Exosomes-Derived MiR-302b Suppresses Lung Cancer Cell Proliferation and Migration via TGFβRII Inhibition.

Background/Aims: Several studies have reported that tumor-derived exosomes contain kinds of miRNAs, including oncogenic miRNAs and tumor suppressor miRNAs. It has been reported that miR-302b could inhibit cancer progression by targeting oncogenes post-transcriptionally. Whether miR-302b is involved in the regulation of tumor-derived exosomes on lung cancer cells proliferation has not yet been demonstrated. This study aimed to examine the effect of exosomes-derived miR-302b on lung cancer cells proliferation and explain the potential mechanism. Methods: The effect of exosomes derived from 95C cells and 95D cells with different metastatic ability on lung cancer cell proliferation and migration were analyzed by MTT assay and Transwell assays, respectively. Exosomes of 95C and 95D cells derived miR-302b was quantified by qRT-PCR, the effect of miR-302b on proliferation and migration of 95D cells was analyzed by MTT assays and Transwell assays respectively after transfection with miR-302b, while the expression of phosphorylated ERK1/2, MMP9 and TGFβRⅡ was analyzed by Western blot. The target gene of miRNA-302b was analyzed by Luciferase reporter assays. Results: 95C-derived exosomes significantly decreased the migration ability of 95D cells. miRNA-302b was significantly overexpressed in 95C cells and 95C-derived exosomes compared with 95D cells and 95D-derived exosomes. Transfection of miR-302b into 95D cells significantly suppressed cells proliferation and migration capabilities along with the down-regulated expression of TGFβRII, phosphorylated ERK1/2 and MMP9 induced by TGF-β1. Conclusions: Exosomes-derived miR-302b could suppress lung cancer cell proliferation and migration via the TGFβRII/ERK pathway and thus provides a potential target for human lung cancer therapy.