CERS6‐AS1 promotes cell proliferation and represses cell apoptosis in pancreatic cancer via miR‐195‐5p/WIPI2 axis

Abstract

Abstract Pancreatic cancer (PC) is a lethal malignancy that threatens human health. Long noncoding RNAs (lncRNAs) act as important mediators in PC development. Our study aimed to investigate the function and mechanism of lncRNA ceramide synthase 6 antisense RNA 1 (CERS6‐AS1) in PC. As shown by RT‐qPCR, CERS6‐AS1 was significantly upregulated in PC cells and tissues. Silencing CERS6‐AS1 suppressed PC cell viability and proliferation while enhancing cell apoptosis according to colony formation assays, EdU assays, and flow cytometry analyses. Mechanistically, CERS6‐AS1 interacted with miR‐195‐5p to elevate the expression level of the WD repeat domain phosphoinositide interacting 2 (WIPI2), which is a downstream target gene of miR‐195‐5p in PC. Moreover, miR‐195‐5p expression was negatively associated with CERS6‐AS1 expression (or WIPI2 expression) in PC tissues. Rescue assays revealed that WIPI2 overexpression rescued the effects of CERS6‐AS1 deficiency on cell viability, proliferation, and apoptosis. In summary, CERS6‐AS1 facilitates PC cell proliferation while inhibiting PC cell apoptosis by upregulating WIPI2 via miR‐195‐5p. This study might provide promising insight into the role of CERS6‐AS1 in PC development.

Keywords

• CERS6‐AS1
• miR‐195‐5p
• pancreatic cancer
• WIPI2