LY294002

GOLPH3, which is overexpressed in PRAD, may enhance glucose metabolic activity in PRAD cells in association with activation of the PI3K/AKT/mTOR pathway, thereby supporting PRAD cell proliferation. These findings provide basic mechanistic evidence for the role of GOLPH3 in PRAD cell metabolism, but further clinical studies are required to determine its prognostic or therapeutic relevance.

Furthermore, the PI3K/AKT inhibitor LY294002 enhanced the effects of sh-MUC1 on the proliferation, apoptosis, migration, invasion and EMT progress, while the activator SC79 partially restored these effects...To conclude, these findings suggested that MUC1 played an important role in lung cancer progression, potentially through the PI3K/AKT pathway. This positioned MUC1 as a molecule worthy of further investigation for its therapeutic potential.

EIF3B activated PI3K/AKT signaling and EMT, both of which were abolished by miR-124-3p or LY294002. These findings define the miR-124-3p/EIF3B/PI3K-AKT axis as a key regulator of OSCC progression and suggest EIF3B as a potential prognostic biomarker and therapeutic target.

PI3K/AKT/mTOR pathway activity was examined by Western blot, and its function validated using SC79 (AKT activator) and LY294002 (PI3K inhibitor)...By modulating the PI3K/AKT/mTOR signaling axis and the pro-angiogenic microenvironment, ADGRD1 facilitates tumor growth and neovascularization. ADGRD1 may serve as a promising prognostic biomarker and therapeutic target for advanced BLCA.

Functional assays in vitro, along with in vivo experiments utilizing the PI3K inhibitor LY294002, confirm that LY6H promotes HCC cell proliferation through a mechanism involving the PI3K/AKT pathway and autophagy...Immunohistochemical analyses reveal positive correlations among LY6H, ATG3, Beclin1, PI3K, and AKT expression in HCC tissues, and their co-overexpression predicts an adverse prognosis. Collectively, this work uncovers a critical regulatory role of the LY6H-p-PI3K-autophagy axis in HCC progression, elucidates the molecular mechanisms underlying LY6H-mediated oncogenic effects, and identifies NSC243928 as a promising therapeutic candidate for targeting LY6H in HCC.

IL-22 promotes LUAD progression by activating the PI3K/AKT signaling pathway and inducing EMT, while its upregulation is modulated by promoter hypomethylation and miR- 21-5p suppression. The IL-22/PI3K/AKT axis represents a potential therapeutic target for LUAD management.

This study identified oxidative stress-correlated DEGs and prognostic risk model in sevoflurane-treated GBM for computationally predicting potential immunotherapy response and drug sensitivity. Therefore, THBS1 mediated a protective response against sevoflurane-induced cytotoxicity and migration inhibition in GBM via PI3K/AKT activation, highlighting a potential molecular interaction between anesthetic exposure and tumor cell behavior.

HMGA1 significantly promoted the proliferation, migration, and invasion of UM cells from different origins (primary C918, metastatic MUM-2B) by activating the PI3K/Akt pathway and upregulating MMP-9 expression, suggesting its potential as a target for molecular targeted therapy in UM.

Mechanistic analyses included pathway enrichment and WB, with validation via rapamycin in HepG2 cells and LY294002 in Hep3B cells. CENPI may function as an oncogenic regulator in HCC through activation of the PI3K/AKT/mTOR-CDK2 cascade, linking cell cycle progression to EMT-associated invasiveness. These findings provide a preclinical rationale for further evaluating CENPI and its related signaling axis as potential prognostic and therapeutic targets in broader HCC models and clinical cohorts.

Western blot, immunofluorescence (IF), and colony-forming unit assays were conducted to assess MTB survival and the expression of phosphatidylinositol 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/AKT/mTOR) signaling pathway components and autophagy-related proteins after transfection with miR-122 inhibitor or mimic. Furthermore, LY294002 treatment confirmed that exosome-derived miR-122 activates the PI3K/AKT/mTOR pathway, suppresses autophagy, and facilitates MTB infection. PstS1-loaded exosomes upregulate miR-122, activating the PI3K/AKT/mTOR pathway to inhibit autophagy and promote MTB infection.

Adding NTS to NSCLC cells increased both P-ERK and P-AKT, which were inhibited by PD98059 and LY294002, respectively. The growth of NCI-H522 or NCI-H661 cells was stimulated by NTS or neuregulin 1 (NRG1), a HER4 ligand, but inhibited by SR48692 or ibrutinib. The results indicate that NTSR1 regulates HER4 transactivation, thereby increasing the proliferation of lung cancer cells.

Huh7 cells were cultured under normoxic (21% O2) or hypoxic (1% O2) conditions, treated with sorafenib alone or combined with PI3K inhibitor LY294002. Our findings suggest that hypoxia reduces the sensitivity of HCC cells to sorafenib, and that GRB2 contributes to this process through activation of the PI3K/AKT pathway. Targeting GRB2 may represent a potential strategy to enhance sorafenib efficacy in HCC treatment under hypoxic conditions.