miR‐105‐5p/PTEN Axis Modulates the Immune Response and Epithelial‐Mesenchymal Transition of Colon Cancer via NF‐κB Activation

The underlying regulating mechanisms of miR-105-5p/PTEN in colon cancer (CC) progression are still unknown. MiR-105-5p and PTEN expressions were determined using RT-PCR. PTEN protein levels were examined by western blot. Also, the contents of inflammatory cytokines (IL-1β, TNF-α, and IL-6) were measured via ELISA. An inflammation model was constructed via LPS. NF-κB p65 expression was assessed via immunofluorescence assay. A xenograft tumor model was constructed in BALB/c nude mice. The functions of miR-105-5p were investigated by establishing a xenograft tumor model, H&E staining, TUNEL assay, immunohistochemistry assay, ELISA, RT-PCR, and western blot. In this research, We found that miR-105-5p expressions were upregulated in CC cells. MiR-105-5p depletion notably augmented PTEN expressions and enhanced immune response, while impeded EMT and distinctly declined the levels of p-IκBα and Nuc-NF-κB p65 in LoVo cells. Whereas, these effects were notably counteracted by PTEN depletion. MiR-105-5p upregulation exerted the opposite effects in CaCo2 cells. LPS markedly increased miR-105-5p expressions and suppressed PTEN expressions in LoVo cells. MiR-105-5p depletion offset LPS-triggered promoting effects on EMT and suppressing effects on the immune response. Meanwhile, in vivo assay proved that miR-105-5p depletion markedly impeded tumor growth and EMT, yet facilitated apoptosis and immune response. It also distinctly deactivated the NF-κB pathway. To sum up, these data indicated that miR-105-5p depletion might impede EMT, yet enhance the immune response in CC by elevating PTEN expressions via deactivation of the NF-κB pathway.