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<p>N6-methyladenosine (m6A), the most abundant internal modification in eukaryotic mRNAs, plays crucial regulatory roles in carcinogenesis through post-transcriptional regulation of mRNA metabolism. Although emerging evidence highlights its significance in tumor biology, the epigenetic mechanism underlying gallbladder carcinoma (GBC) progression remains poorly characterized. In the present study, KIAA1429, a key component of the m6A methyltransferase complex, was significantly upregulated in GBC and correlated with aggressive tumor characteristics and poor patient survival. Functionally, KIAA1429 knockdown substantially impaired cellular proliferation, migration, and invasion in vitro and suppressed xenograft tumor growth in vivo. Conversely, KIAA1429 overexpression promoted malignant phenotypes in GBC. Mechanistically, an integrated analysis of MeRIP-seq and GEO data identified KIF20A as a downstream effector of KIAA1429. Further experiments demonstrated that KIAA1429 upregulates KIF20A expression. Overexpression of KIF20A partially restored the proliferation and invasion abilities of GBC cells curtailed by KIAA1429 knockdown. Taken together, our work uncovers a critical function for KIAA1429 in driving GBC progression and reveals novel mechanistic insights into m6A methylation in gallbladder carcinogenesis.</p>

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KIAA1429 promotes gallbladder cancer progression through m6A-dependent post-transcriptional modification of KIF20A

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月12日

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  • Dongdong Song,
  • Yun Wang,
  • Guizhen Zhang,
  • Zishuo Wang,
  • Yihang Song,
  • Ranran Sun,
  • Liwen Liu

摘要

N6-methyladenosine (m6A), the most abundant internal modification in eukaryotic mRNAs, plays crucial regulatory roles in carcinogenesis through post-transcriptional regulation of mRNA metabolism. Although emerging evidence highlights its significance in tumor biology, the epigenetic mechanism underlying gallbladder carcinoma (GBC) progression remains poorly characterized. In the present study, KIAA1429, a key component of the m6A methyltransferase complex, was significantly upregulated in GBC and correlated with aggressive tumor characteristics and poor patient survival. Functionally, KIAA1429 knockdown substantially impaired cellular proliferation, migration, and invasion in vitro and suppressed xenograft tumor growth in vivo. Conversely, KIAA1429 overexpression promoted malignant phenotypes in GBC. Mechanistically, an integrated analysis of MeRIP-seq and GEO data identified KIF20A as a downstream effector of KIAA1429. Further experiments demonstrated that KIAA1429 upregulates KIF20A expression. Overexpression of KIF20A partially restored the proliferation and invasion abilities of GBC cells curtailed by KIAA1429 knockdown. Taken together, our work uncovers a critical function for KIAA1429 in driving GBC progression and reveals novel mechanistic insights into m6A methylation in gallbladder carcinogenesis.