LncRNA SNHG12 promotes EMT and metastasis of colorectal cancer via regulating TGF-β/Smad2/3 signaling pathway

Objective: In this study, we aimed to explore the molecular mechanism of SNHG12 promoting colorectal cancer (CRC) progression. Methods: 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-(3 and p-Smad2/3. Additionally, the rescue test of overexpressing TGF-(3 and a nude mouse subcutaneous tumor model were established to validate the pivotal role of SNHG12 in driving the progression of CRC. Results: 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-(3 and p-Smad2/3. Meanwhile, the rescue experiment proved that overexpressed TGF-(3 had the ability to reverse the impact of SNHG12 knockout on cell function and phenotype. In vivo, SNHG12 knockdown significantly reduced tumor growth. Conclusion: SNHG12 promotes EMT and metastasis of CRC by modulating the TGF-(3/Smad2/3 signaling pathway and EMT process, which could function as a prognostic biomarker and a treatment target for CRC.