In the present study, we found that in patients with gastric cancer in different clinical stages (from stageⅠto stage Ⅳ), both C5aR and p-PI3K/AKT levels were significantly higher in tumoral tissues than in adjacent non-tumoral tissues.
In conclusion, CAF‑derived HGF promotes angiogenesis, VM and mosaic vessel formation via PI3K/AKT and ERK1/2 signaling in gastric cancer and HGF may serve as a potential therapeutic target for cancer anti‑vascular treatment.
To clarify the role of TIPE2 in the progression of human GC and to elucidate the underlying mechanism, the association between TIPE2 and phosphatidylinositol 3‑kinase (PI3K)/AKT, the cell cycle, the caspase‑related apoptosis pathway and the NF‑κB signaling pathway were investigated through western blot and flow cytometric analysis.
Taken together, our findings contribute to current understanding of the functions of FBXO11 and suggest a mechanism by which FBXO11 plays an oncogenic role in the development of GC possibly by inhibiting PTEN and subsequently promoting PI3K/AKT pathway activation.
Furthermore, overexpression of ciRS-7 blocked the miR-7-induced tumor suppression in MGC-803 and HGC-27 cells and led to a more aggressive oncogenic phenotype, via antagonizing miR-7-mediated PTEN/PI3K/AKT pathway. ciRS-7 may act as a prospective prognostic biological marker and a promising therapeutic target for GC..
Correlations between the expression levels of miR-21, PTEN, and p-AKT were analyzed by real-time PCR and Western blot test in HER2-positive GC cell lines.
Deregulation of MicroRNA-375 Inhibits Proliferation and Migration in Gastric Cancer in Association With Autophagy-Mediated AKT/mTOR Signaling Pathways.
MALAT1-miR-183-SIRT1 axis and PI3K/AKT/mTOR pathway may be mechanisms to mediate autophagy in GC. miR-183 may serve as a towardly therapeutic target for GC.
Moreover, we demonstrated that the miR-20a/LRIG1 axis regulated GC cell MDR through epidermal growth factor receptor (EGFR)-mediated PI3K/AKT and MAPK/ERK signaling pathways.
Overexpression of miR-592 promotes GC proliferation, migration, and invasion and induces the EMT via the PI3K/AKT and MAPK/ERK signaling pathways by inhibiting Spry2, suggesting a potential therapeutic target for GC.
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.
AdP promoted apoptosis in CDDP-resistant GC cells by suppressing the PI3K/AKT/ARNT signaling pathway and might be considered a candidate agent for the clinical treatment of cisplatin-resistant GC.
The serine/threonine-protein kinase PFTAIRE 1 (PFTK1) is a member of the cyclin‑dependent kinase family that is highly expressed in several malignant tumors, including hepatocellular carcinoma, esophageal, breast and gastric cancers, and glioma.
Taken together, Rab1A regulates the PI3K-AKT-mTORC1 pathway through the mTORC1 complex consisting of mTORC1, Rheb and Rab1A, and is a promising therapeutic target in GC.
In this review, a basic overview of the role of AKT in normal and malignant tissues is provided, along with an in-depth discussion of its role in gastric cancer and its potential as a target for therapy.
Our results suggest that the potentially functional AKT1rs2494752 SNP may affect GCa susceptibility, likely by modulating the AKT1 promoter transcriptional activity.