|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
We have investigated the frequency of molecular changes in the PI3K pathway in gastric cancer.
|
23813545 |
2013 |
|
Stomach Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Up-regulation of PIK3CA may promote the metastasis of gastric cancer through aberrant activation of PI3K/Akt signaling.
|
20954287 |
2010 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Ultimately, PI3K p110α represents a novel target for gastric cancer.
|
26543351 |
2015 |
|
Stomach Carcinoma
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
To define the inhibitory and pro-apoptotic effects of the two PI3K inhibitors BEZ235 and BKM120 in three human colon cancer (HT-29, HCT-116 and DLD-1) and three gastric cancer (NCI-n87, AGS and MKN-45), cell lines with different PIK3CA gene mutation status were used.
|
22543857 |
2012 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Thus far, the human epidermal growth factor receptor (HER) pathway, angiogenic pathway, and phosphatidylinositol-3-kinase (PI3K)-Akt-mammalian target of rapamycin pathway have emerged as potential avenues for targeted therapy in AGC patients.
|
22334453 |
2012 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Through in vitro experiments, we proved that m6A suppression (represented by METTL14 knockdown) promoted GC cell proliferation and invasiveness through activating Wnt and PI3K-Akt signaling, while m6A elevation (represented by FTO knockdown) reversed these phenotypical and molecular changes. m6A may also be involved in interferon signaling and immune responses of GC.
|
31243897 |
2019 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
This study revealed that (1) PIK3CA hotspot mutations occurred with low frequency in gastric cancer; (2) PIK3CA hotspot mutations were not directly associated with PI3K pathway activation; and (3) p-AKT (+) may be a biomarker for better outcomes for gastric cancer patients undergoing gastrectomy regardless of the PIK3CA mutation status.
|
28550907 |
2017 |
|
Stomach Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
This study demonstrates, for the first time, that SHIP2 is frequently downregulated in gastric cancer, and reduced SHIP2 expression promotes tumorigenesis and proliferation of gastric cancer via activation of the PI3K/Akt signaling.
|
26201869 |
2016 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
This is the first time this extensive panel of 9 genes within PI3K/AKT/mTOR pathway has been studied in GC to clarify the biological role of this pathway in GC and develop new strategies for this malignancy.
|
27156070 |
2016 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results suggested that the PI3K/Akt inhibitor LY294002 can enhance chemosensitivity of human gastric cancer to VCR.
|
23743572 |
2013 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results suggest that LMO4 promotes GC cell invasion and proliferation mainly through PI3K-Akt-mTOR signaling.
|
31737204 |
2019 |
|
Stomach Carcinoma
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
These results show that H. pylori infection induces AKT/PI3K-mediated phosphorylation of p27 at T157 and T198 to cause cytoplasmic p27 mislocalization in gastric cancer, and that p27 mislocalization is an adverse prognostic feature in gastric cancer.
|
21841827 |
2012 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
These data suggest that EGF-induced activation of MMP7 and MMP13 in GC is through phosphatidylinositol 3-kinase (PI3K) and extracellular-related kinase/mitogen-activated protein kinase (ERK/MAPK) signaling pathway, respectively.
|
25085584 |
2014 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therefore, in the present review, the disorder and function of miRNAs and PTEN/PI3K/Akt signaling in GC are discussed.
|
30628706 |
2019 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
Therefore, how PTEN lipid phosphatase inactivation contributes to the occurrence and development of gastric cancer and the potential role of the Hippo and PI3K/Akt pathways in PTEN lipid phosphatase inactivation mediated gastric tumorigenesis remain to be explored.
|
30134988 |
2018 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The Wnt/β-catenin and PI3K/Akt signaling pathways promote EMT in gastric cancer by epigenetic regulation via H3 lysine 27 acetylation.
|
28671020 |
2017 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The present study was designed to test whether semaphorin 5A mediates the invasion and metastasis of gastric cancer via PI3K/Akt/uPA signaling.
|
23661031 |
2013 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The miR-92b/DAB2IP/PI3K/AKT signalling axis may be a potential therapeutic target to prevent GC progression.
|
31713929 |
2020 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The mechanism analyses further found that SLC25A5-AS1 might act as a competing endogenous RNAs (ceRNA), which was involved in the derepression of PTEN expression, a target gene of miR-19a-3p, and regulate malignant phenotype via PI3K/AKT signalling pathway in GC.
|
30793479 |
2019 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The HER-2 positive SGC-7901 secreted more transforming growth factor beta 1 (TGF-β1) and resultantly activated MMP-9 to enhance s-ICAM-1 secretion and further studies showed that phosphatidylinositol-3 kinase (PI3K)/Akt/NF-κB signaling pathway was involved in GC pathogenesis.
|
25613482 |
2015 |
|
Stomach Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The expression of phosphatidylinositol 3' -kinase (PI3K)/ protein kinase B (AKT) and c-Jun N-terminal kinase (JNK) was down-regulated by GEN (all P < .05) while reversed by HULC overexpression.HULC was up-regulated in GC.
|
30176223 |
2018 |
|
Stomach Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The experimental methods are as follows: (1) The proliferation of HGC-27 cells inhibited by Apatinib and LY294002 was observed by 3-(4,5)-dimethylthiahiazo-(z-y1)-3,5-diphenytetrazoli- umromide (MTT) assay; (2) flow cytometry was adopted to detect the apoptosis of cells after they were treated with drugs and the positive control; (3) different effects of varying concentrations of Apatinib on apoptosis-related genes and proteins, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase) 9, were detected via fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting (WB), and the effects of different concentrations of Apatinib on the protein expressions of PI3K, phosphorylated (p)-PI3K, Akt and p-Akt were detected by Western blotting.
|
31786865 |
2020 |
|
Stomach Carcinoma
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
The effects of miR-34a ectopic expression on the AKT and p-AKT expression of cisplatin-induce gastric cancer cells were determined by Western blot and flow cytometry with the PI3K pathway inhibitor Wortmannin.
|
24068565 |
2014 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The cooperation between RUNX3 and the PI3K/Akt signaling pathway component FoxO3a/FKHRL1 suggests the putative role of RUNX3 in the homoeostasis of gastric cells and in stomach cancer control.
|
16627973 |
2006 |
|
Stomach Carcinoma
|
0.100 |
Biomarker
|
disease |
BEFREE |
The aim of the present study was to investigate the mechanism of microRNA-4295 (miR-4295), which regulates cisplatin (DDP)-induced apoptosis in GC cells through the leucine-rich repeats and immunoglobulin-like domains 1 (LRIG1)-mediated epidermal growth factor receptor (EGFR)/phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway.
|
30320337 |
2018 |