| Affiliation: | 1. Department of Pancreatic Biliary Surgery, Xiangya Hospital, Central South University, Changsha, China Department of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Guilin Medical College, Guilin, Guangxi, China;2. Department of Pancreatic Biliary Surgery, Xiangya Hospital, Central South University, Changsha, China;3. Department of Pathology, The Affiliated Hospital of Guilin Medical College, Guilin, Guangxi, China;4. Department of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Guilin Medical College, Guilin, Guangxi, China |
| Abstract: | Pancreatic cancer (PC) has a high mortality rate in all cancers worldwide. According to recent studies, long noncoding RNA-CASC2 is involved in the development and progression of many malignant tumors; in the present study, we demonstrated that lncRNA-CASC2 was specifically downregulated in PC tissues and cell lines, and a lower CASC2 expression in PC was related with a poorer prognosis. CASC2 suppressed PC cell proliferation. Hepatocyte nuclear factor 1 alpha (HNF1A) is a transcription factor known to regulate pancreatic differentiation and maintain the homeostasis of the endocrine pancreas. Recently, HNF1A is considered to be a possible tumor suppressor in PC. In the present study, we observed that HNF1A positively regulated CASC2 expression. Through luciferase assays, we demonstrated that CASC2 gene possessed an HNF1A-responsive element (CASC2-HNF1A RE); HNF1A could promote CASC2 expression through direct binding to CASC2-HNF1A RE. Further, PTEN/Akt signaling was involved in HNF1A regulation of CASC2. Finally, we evaluated the expression level of HNF1A in PC tissues; lower HNF1A expression was correlated with shorter overall survival in patients with PC. Taken together, these findings will shed light on the role and mechanism of HNF1A/CASC2 in regulating PC cells proliferation through PTEN/Akt signaling. CASC2 may serve as a potential therapeutic target in PC in the future. |
