Circ_0001658 regulates PI3K/AKT signaling via the miR-671-5p/ITGA2 axis and affects the progress of papillary thyroid carcinoma

Circ_0001658 通过 miR-671-5p/ITGA2 轴调控 PI3K/AKT 信号传导并影响甲状腺乳头状癌的进展

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作者:Xiaoyu Liu, Congren Wang, Zijian Su, Shaoyang Cai, Qunxiong Pan, Xiangjin Chen

Background

Circular RNAs (circRNAs) are a newly described class of non-coding RNAs that play essential roles in regulating gene expression. However, to date, few studies have examined the roles of circRNAs in papillary thyroid carcinoma (PTC). In this study, we analyzed the expression of circ_0001658 in PTC as well as its functions and associated mechanisms of action in PTC cells.

Conclusions

Our findings provide a theoretical basis for further molecular biological studies on the treatment of PTC.

Methods

Real-time quantitative polymerase chain reaction was used to determine the expression of circ_0001658, miR-671-5p, and integrin subunit alpha 2 (ITGA2), and western blotting was performed to determine the levels of ITGA2 and phosphatidylinositide 3-kinase/protein kinase B pathway-related proteins in PTC cell lines. Cell Counting Kit-8 and Transwell analyses were conducted to examine the effects of circ_0001658 on PTC cell function following the knockdown of circ_0001658 expression. In addition, the targeting of circ_0001658 and ITGA2 by miR-671-5p was verified using dual-luciferase reporter assays.

Results

We demonstrated that circ_0001658 and ITGA2 were significantly up-regulated in PTC tissues and cell lines. Knockdown of circ_0001658 inhibited the growth and metastatic potential of PTC cells. MiR-671-5p targeted both circ_0001658 and ITGA2. Mechanistically, circ_0001658 promoted PTC progression by sponging miR-671-5p, up-regulating ITGA2 expression, and activating the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway. In summary, circ_0001658 is a carcinogenesis-associated circRNA that regulates PI3K/AKT signaling via the miR-671-5p/ITGA2 axis and plays a role in promoting the progression of PTC. Conclusions: Our findings provide a theoretical basis for further molecular biological studies on the treatment of PTC.

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