Ye Yibiao, Li Yanshan, Wei Yunping, Xu Yunxiuxiu, Wang Ruomei, Fu Zhiqiang, Zheng Shangyou, Zhou Quanbo, Zhou Yu, Chen Rufu, Chen Tao
Department of Hepatobiliary Surgery, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong 510120, P.R. China.
Key Laboratory of Malignant Tumor Gene Regulation and Target Therapy of Guangdong Higher Education Institutes, Guangzhou, Guangdong 510120, P.R. China.
Oncol Lett. 2018 Aug;16(2):1937-1942. doi: 10.3892/ol.2018.8870. Epub 2018 Jun 1.
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.
本研究旨在确定HOTTIP的表达和功能如何改变并调节代谢型谷氨酸受体1（mGluR1），从而影响人胰腺癌细胞的活力。与癌旁组织相比，人胰腺癌组织中HOTTIP的表达更高。然而，研究发现HOTTIP表达的下调可显著降低细胞活力，诱导细胞凋亡，促进半胱天冬酶-3和半胱天冬酶-8的活性，并增加胰腺癌细胞中Bax的表达。此外，HOTTIP表达的下调显著抑制了mGluR1，并减轻了胰腺癌细胞中磷酸肌醇3激酶（PI3K）/蛋白激酶B（Akt）/雷帕霉素机制靶点（mTOR）通路的激活。据我们所知，本研究首次确定HOTTIP对人胰腺癌的抗癌作用是通过mGluR1通路发挥的。
