M6A methylation in thyroid cancer: Functions, mechanisms, and clinical significance

Area of Science:

• Molecular Biology
• Oncology
• Epigenetics

Background:

• Thyroid cancer (TC) is the most common endocrine malignancy, with significant heterogeneity and treatment challenges in advanced cases.
• N6-methyladenosine (m6A) is a key epigenetic regulator of RNA processing, impacting gene expression and cellular functions.
• Dysregulated m6A pathways are implicated in TC, but their complex roles require further elucidation.

Purpose of the Study:

• To review the current understanding of m6A modifications in thyroid cancer pathogenesis.
• To explore m6A's role in cellular behaviors, metabolism, cell death, and therapeutic resistance in TC.
• To examine the interplay between m6A and non-coding RNAs in oncogenic networks and assess m6A's translational potential.

Main Methods:

• Literature review and synthesis of current research on m6A in thyroid cancer.
• Analysis of m6A's involvement in proliferation, migration, metabolic reprogramming, apoptosis, ferroptosis, and treatment resistance.
• Investigation of the m6A-non-coding RNA axis and its impact on oncogenic pathways.

Main Results:

• m6A modifications significantly influence TC initiation and progression by altering cellular functions and promoting stemness.
• m6A regulators are implicated in metabolic reprogramming, programmed cell death (apoptosis and ferroptosis), and resistance to various therapies.
• The m6A-non-coding RNA axis plays a critical role in rewiring oncogenic networks within thyroid cancer.

Conclusions:

• m6A modifications are integral to thyroid tumorigenesis, affecting key biological processes and therapeutic responses.
• m6A regulators represent promising diagnostic and prognostic biomarkers for TC.
• Targeting the epitranscriptome via m6A modulation holds potential for developing novel precision oncology strategies in TC.