Aloperine inhibits colorectal cancer cell proliferation and metastasis progress via regulating miR-296-5p/STAT3 axis.

Anti-tumorous effect of Aloperine (ALO) has been previously found. This study examined the role and the underlying mechanism of ALO in colorectal cancer (CRC). CRC cells were processed by different concentrations of ALO, and subsequently the cell proliferation was detected by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and miR-296-5p expression was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Moreover, the target gene of miR-296-5p was predicted by TargetScan and confirmed by dual-luciferase reporter assay. The expressions of signal transducer and activator of transcription 3 (STAT3), apoptosis-related proteins and epithelial-mesenchymal transition (EMT)-related markers were measured by Western blot. Clone formation assay, flow cytometry, wound-healing and Transwell assays were respectively employed to detect cell proliferation, apoptosis, migration and invasion. ALO inhibited CRC cell proliferation in a dose-dependent manner. MiR-296-5p was low-expressed in CRC tissues and cells, and ALO promoted miR-296-5p expression. STAT3 was targeted by miR-296-5p. Up-regulation of miR-296-5p and ALO treatment both suppressed STAT3 expression, inhibited CRC cell proliferation, migration, invasion as well as the expressions of Bcl-2 and N-cadherin, but promoted apoptosis and expressions of Bax and E-cadherin, which were all reversed by overexpressed STAT3. ALO inhibited CRC cell proliferation, metastasis and EMT but promoted apoptosis via regulating miR-296-5p/STAT3 axis.