MiR-216b functions as a tumor suppressor by targeting HMGB1-mediated JAK2/STAT3 signaling way in colorectal cancer.

MiR-216b is implicated in the development of multiple types of cancers, however, a role for miR-216b in colorectal cancer (CRC) remains elusive. The present study aimed to investigate the function and underlying mechanism of miR-216b in human CRC. In this study, we found miR-216b in CRC tissues and cell lines was markedly decreased compared with corresponding adjacent normal tissues (ANTs) and colonic mucosal epithelial cell line (FHC), and was obviously associated with the TNM stage, lymph node metastases, differentiation and poor overall survival (OS) (P<0.05). Furthermore, we demonstrated that miR-216b inhibited cell proliferation, migration, invasion and angiogenesis by targeting HMGB1 which was highly expressed in CRC. Additionally, we proved that miR-216b promoted the development and progression of CRC, at least partially through HMGB1-mediated JAK2/STAT3 pathway. Lastly, we showed that plasma miR-216b expression was reduced in CRC when compared to healthy controls and might be a potential diagnostic biomarker for CRC. The findings indicated that miR-216b might function as a suppressor in CRC and could serve as a promising diagnostic and prognostic biomarker for CRC.