LY294002

Mechanistically, we not only regulated the PI3K/AKT pathway using inhibitor LY294002 and activator 740Y-P but also specifically knocked down PI3K via small interfering RNA (siRNA) to confirm if SPINK4's function depends on this pathway...In vivo, SPINK4 overexpression activated PI3K/AKT, promoting tumor growth and M2 macrophage infiltration. Collectively, SPINK4 acts as an oncogene to promote macrophage recruitment and M2 polarization via PI3K/AKT, driving CRC malignant progression.

The PI3K inhibitor LY294002 reversed these pro-tumor and immunosuppressive effects. High COQ10B expression is closely associated with ESCC progression and poor prognosis. These malignant biological behaviors and the associated immunosuppressive tumor microenvironment are potentially mediated via the activation of the PI3K/AKT/HIF-1A signaling pathway.

The study identified CHEK1 as a key diagnostic gene for BC through 127 ML algorithms and SMR causal inference. By combining AI-assisted virtual screening and molecular docking, computational candidate compounds targeting CHEK1 were prioritized. These findings represent hypothesis-generating in silico predictions and require experimental validation before any therapeutic conclusions can be drawn.

The PI3K inhibitor LY294002 significantly reduces AP2A1 levels and inhibits MDK-induced malignant behaviors. Targeting MDK-related signaling pathways may offer new strategies for CRC treatment.

Functionally, BPA exposure promoted prostate cancer cell invasion and EMT, which were associated with activation of the PI3K/AKT and MMP signaling pathways, whereas the PI3K inhibitor LY294002 effectively attenuated BPA-induced invasive phenotypes in vitro and reduced tumor progression in vivo. Collectively, these findings provide mechanistic insights into BPA-driven prostate cancer progression and highlight the value of network toxicology-based approaches in environmental toxicology research.

Mechanistic investigations utilized PFKFB3 overexpression, PI3K activator (740 Y-P), and inhibitor (LY294002) intervention experiments...In vivo experiments confirmed that Res treatment markedly diminished tumor size and mass, lowered Ki-67 proliferation marker, enhanced programmed cell death, suppressed PI3K/AKT signaling, decreased glycolytic enzyme levels, and elevated copper-dependent cell death mediators. Res exerts anti-AML effects by inhibiting the PI3K/AKT pathway while coordinately regulating aerobic glycolysis and cuproptosis in AML cells.

The PI3K/AKT agonist 740Y-P and inhibitor LY294002 were employed to determine the contribution of this pathway to EMT regulation in breast cancer cells...In contrast, the agonist 740Y-P restored the decreased migration, invasion, and EMT phenotypes induced by UBD knockdown. Collectively, our data demonstrated that UBD plays a critical role in the malignant progression of breast cancer, highlighting its potential as a novel therapeutic target for breast cancer patients.

Mechanistically, WB analysis indicated that OSM upregulates PD-L1 expression via activation of the PI3K/AKT axis, and the PI3K inhibitor LY294002 abrogated the OSM-driven immunosuppressive and promigratory phenotypes. In vivo imaging, immunofluorescence, and hematoxylin-eosin (HE) staining further confirmed that OSM promotes tumor growth and metastasis, elevates PD-L1 expression, reduces immune infiltration, and suppresses the production of key effector cytokines such as IFN-γ. Collectively, our findings demonstrate that OSM enhances PD-L1 expression through the PI3K/AKT pathway, thereby facilitating immune evasion and metastatic progression in pancreatic cancer, and reveal a potential therapeutic window for immunomodulatory intervention.

NBL1 functions as a tumor suppressor in ESCC. Its downregulation enhances radioresistance and chemoresistance in ESCC by activating the PI3K-AKT signaling pathway through BMP2,4,7. Inhibition of the PI3K-AKT pathway with LY294002 or BYL719 increases the cytotoxic effects of chemotherapy and radiation, offering a novel therapeutic strategy for ESCC patients, particularly those with low NBL1 expression.

Notably, LY294002 (a PI3K inhibitor) and Anisomycin (a JNK activator) partially reversed the anti-apoptotic and anti-inflammatory effects of PTE, respectively. This study provides the first integrated evidence combining network pharmacology and experimental validation that PTE protects against LIRI by modulating the PI3K/AKT and JNK/c-Jun signaling pathways, offering novel pharmacological insights into its translational potential in LIRI.

FGFR2 is lowly expressed in DFU and can exert a protective effect by activating the PI3K/Akt pathway. It is a candidate diagnostic biomarker and potential therapeutic target for DFU.

Mechanistically, APOE overexpression significantly activated the PI3K/AKT signaling pathway, and this effect was effectively reversed by the PI3K inhibitor LY294002. Consistently, APOE overexpression enhanced tumor growth in vivo. These findings indicate that APOE promotes glioma progression through nuclear activity and activation of the PI3K/AKT signaling pathway, highlighting APOE-related signaling as a potential therapeutic target in glioma.