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Identification of Circular RNAs using RNA Sequencing
Published on: November 14, 2019
Transcriptomic analysis reveals potential novel circRNA in goiters progression
Guanying Nie1, Zixuan Ru2, Wei Zhang1
1Key Lab of Etiology and Epidemiology, National Health Commission & Education Bureau of Heilongjiang Province (23618504), Key Laboratory of Trace Elements and Human Health, Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, China.
Abstract:
Goiter is predominantly caused by iodine deficiency, and mainstream treatments currently fail to restore normal thyroid morphology and irreversibly damage the organ's function. In this study, involvement of circRNA molecules in goiter was investigated. A mouse model of iodine deficiency induced goiter was established and analyzed their transcriptomes via transcriptomic sequencing. Subsequent real-time quantitative PCR, western blot and immunohistochemistry were used to verify the bioinformatics analysis. Transcriptomic sequencing revealed insulin-like growth factor 1 (IGF1) was upregulated in the goiter and enriched in Ras, mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3-kinase (PI3K)-Akt signaling pathways. Bioinformatics analysis identified the involvement of a mmu-circ-0000554/hsa-circ-0030239-miR-363-5p-IGF1 axis and mmu-circ-0000554 and IGF1 expression were shown to be increased in goiter tissues by real-time polymerase chain reaction, an effect that was reversed by iodine-repletion treatment. Mmu-miR-363-5p expression was decreased in goiter but increased on iodine repletion. Hsa-circ-0020309, IGF1 and miR-363-5p expression were associated with goiter and may have diagnostic value for patients. A novel mmu-circ-0000554 /hsa-circ-0030239-miR-363-5p-IGF1 axis may influence goiter progression and may have potential as a biomarker and a treatment target.
Insights
This study reveals a novel circRNA-miR-IGF1 axis involved in goiter development due to iodine deficiency. This pathway, including mmu-circ-0000554 and insulin-like growth factor 1 (IGF1), may offer new diagnostic and therapeutic targets for goiter.
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.
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