In this study, we aimed to explore the molecular mechanism of SNHG12 promoting colorectal cancer (CRC) progression.

Bioinformatics technology was utilized to identify SNHG12-targeted mRNA and the correlation with the prognosis of CRC patients. Transfected sequence of knockdown SNHG12 in HCT-116 cell line was established. CCK8 assay, colone formation assay, flow cytometry, cell migration and transwell assay were applied to detect the impact of SNHG12 on HCT-116 cells. Besides, qRT-PCR and western blot were employed to evaluate the apoptotic and EMT markers as well as the expression of TGF-β and p-Smad2/3. Additionally, the rescue test of overexpressing TGF-β and a nude mouse subcutaneous tumor model were established to validate the pivotal role of SNHG12 in driving the progression of CRC.

SNHG12 could predict the prognosis of CRC patients, and a target mRNA GOLT1B was obtained from bioinformatics. In vitro results indicated that SNHG12 facilitated the proliferation, migration, and invasion of HCT-116 cells. qRT-PCR and western blot showed SNHG12 was related to the expression of Caspase 3, EMT markers as well as TGF-β and p-Smad2/3. Meanwhile, the rescue experiment proved that overexpressed TGF-β had the ability to reverse the impact of SNHG12 knockout on cell function and phenotype. In vivo, SNHG12 knockdown significantly reduced tumor growth.

SNHG12 promotes EMT and metastasis of CRC by modulating the TGF-β/Smad2/3 signaling pathway and EMT process, which could function as a prognostic biomarker and a treatment target for CRC.