Journal
EPIGENETICS
Volume 18, Issue 1, Pages -Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15592294.2023.2210339
Keywords
Thyroid carcinoma (TC); circ_0003747; MiR-338-3p; PLCD3
Ask authors/readers for more resources
The study investigated the role of circRNAs in the development of thyroid carcinoma (TC). It was found that circ_0003747 was highly expressed in TC cells and its knockdown inhibited TC cell viability, proliferation, migration, and invasion while promoting apoptosis. Circ_0003747 negatively regulated miR-338-3p expression, which in turn interacted with PLCD3 to suppress its expression. Overexpression of miR-338-3p inhibited TC cell progression, and PLCD3 reversed these effects.
The circular RNAs (circRNAs) involved in competitive endogenous RNA (ceRNA) mechanism are critical modulators affecting pathogenesis of thyroid carcinoma (TC). The study's goal was to investigate the effects of circ 0003747 on the biological progression of papillary thyroid cancer (PTC). Normal thyroid cells Nthy-ori3-1 and TC derived cell lines were used in our study. Sanger sequencing and RNase R treatment were utilized for validating the circular structure of circ_0003747. In our work, circ_0003747 was found to be highly expressed in TC cells. Circ_0003747 knockdown reduced TC cell viability, proliferation, migration, and invasion while increasing cell apoptosis. Circ_0003747 targeted and negatively regulated miR-338-3p expression. Besides, miR-338-3p interacted with PLCD3 to repress its expression. Overexpression of miR-338-3p inhibited TC cell progression, and PLCD3 reversed these effects. Furthermore, PLCD3 overexpression reversed the effects of circ_0003747 knockdown on TC cells. Additionally, the knockdown of circ_0003747 remarkably suppressed tumour size and growth, restrained PLCD3 expression and promoted miR-338-3p expression in nude mice. In conclusion, circ_0003747 facilitated the biological progression of TC by modulating the miR-338-3p/PLCD3 axis, and it may be a new target for TC treatment.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available