Transcriptomic analysis reveals potential novel circRNA in goiters progression.

Area of Science:

• Endocrinology
• Molecular Biology
• Genetics

Background:

• Goiter, often caused by iodine deficiency, presents challenges with current treatments that fail to restore thyroid function.
• The role of circular RNA (circRNA) molecules in goiter pathogenesis remains largely unexplored.

Purpose of the Study:

• To investigate the involvement of circRNA molecules in the development of goiter.
• To identify potential molecular mechanisms and biomarkers associated with iodine deficiency-induced goiter.

Main Methods:

• Establishment of a mouse model for iodine deficiency-induced goiter.
• Transcriptomic sequencing to analyze gene expression profiles.
• Validation using real-time quantitative PCR, western blot, and immunohistochemistry.

Main Results:

• Transcriptomic analysis identified upregulated insulin-like growth factor 1 (IGF1) in goiter, enriched in Ras, MAPK, and PI3K-Akt pathways.
• A novel axis involving mmu-circ-0000554/hsa-circ-0030239-miR-363-5p-IGF1 was identified.
• Expression of mmu-circ-0000554 and IGF1 increased in goiter tissues and reversed with iodine repletion; miR-363-5p showed inverse regulation.

Conclusions:

• A novel circRNA-miR-IGF1 axis (mmu-circ-0000554/hsa-circ-0030239-miR-363-5p-IGF1) may play a significant role in goiter progression.
• The identified molecules, including hsa-circ-0020309, IGF1, and miR-363-5p, show potential as diagnostic biomarkers for goiter patients.
• This axis represents a potential therapeutic target for managing goiter.