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Background <p>m1A, a prevalent RNA modification found in various RNA species, has recently been reported to modulate cancer progression. However, its effects on neuroblastoma remain uninvestigated.</p> Methods <p>The PCAT database was utilized to analyze the mRNA levels and survival probabilities of m1A regulator genes (TRMT6, TRMT61A, ALKBH1, and ALKBH3) in neuroblastoma patients. Silencing and recovery of TRMT6 were employed to investigate its role in neuroblastoma in vitro and in vivo. m1A-seq and RIP-qPCR were performed to identify and confirm the downstream targets of TRMT6. Additionally, Actinomycin D treatment was administered to assess mRNA stability.</p> Results <p>m1A transmethylase TRMT6 expression was significantly elevated in high-risk and late-stage neuroblastoma patients. Functionally, TRMT6 promotes the malignancy of neuroblastoma cells in vitro and promotes tumor growth and metastasis in vivo. Mechanistically, TRMT6 reduces SST mRNA levels by inhibiting its stability in an m1A-YTHDF2-dependent manner, thereby promoting the development of neuroblastoma. Furthermore, SST analog octreotide suppresses neuroblastoma cell malignancy, tumor growth, and metastasis.</p> Conclusions <p>TRMT6 mediates m1A modification of SST to promote neuroblastoma progression, suggesting that targeting TRMT6 may be a novel potential therapeutic approach for treating neuroblastoma.</p>

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m1A methylase TRMT6 promotes neuroblastoma development by demethylating SST mRNA in an m1A/YTHDF2-dependent manner

  • 期刊论文

  • 发表日期：

    2025年9月2日

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  • Xinxin Zhang,
  • Huiran Lin,
  • Huimin Yin,
  • Yufeng Han,
  • Liping Chen,
  • Mengzhen Zhang,
  • Hongxia Chen,
  • Jing He,
  • Zhenjian Zhuo

摘要

Background

m1A, a prevalent RNA modification found in various RNA species, has recently been reported to modulate cancer progression. However, its effects on neuroblastoma remain uninvestigated.

Methods

The PCAT database was utilized to analyze the mRNA levels and survival probabilities of m1A regulator genes (TRMT6, TRMT61A, ALKBH1, and ALKBH3) in neuroblastoma patients. Silencing and recovery of TRMT6 were employed to investigate its role in neuroblastoma in vitro and in vivo. m1A-seq and RIP-qPCR were performed to identify and confirm the downstream targets of TRMT6. Additionally, Actinomycin D treatment was administered to assess mRNA stability.

Results

m1A transmethylase TRMT6 expression was significantly elevated in high-risk and late-stage neuroblastoma patients. Functionally, TRMT6 promotes the malignancy of neuroblastoma cells in vitro and promotes tumor growth and metastasis in vivo. Mechanistically, TRMT6 reduces SST mRNA levels by inhibiting its stability in an m1A-YTHDF2-dependent manner, thereby promoting the development of neuroblastoma. Furthermore, SST analog octreotide suppresses neuroblastoma cell malignancy, tumor growth, and metastasis.

Conclusions

TRMT6 mediates m1A modification of SST to promote neuroblastoma progression, suggesting that targeting TRMT6 may be a novel potential therapeutic approach for treating neuroblastoma.