IGF2BP3 Regulates TMA7-mediated Autophagy and Cisplatin Resistance in Laryngeal Cancer via m6A RNA Methylation

Like Yang1, Bingrui Yan1, Lingmei Qu2

  • 1Department of Otorhinolaryngology, Head and Neck Surgery, The Second Affiliated Hospital, Harbin Medical University, Harbin 150086, China.

Insights

Translation machinery associated 7 homolog (TMA7) promotes laryngeal squamous cell carcinoma (LSCC) progression. Its stability is enhanced by IGF2BP3, inhibiting autophagy via the TMA7-UBA2-PI3K pathway, leading to poor prognosis and cisplatin resistance.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • Translation machinery associated 7 homolog (TMA7) is linked to proliferation diseases.
  • The specific role and regulation of TMA7 in laryngeal squamous cell carcinoma (LSCC) are not well understood.

Purpose of the Study:

  • To investigate the impact of TMA7 on LSCC development and progression.
  • To elucidate the underlying regulatory mechanisms of TMA7 in LSCC.

Main Methods:

  • Assessed TMA7 expression in LSCC tissues.
  • Downregulated TMA7 to observe effects on cell proliferation, migration, and invasion.
  • Investigated the interaction between TMA7, IGF2BP3, UBA2, and the PI3K pathway.
  • Analyzed the role of m6A modification in TMA7 regulation.

Main Results:

  • TMA7 is upregulated in LSCC and correlates with poor prognosis.
  • TMA7 downregulation inhibited LSCC cell proliferation, migration, and invasion while increasing autophagy.
  • IGF2BP3 stabilized TMA7, reduced autophagy, and promoted LSCC progression via the TMA7-UBA2-PI3K pathway.
  • TMA7 promotes cisplatin resistance in LSCC.

Conclusions:

  • TMA7 promotes LSCC progression and cisplatin resistance.
  • The IGF2BP3-TMA7-UBA2-PI3K pathway is crucial for TMA7's oncogenic function by inhibiting autophagy.
  • TMA7 is a potential biomarker and therapeutic target for LSCC.

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