| Literature DB >> 30008887 |
Yibiao Ye1,2, Yanshan Li2,3, Yunping Wei1,2, Yunxiuxiu Xu1,2, Ruomei Wang1,2, Zhiqiang Fu2,4, Shangyou Zheng2,4, Quanbo Zhou2,4, Yu Zhou5, Rufu Chen2,4, Tao Chen1,2.
Abstract
The present study aimed to determine how the expression and function of HOTTIP modifies, and regulates the metabotropic glutamate receptor 1 (mGluR1) to affect human pancreatic cancer cell viability. HOTTIP expression was higher in human pancreatic cancer tissue compared with in para-carcinoma tissue. However, downregulation of HOTTIP expression was revealed to significantly reduce cell viability, induce apoptosis, promote caspase-3 and caspase-8 activities and increase Bax expression in pancreatic cancer cells. Additionally, downregulation of HOTTIP expression significantly suppressed mGluR1 and mitigated activation of the phosphoinositide 3-kinase (PI3K)/Akt/mechanistic target of rapamycin (mTOR) pathway in pancreatic cancer cells. To the best of our knowledge, the present study is the first to identify that the anticancer effect of HOTTIP against human pancreatic cancer functions the mGluR1 pathway.Entities:
Keywords: HOTTIP; metabotropic glutamate receptor 1; pancreatic cancer; phosphoinositide 3-kinase
Year: 2018 PMID： 30008887 PMCID： PMC6036435 DOI： 10.3892/ol.2018.8870
Source DB: PubMed Journal: Oncol Lett ISSN： 1792-1074 Impact factor: 2.967