Inactivation of the Phosphatidylinositol 3-Kinase/Akt Pathway is Involved in BMP9-mediated Tumor-suppressive Effects in Gastric Cancer Cells

2015 ◽  
Vol 116 (6) ◽  
pp. 1080-1089 ◽  
Author(s):  
Liang Duan ◽  
Liwei Ye ◽  
Rui Wu ◽  
Haiyan Wang ◽  
Xueru Li ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Akt Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Gastric Cancer Cells ◽  
Phosphatidylinositol 3

scholarly journals Down-regulation of HIF-1α inhibits the proliferation, migration, and invasion of gastric cancer by inhibiting PI3K/AKT pathway and VEGF expression

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Jingjing Zhang ◽  
Jun Xu ◽  
Yonghong Dong ◽  
Bo Huang
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Patients ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Vegf Expression ◽  
Gastric Cancer Cells ◽  
Tumor Tissues ◽  
Sirna Silencing ◽  
Gastric Cancer Patients

In view of the high incidence of gastric cancer and the functions of hypoxia-inducible factor 1α (HIF-1α), our study aimed to investigate the functionality of HIF-1α in gastric cancer, and to explore the diagnostic and prognostic values of HIF-1α for this disease. Expression of HIF-1α in tumor tissues and adjacent healthy tissues as well as serum collected from both gastric cancer patients and normal healthy controls was detected by qRT-PCR. Survival analysis was performed using Kaplan–Meier method. HIF-1α siRNA silencing cell lines were established. Effects of HIF-1α siRNA silencing as well as PI3K activator sc3036 on proliferation, migration, and invasion of gastric cancer cells were detected by Cell counting kit (CCK-8) assay, and Transwell migration and invasion assay. Effects of HIF-1α siRNA silencing on AKT and VEGF were detected by Western blot. Expression of HIF-1α was significantly down-regulated in tumor tissues than in adjacent healthy tissues in most gastric cancer patients. Serum levels of HIF-1α were also higher in gastric cancer patients than in normal healthy people. Serum HIF-1α showed promising diagnostic and prognostic values for gastric cancer. HIF-1α siRNA silencing inhibited the proliferation, migration, and invasion of gastric cancer cells, while PI3K activator sc3036 treatment reduced those inhibitory effects. Down-regulation of HIF-1α can inhibit the proliferation, migration, and invasion of gastric cancer possibly by inhibiting PI3K/AKT pathway and VEGF expression.

scholarly journals 2-Methoxyestradiol attenuates phosphatidylinositol 3-kinase/Akt pathway-mediated metastasis of gastric cancer

2007 ◽  
Vol 121 (11) ◽  
pp. 2547-2555 ◽  
Author(s):  
Heng-Liang Lin ◽  
Muh-Hwa Yang ◽  
Chew-Wun Wu ◽  
Po-Min Chen ◽  
Yi-Ping Yang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Akt Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

scholarly journals miR-106a confers cisplatin resistance by regulating PTEN/Akt pathway in gastric cancer cells

2013 ◽  
Vol 45 (11) ◽  
pp. 963-972 ◽  
Author(s):  
Y. Fang ◽  
H. Shen ◽  
H. Li ◽  
Y. Cao ◽  
R. Qin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cisplatin Resistance ◽  
Akt Pathway ◽  
Gastric Cancer Cells

scholarly journals miR193b Promotes Apoptosis of Gastric Cancer Cells via Directly Mediating the Akt Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Ruyue Tian ◽  
Hailun Jiang ◽  
Linlin Shao ◽  
Yang Yu ◽  
Qingdong Guo ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Critical Role ◽  
Pik3ca Mutation ◽  
Akt Pathway ◽  
Human Gastric Cancer ◽  
Tumor Type ◽  
Gastric Cancer Cells ◽  
Induced Apoptosis

Gastric cancer (GC) is one of the most common and fatal malignancies worldwide. MicroRNAs (miRNAs) play a critical role in tumor initiation, proliferation, and metastasis of gastric cancer. miR193b has been identified as a tumor suppressor in a variety of tumor types; however, its role in gastric cancer is yet to be determined. Here, we found a significant downregulation of miR193b expression in both human gastric cancer tissues (p<0.05) and human gastric cancer cell lines (p<0.01). Furthermore, the expression level of miR193b correlated with the tumor type, tumor size, and clinical stage (p<0.05). In vitro, miR193b overexpression inhibited cell survival and induced apoptosis in GC cell lines, indicating that miR193b plays a role in the development of gastric cancer. KRAS was verified as the target of miR193b, and KRAS overexpression attenuated miR193b-induced apoptosis (p<0.05). Moreover, we found that the Akt pathway negatively regulated miR193b, also affecting apoptosis. Further analyses indicated that PIK3CA mutation and KRAS amplification are two mutually exclusive pathways (p<0.01), and we hypothesize that both two pathways could result in the carcinogenic overactivation of KRAS. Thus, our results suggest that the Akt-miR193b-KRAS axis may act as a mechanism affecting apoptosis in gastric cancer cells.

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