ArticleCancer cell international2025
HNRNPC promotes progression of non-small cell lung cancer by maintaining TFAP2A mRNA stability.
Article in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- HNRNPC contributes to ccRCC progression by stabilizing AURKB mRNA in an m6A-dependent manner.Human cell · 2026Article
- The Role of Alternative Splicing in Lung Cancer: Mechanisms, Regulators, and Therapeutic Implications.International journal of molecular sciences · 2026Review
- RNA Regulatory Networks: Key Hubs in the Panorama of Cancer and Emerging Therapeutic Targets.MedComm · 2026Review
- Prognostic role and mutational characteristics of N6-methyladenosine-related genes in lung adenocarcinoma.Oncology letters · 2025Article
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9 authors.
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Abstract
backgroundHNRNPC is an RNA-binding protein that is overexpressed in a variety of cancers and is well known as an m6A "reader", but its specific function and molecular mechanism in NSCLC have not been fully understood. This study aimed to discuss molecular mechanism of HNRNPC in NSCLC.
methodsHNRNPC expression and clinically relevant data in pan-cancer and LUAD were extracted through these websites, including UALCAN, TIMER2 and GEPIA. The target gene of HNRNPC were identified through RIP-seq, meRIP-qPCR and mRNA stability test. The differential expression of target gene in NSCLC was explored by immunohistochemistry. Lentivirus was selected to knock down HNRNPC and plasmid was selected to overexpress downstream target genes. The transfection efficiency was verified by RT-qPCR and Western Blot. In vitro colony formation assay, CCK-8, wound healing, transwell assays were performed to determine the biological functions of HNRNPC and target gene in lung adenocarcinoma cells.
resultsHNRNPC can promotes the expression of TFAP2A by recognizing the m6A modification of TFAP2A mRNA and maintaining its stability, activates the TFAP2A/CTNNB1 axis, enhances EMT, and ultimately promotes the malignant process of NSCLC and promote distant metastasis of NSCLC.
conclusionsThese results supported that HNRNPC regulate TFAP2A to promote the malignant progression and EMT of NSCLC. These findings connect m6A modification with EMT, providing a new perspective on the regulation of m6A modification in tumors.
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