Circ_0000526 Blocks the Progression of Breast Cancer by Sponging miR-492

Aim: Breast cancer is one of the leading causes of cancer-associated death. This work aimed to explore the expression, function, and mechanism of circ_0000526 on the progression of breast cancer. Materials and Methods: The expressions of circ_0000526, miR-492, and suppressor of cytokine signaling 2 (SOCS2) in breast cancer samples were measured using quantitative real-time polymerase chain reaction. The correlation between pathological indexes of patients and the expression of circ_0000526 was also analyzed. Human breast cancer cell lines MCF-7 and MDA-MB-231 were applied to investigate the associated mechanism. Cell counting kit-8 assays were used to assess the effect of circ_0000526 on proliferation, and together with the wound healing assay, transwell assay was conducted to detect the effects of circ_0000526 on migration and invasion. Furthermore, luciferase reporter assay was used to verify the targeting relationship between miR-492 and circ_0000526. In addition, Western blot was performed to detect the regulatory effects of circ_0000526 on SOCS2. Results: Circ_0000526 expression in breast cancer samples was downregulated, which was correlated with unfavorable pathological indexes. It significantly inhibited the proliferation and metastasis of breast cancer cells, and facilitated apoptosis. The overexpression of circ_0000526 remarkably inhibited the expression of miR-492 by sponging it, and in turn promoted the expression of SOCS2. Conclusions: Circ_0000526 served as a tumor suppressor, which could function as the sponge of miR-492, an oncogenic microRNA, in breast cancer, and enhance the expression of tumor suppressor SOCS2 indirectly.

Automated summary

The study showed that circ_0000526 was downregulated in breast cancer samples and correlated with unfavorable pathological indexes. Circ_0000526 significantly inhibited the proliferation and metastasis of breast cancer cells, and promoted apoptosis. By binding with miR-492, circ_0000526 indirectly enhanced the expression of tumor suppressor SOCS2.