Astragalus mongholicus and Hedyotis diffusa willd inhibit cell proliferation by attenuating the miR-582-3p-p27 signaling pathway in LUAD.

Previous studies conducted by the same group of researchers found that Traditional Chinese Medicine Astragalus mongholicus Bunge and Hedyotis diffusa Willd (A-H) significantly suppressed the cell proliferation of lung adenocarcinoma (LUAD). MicroRNAs are considered promising candidates for cancer diagnosis and treatment. This study focused on miR-582-3p as the primary subject of investigation to explore the mechanism by which A-H inhibits cell proliferation through miR-582-3p. The overexpressing and silencing miR-582-3p cell models were established by using lentiviral transfection technology. CCK-8 assay (24 h, 48 h, 72 h) and clone formation assay (1 w) were employed to detect the proliferation of A549 cells. Moreover, flow cytometry analysis (24 h) was performed to detect the cell cycle. Western blotting (WB) and a luciferase reporter assay were also used to measure the expression of cell cycle-related proteins and verify the direct interaction between miR-582-3p and p27, respectively. The LV-miR-582-3p inhibitor + shRNA-p27 stable A549 cells were constructed in the same manner to repeat the above-mentioned procedure. The CCK-8 assay was conducted to assess the effects of various concentrations of A-H on the proliferation of A549 cells. A-H-containing serum was prepared to intervene in LV-miR-582-3p and mimic A549 cells. Subsequently, the same procedure was repeated, as described earlier. Results indicated a direct interaction between miR-582-3p and p27. Furthermore, miR-582-3p was found to enhance the proliferation of A549 cells by regulating cell cycle-related proteins, specifically p27. It was also observed that A-H-containing serum inhibited the proliferation of A549 cells through the miR-582-3p-p27 signaling pathway. The study findings revealed the underlying molecular mechanisms of miR-582-3p in the development and prognosis of A549 LUAD cells. In addition, A-H inhibited LUAD proliferation through the miR-582-3p-p27 signaling pathway. These findings may provide a new understanding of the use of Chinese medicine in treating lung cancer.