据观察，β-榄香烯主要通过多种途径对多种肿瘤发挥抑制作用，例如抑制癌细胞增殖和诱导细胞凋亡。本研究旨在阐明β-榄香烯在非小细胞肺癌（NSCLC）治疗干预中的作用和潜在机制。体外和体内实验模型均证实了 β-榄香烯对 NSCLC 的抑制效力。我们的研究结果表明，β-榄香烯通过抑制 CBX8 促进 miR-127-3p 的成熟。作为 MAPK4 的上游调节因子，miR-127-3p 通过靶向 MAPK4 使 Akt/mTOR/p70S6K 通路失活，从而诱导 NSCLC 中的自噬。此外，β-榄香烯通过 SYNCRIP 增强 miR-127-3p 的包装到外泌体中。外泌体 miR-127-3p 通过抑制 ZC3H4 进一步刺激巨噬细胞的 M1 极化。总而言之，对 β-榄香烯在 NSCLC 中诱导自噬并促进巨噬细胞 M1 极化的机制的详细了解，提供了令人信服的科学证据，支持其在 NSCLC 治疗中的潜在用途。© 2024 作者。

β-elemene has been observed to exert inhibitory effects on a multitude of tumors, primarily through multiple pathways such as the inhibition of cancer cell proliferation and the induction of apoptosis. The present study is designed to elucidate the role and underlying mechanisms of β-elemene in the therapeutic intervention of non-small cell lung cancer (NSCLC). Both in vitro and in vivo experimental models corroborate the inhibitory potency of β-elemene on NSCLCs. Our findings indicate that β-elemene facilitates the maturation of miR-127-3p by inhibiting CBX8. Functioning as an upstream regulator of MAPK4, miR-127-3p deactivates the Akt/mTOR/p70S6K pathway by targeting MAPK4, thereby inducing autophagy in NSCLCs. Additionally, β-elemene augments the packaging of miR-127-3p into exosomes via SYNCRIP. Exosomal miR-127-3p further stimulates M1 polarization of macrophages by suppressing ZC3H4. Taken together, the detailed understanding of the mechanisms through which β-elemene induces autophagy in NSCLCs and facilitates M1 polarization of macrophages provides compelling scientific evidence supporting its potential utility in NSCLC treatment.© 2024 The Authors.