ArticleFASEB bioAdvances2024
The m6 RNA methylation regulator KIAA1429 is associated with autophagy-mediated drug resistance in lung cancer.
Article in FASEB bioAdvances, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Research progress and trends on DNA methylation research in non-small cell lung cancer: a bibliometric analysis.Journal of thoracic disease · 2026Article
- Research progress on the characteristics and functions of m6A modification in lung cancer tumor stem cells.American journal of cancer research · 2026Review
- Targeting proteostasis pathways for cancer therapy.Journal of pharmaceutical analysis · 2025Review
- The Multifaceted Role of VIRMA, a Core Component of the Methyltransferase Complex, in Cancer and Cancer Therapy.Biomolecules · 2025Review
- KIAA1429 in non-small cell lung cancer: bridging m6A epigenetics to therapeutic innovation.Frontiers in surgery · 2025Review
- N6-Methyladenosine Methyltransferase Component KIAA1429 Is a Potential Target of Cancer Therapy.Biomolecules · 2024Review
- The m6 RNA methylation regulator KIAA1429 is associated with autophagy-mediated drug resistance in lung cancer.FASEB bioAdvances · 2024Article
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Authors and funding
3 authors.
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Abstract
N6-methyladenosine (m6A) modification plays a crucial role in cancer progression. However, the role of m6A modification-mediated autophagy underlying non-small cell lung cancer (NSCLC) gefitinib resistance remains unknown. Here, we discovered that m6A methyltransferase KIAA1429 was highly expressed in NSCLC gefitinib-resistant cells (PC9-GR) as well as tissues, and KIAA1429 high expression was associated with poor survival. In addition, silent KIAA1429 repressed gefitinib resistance in NSCLC and reduced tumor growth in vivo. Mechanistically, KIAA1429 stabilized WTAP, a significant player in autophagy, by binding to the 3' untranslated regions (3'-UTR) of WTAP. In a word, our findings indicated that KIAA1429 could elevate NSCLC gefitinib resistance, which may provide a promising targeted therapy for NSCLC patients.
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