miR-29b Derived from Bone Marrow Stromal Cell (BMSC) Exosomes Improves Laryngeal Carcinoma by Inhibiting Forkhead Box Protein P1 (FOXP1) to Decrease Cyclin E2 Transcription

This study intends to investigate whether miR-29b derived from BMSC exosomes (BMSC-exos) affects laryngeal cancer progression. RT-qPCR detected miR-29b level in BMSCs and BMSC-exos. After miR-29b was overexpressed in BMSCs, exos were extracted from BMSCs and used to treat laryngeal cancer cells, followed by CCK-8 assay and soft agar assay. When cells were treated with FOXP1 inhibitor or cyclin E2 vector, Western blot analyzed the expression of related proteins and flow cytometry assessed cell cycle distribution. In vivo experiment was conducted to assess miR-29b's effect on tumor growth. miR-29b was upregulated in BMSC-exos, but lowly expressed in cancer cells. miR-29b upregulation inhibited the proliferation of laryngeal cancer cells and delayed tumor progression in vivo by inducing cell cycle arrest. Importantly, miR-29b bound 3'UTR of FXOP1 to inhibit its expression, and further reduced cyclin E2 level. sh-FXOP1 or cyclin E2 vector can restore the cell cycle and proliferation caused by miR-29b. In conclusion, miR-29b enriched in BMSC-exo can down-regulate cyclin E2 expression through targeted inhibition of FXOP1, thereby inhibiting the progression of laryngeal cancer.