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.
In this study, we aimed to investigate the effects of combined treatment with Notch1 signaling blocker DAPT and PI3K/Akt signal blocker LY294002 on metastasis of gastric cancer.
PIK3CA mutations were identified in formalin-fixed and paraffin-embedded surgical specimens from 112 patients with EBV-GC with available tumor tissue samples.
Our findings suggested that CSNK2A1 plays important oncogenic roles in GC invasion via EMT and the PI3K-Akt-mTOR signaling pathway and that CSNK2A1 may serve as a novel prognostic and/or therapeutic target in GC.
Moreover, research on molecular mechanisms indicated that both miRNA-32-5p and shKLF2 downregulated the expression of PTEN and activated the PI3K/AKT signaling to promote the development of gastric cancer.
In conclusion, the polymorphisms of the two loci, PIK3R3 rs7536272 and mTOR rs2295080, on the PI3K/AKT/mTOR signaling pathway genes are associated with genetic susceptibility to gastric cancer in Chinese population.
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.
In conclusion, the results of the present study revealed that isoforms S and L of MRPL33, which arise from alternative splicing, exhibited opposing roles in the chemoresponse to epirubicin in gastric cancer via the PI3K/AKT signaling pathway.
Taken together, LINC02465 is an oncogenic lncRNA that facilitates the tumorigenesis and progression of GC via PI3K/AKT pathway, demonstrating a novel effective therapeutic target and prognostic biomarker for GC patients.
LOC101928316 molecular mechanism investigates suggested that LOC101928316 can regulate PI3K-Akt-mTOR signaling pathway and change the GC development progression in vivo and in vitro.
Patients with GC with HP infection were associated with fewer <i>PI3K/AKT</i> pathway genetic mutations and better survival than those without HP infection, especially for EBV-negative and intestinal-type GC.
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.
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.
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.