MicroRNA‐203a‐3p may prevent the development of thyroid papillary carcinoma via repressing MAP3K1 and activating autophagy

Background Papillary thyroid carcinoma (PTC) grows slowly but has a great risk of metastasis. MicroRNAs are well known as vital tumor‐related gene regulators. In PTC, the role of miR‐203a‐3p and the underlying mechanisms remain not completely understood. Methods We conducted CCK8 assay, wound healing assay, transwell experiment and flow cytometry analyses to investigate the function of miRNA‐203a‐3p. The interaction of miRNA‐203a‐3p with its gene MAP3K1 was characterized by quantitative real‐time polymerase chain reaction, western blotting and luciferase assay. Results We found that the levels of miRNA‐203a‐3p were statistically decreased in PTC tissues. When mimics were delivered to TPC‐1 and KTC‐1 cells to upregulate miR‐203a‐3p, it was observed that cell proliferation, metastatic abilities and cell cycle process were prevented but cell apoptosis was enhanced. Furthermore, we proved the interaction between MAP3K1 and miR‐203a‐3p. Intriguingly, similar to miR‐203a‐3p mimics, siMAP3K1 showed a tumor‐suppressive effect, and this effect could be reversed when miR‐203a‐3p was simultaneously inhibited. Finally, selected autophagy‐linked proteins such as LC3 Beclin‐1 were detected and found to be increased when miR‐203a‐3p was upregulated or MAP3K1 was inhibited. Conclusion Overall, miR‐203a‐3p inhibits the oncogenic characteristics of TPC‐1 and KTC‐1 cells via suppressing MAP3K1 and activating autophagy. Our findings might enrich the understanding and the therapeutic strategies of PTC. Mi‐RNA‐203a‐3p inhibits cell proliferation, migration, invasion and the process of the cell cycle, and promotes apoptosis through targeting MAP3K1 and activating autophagy in PTC.