RBM10 suppresses colorectal cancer invasion by regulating LncRNA SNHG17 alternative splicing.

To explore the role of RBM10 in colorectal cancer (CRC) and the regulatory mechanism of CRC invasion through alternative splicing (AS) of long non-coding RNA (lncRNA) SNHG17 by RBM10. Samples were collected from sixty cases of CRC and their corresponding adjacent normal tissues. Immunohistochemistry and Western blot were performed to analyze the expression of RBM10. A Transwell invasion assay was conducted to evaluate the effect of RBM10 on the invasion of HCT116 cells, and a Western blot was performed to detect the expression of EMT-related proteins. Moreover, CLIP-seq and RIP experiments were performed to explore the interaction between RBM10 and SNHG17. The expression of RBM10 was significantly decreased in CRC tissues and cells compared to the normal adjacent tissues. Overexpression of RBM10 inhibited CRC invasion, while knockdown of RBM10 had the opposite effect. RBM10 was found to interact with SNHG17 and regulate its splice isoform balance. Specifically, the splice variant SNHG17_2 regulated by RBM10 was upregulated in CRC and was positively correlated with CRC invasion. RBM10 inhibits CRC invasion by regulating the alternative splicing of SNHG17, providing new research directions and potential targets for CRC treatment.