Downregulation of long noncoding RNA SNHG1 inhibits cell proliferation, metastasis, and invasion by suppressing the Notch-1 signaling pathway in pancreatic cancer.

Abstract

Pancreatic cancer (PC) has become the fourth most lethal among human cancers. Long noncoding RNAs (lncRNAs) have been reported to play a role in the progression of a variety of cancers. However, the role of lncRNA SNHG1 in PC is not clear. Real-time Quantitative PCR Detection System (qPCR) was used to detect the expression of SNHG1 in PC cells. Then, the SNHG1 knockdown cell was constructed with si-SNHG1. AsPC-1 and PANC1 cells were used to analyze the ability of cell proliferation, invasion, and migration. MTT assay was used to analyze the proliferation ability. Transwell experiments and wound healing experiments were used to detect the capacity of invasion and migration. Finally, Western blot analysis was used to explore the mechanism of SNHG1 in PC. SNHG1 was significantly upregulated in PC cells. Knockdown of SNHG1 could obviously suppress cell proliferation, invasion, and migration. Furthermore, SNHG1 knockdown inhibited the activation of the Notch-1 signaling pathway and inhibited the expression of N-cadherin, Hes1, Vimentin, Notch-1. The inhabitation was reversed when Notch-1 was overexpressed in si-SNHG1 cells. The lncRNA SNHG1 promotes cell growth and metastasis in PC through activation of the Notch-1 signaling pathway in PC.