Abstract
Background Breast cancer (BC) progression is related to the disorder of circular RNAs (circRNAs). This study aims to characterize the role of circ_0075943 in BC. Methods Real-time fluorescent quantitative PCR (real-time PCR) technology was implemented to investigate circ_0075943, AK2 mRNA, and microRNA-141-3p levels. MTT, colony formation method, Transwell, and flow cytometry technique were adopted to investigate cell function. The connection between miR-141-3p and circ_0075943 or AK2 was confirmed by the dual-luciferase reporter gene or RNA immunoprecipitation (RIP). The influence on circ_0075943 in vivo was confirmed by animal experiments. Results circ_0075943 was augmented in BC cell lines and tumor specimens. Dwindling of circ_0075943 could dramatically suppress the phenotype of BC cells and induce apoptosis. MiR-141-3p is a target of circ_0075943, and its repression largely reverses the influence of knocking down circ_0075943 on cell behavior. Moreover, AK2, as a target of miR-141-3p, is augmented in BC cells and specimens. AK2 overexpression could restore the phenotype of BC cells blocked by miR-141-3p redevelopment. Moreover, knocking down circ_0075943 could suppress the growth of tumors in vivo. Conclusion The abnormal regulation of circ_0075943 participates in part of the expansion of BC by dominating the miR-141-3p/AK2 regulatory network.
Highlights
Breast cancer is the second incidence of malignant tumors in the world, and the incidence and mortality of breast cancer are consistently ranked first in terms of female-related malignancies [1, 2]
It is hoped that through the construction of circTADA2As/miR-203a-3p/SOCS3 network targeted therapy for breast cancer is a good prognostic molecular marker for triple-negative breast cancer [14]; other studies have shown that circular RNA plays an important role in breast cancer resistance; for example, hsa_circ_0025202 in HR-positive breast cancer has an anticancer effect, which can be achieved through the miR-182-5p/FOXO3a axis and can be used as a new marker for tamoxifen resistance [15]
Figure 5: circ_0075943 dominates AK2 level by targeting miR-141-3p. (a) e binding site of AK2 3′UTR and miR-141-3p is provided by TargetScan. (b, c) e interaction between AK2 and miR-141-3p was affirmed by the dual-luciferase reporter gene. (d) AK2 level in the normal specimen and Breast cancer (BC) tumor specimen from the GEPIA database. (e, f ) Detect AK2 level in our tissue samples by real-time PCR and immunoblotting technique. (g) e immunoblotting technique was adopted to check AK2 protein level in MCF-10A, BC cells. (h) e immunoblotting technique was adopted to check the influence on miR-141-3p redevelopment on AK2 level protein. (i) Immunoblotting technique checked AK2 protein in BC cells. ∗∗∗P < 0.001
Summary
Breast cancer (BC) progression is related to the disorder of circular RNAs (circRNAs). is study aims to characterize the role of circ_0075943 in BC. MTT, colony formation method, Transwell, and flow cytometry technique were adopted to investigate cell function. E connection between miR-141-3p and circ_0075943 or AK2 was confirmed by the dual-luciferase reporter gene or RNA immunoprecipitation (RIP). E influence on circ_0075943 in vivo was confirmed by animal experiments. Circ_0075943 was augmented in BC cell lines and tumor specimens. Dwindling of circ_0075943 could dramatically suppress the phenotype of BC cells and induce apoptosis. MiR-141-3p is a target of circ_0075943, and its repression largely reverses the influence of knocking down circ_0075943 on cell behavior. AK2, as a target of miR-141-3p, is augmented in BC cells and specimens. AK2 overexpression could restore the phenotype of BC cells blocked by miR-141-3p redevelopment. Knocking down circ_0075943 could suppress the growth of tumors in vivo. E abnormal regulation of circ_0075943 participates in part of the expansion of BC by dominating the miR-141-3p/AK2 regulatory network
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