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<p>N6-methyladenosine (m6A), a key internal and reversible RNA modification plays a crucial role in cancer development and progression. Among m6A-modifying enzymes, the m6A erasers (m6A demethylases), fat mass and obesity-associated protein (FTO), and Alkb homolog 5 (ALKBH5) are frequently dysregulated in various cancer types. In this study, we investigated the biological significance of FTO and ALKBH5 in oral squamous cell carcinoma (OSCC) via loss-of-function studies coupled with in vitro pathophysiological assays. Our results demonstrate significantly reduced transcript and protein levels of FTO and ALKBH5 in OSCC cells compared to control normal oesophageal epithelial cells. Furthermore, siRNA-mediated transient knockdown of FTO and ALKBH5 enhanced cell viability, colony formation, migration, and invasion while decreasing apoptosis in OSCC cells. Notably, RT-qPCR analysis revealed upregulated expression of integrin alpha 6 (ITGA6) and apolipoprotein (APOE) mRNAs, two known m6A-regulated transcripts, upon depletion of FTO or ALKBH5. These findings highlight the tumor-suppressive function of FTO and ALKBH5 in OSCC and underscore their potential as prognostic biomarkers and therapeutic targets in this malignancy.</p>

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Tumor-suppressive role of m6A eraser proteins FTO and ALKBH5 in oral squamous cell carcinoma

  • 期刊论文

  • 发表日期：

    2025年6月11日

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  • Jayasree Peroth Jayaprakash,
  • Sridhanya Velayudham Muralidharan,
  • Piyush Khandelia

摘要

N6-methyladenosine (m6A), a key internal and reversible RNA modification plays a crucial role in cancer development and progression. Among m6A-modifying enzymes, the m6A erasers (m6A demethylases), fat mass and obesity-associated protein (FTO), and Alkb homolog 5 (ALKBH5) are frequently dysregulated in various cancer types. In this study, we investigated the biological significance of FTO and ALKBH5 in oral squamous cell carcinoma (OSCC) via loss-of-function studies coupled with in vitro pathophysiological assays. Our results demonstrate significantly reduced transcript and protein levels of FTO and ALKBH5 in OSCC cells compared to control normal oesophageal epithelial cells. Furthermore, siRNA-mediated transient knockdown of FTO and ALKBH5 enhanced cell viability, colony formation, migration, and invasion while decreasing apoptosis in OSCC cells. Notably, RT-qPCR analysis revealed upregulated expression of integrin alpha 6 (ITGA6) and apolipoprotein (APOE) mRNAs, two known m6A-regulated transcripts, upon depletion of FTO or ALKBH5. These findings highlight the tumor-suppressive function of FTO and ALKBH5 in OSCC and underscore their potential as prognostic biomarkers and therapeutic targets in this malignancy.