis of CRC patients. The role of MFAP2 in the invasiveness of CRC cells was evaluated by transwell assays and peritoneal metastatic model in nude mice. The downstream targets of MFAP2 was screened by mass spectrometry analysis. Then the role of MFAP2-CLK3 signaling axis was verified by cotransfecting MFAP2 siRNA and CLK3 plasmid in CRC cells.
resultsMicrofibril associated protein 2 (MFAP2) mRNA was overexpressed and m1A-hypermethylated in CRC. High expression of MFAP2 was closely related to lymph node metastasis and distant metastasis, leading to poor prognosis in patients with CRC. In vivo and in vitro studies showed that silencing of MFAP2 inhibited the migration, invasion and metastasis of CRC cells. CDC Like Kinase 3 (CLK3) was a potential downstream target of MFAP2. Further studies showed that MFAP2 depletion might induce autophagic degradation of CLK3, and the role of MFAP2 in the invasiveness of CRC cells was dependent on CLK3.
conclusionsOur results uncover a newly identified MFAP2-CLK3 signaling axis, which is a potential therapeutic target for CRC metastasis.
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