β‐Elemene Inhibits Adrenocortical Carcinoma Cell Proliferation and Migration, and Induces Apoptosis by Up‐Regulating miR‐486‐3p/Targeting NPTX1 Axis

ABSTRACT β‐elemene has a variety of anti‐inflammatory, antioxidant, and antitumor effects. Currently, the influence of β‐elemene on adrenocortical carcinoma (ACC) malignant progression and action mechanism remains unclear. This research aims to explore the influence and action mechanism of β‐elemene on ACC progression. The impacts of β‐elemene on ACC cell viability, proliferation, migration, and apoptosis were investigated through CCK‐8 assay, clone formation assay, Transwell experiment, Wound healing assay, and flow cytometry. The miR‐486‐3p expression was analyzed utilizing RT‐qPCR. According to different databases, neuronal pentraxin 1 (NPTX1) is the predicted downstream target gene of miR‐486‐3p. Western blot and RT‐qPCR were utilized to examine NPTX1 expression. Silencing miR‐486‐3p or Overexpression NPTX1 in ACC cells further explored whether β‐elemene affects ACC cells by regulating miR‐486‐3p/NPTX1. Finally, a subcutaneous graft tumor model was constructed to investigate how β‐elemene may impact tumor growth in vivo. β‐elemene decreased the cell viability, hindered cell proliferation and migration capacity, and induced apoptosis of ACC cells. miR‐486‐3p level in ACC cells was notably reduced in comparison to normal cells, but treatment with β‐elemene markedly increased miR‐486‐3p expression. Additionally, ACC cells showed high level of NPTX1, while miR‐486‐3p targeted negative regulation of NPTX1. Overexpression miR‐486‐3p hindered the malignant progression of ACC cells, whereas overexpression NPTX1 reversed the impact of overexpression miR‐486‐3p. Silencing miR‐486‐3p or overexpression NPTX1 both attenuated the suppressive influence of β‐elemene on the malignant behavior of ACC cells. Additionally, tumor growth was suppressed and apoptosis was induced in tumor cells in vivo by β‐elemene. In conclusion, β‐elemene reduces ACC cell viability, hinders proliferation and migration, and induces apoptosis through the miR‐486‐3p/NPTX1 axis.