LY294002

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.

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.