外泌体 miRNA 在介导细胞间通讯以及肿瘤发生和发展中具有重要功能。因此，我们的研究旨在探索外泌体miR-130b-3p/DEP结构域含有1（DEPDC1）/转化生长因子-β（TGF-β）信号通路在非小细胞肺癌（NSCLC）中的调控机制。我们发现NSCLC患者血清中外泌体miR-130b-3p表达降低，具有重要的诊断价值。此外，miR-130b-3p水平升高抑制NSCLC细胞的增殖和迁移，并增强其凋亡。相反，miR-130b-3p 下调会产生相反的效果。 miR-130b-3p作为DEPDC1的上游，直接结合DEPDC1的3'UTR来调控其表达。 DEPDC1水平通过TGF-β信号通路影响NSCLC细胞的增殖、迁移和凋亡。外泌体miR-130b-3p在BEAS-2B细胞中高表达，此外，BEAS-2B细胞将外泌体miR-130b-3p转移至NSCLC细胞。最后，外泌体miR-130b-3p抑制NSCLC细胞的生长和迁移，通过减少DEPDC1表达通过TGF-β信号通路促进其凋亡，并抑制NSCLC细胞中的上皮间质转化（EMT）。总之，外泌体 miR-130b-3p 有潜力成为 NSCLC 的预测生物标志物，从而刺激针对 NSCLC 的诊断和治疗方法的探索。版权所有 © 2024。由 Elsevier B.V 出版。

Exosomal miRNAs have vital functions in mediating intercellular communication as well as tumor occurrence and development. Thus, our research was aimed at exploring the regulatory mechanisms of exosomal miR-130b-3p/DEP domain containing 1 (DEPDC1)/transforming growth factor-β (TGF-β) signaling pathway in non-small cell lung cancer (NSCLC). Here we indicated that exosomal miR-130b-3p expression decreased in the serum of NSCLC patients, and it was of significant diagnostic value. Moreover, elevated miR-130b-3p levels suppressed the proliferation and migration of NSCLC cells, and enhanced their apoptosis. Conversely, miR-130b-3p down-regulation led to an opposite effect. As the upstream of DEPDC1, miR-130b-3p directly bound to 3'UTR in DEPDC1 to regulate its expression. DEPDC1 level affected the proliferation, migration, and apoptosis of NSCLC cells via TGF-β signaling pathway. Exosomal miR-130b-3p was highly expressed in BEAS-2B cells, besides, BEAS-2B cells transferred exosomal miR-130b-3p to NSCLC cells. Finally, exosomal miR-130b-3p suppressed NSCLC cell growth and migration, promoted their apoptosis via TGF-β signaling pathway by decreasing DEPDC1 expression, and suppressed epithelial-mesenchymal transition (EMT) in NSCLC cells. In conclusion, exosomal miR-130b-3p has the potential to be a predictive biomarker for NSCLC, thereby stimulating the exploration of diagnostic and therapeutic approaches targeting NSCLC.Copyright © 2024. Published by Elsevier B.V.