LY294002

This study demonstrated that the combination of Aconiti Lateralis Radix Praeparata and Angelicae Sinensis significantly protected H/R cardiomyocytes in vitro. This protective effect was achieved through enhancing cell viability, reducing oxidative stress-induced injury, and modulating the expression and distribution of key proteins and genes. The underlying mechanisms involved the activation of the PI3K/Akt/GSK-3β signaling pathway and the autophagy pathway, as confirmed by the inhibitory effect of LY294002.

Further experiments revealed that the expression of polarization-related markers in M1-type macrophages was significantly suppressed after treatment with the SUCNR1-neutralizing antibody or the PI3K inhibitor LY294002. These findings suggest that succinate may activate the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway via SUCNR1 to promote the polarization of NEC macrophages toward the M1 phenotype, thereby accelerating NEC progression.

DACT1 promotes the malignant behavior of LSCC cells and suppresses cuproptosis by activating the PI3K/AKT signaling.

To investigate how dexmedetomidine (DEX) controls the proliferation and death of breast cancer cells. DEX also abrogated LY294002-induced down-regulation of MMP, p-PI3K/PI3K, p-AKT/AKT and Bcl-2 and up-regulation of Bax in breast cancer cells. DEX may promote the development of breast cancer cells while preventing cancer cell autophagy and apoptosis in vitro via PI3K/AKT signaling.

This mechanism was substantiated by the findings that the PI3K inhibitor LY294002 mimicked cetrorelix's effects without producing an additive apoptotic response, and that GnRHR knockdown abrogated cetrorelix-induced apoptosis, confirming receptor specificity. These findings suggest that cetrorelix may induce EOC apoptosis via the PI3K/AKT-FOXO1 pathway, which provides mechanistic support for the therapeutic potential of GnRH antagonists in EOC management. Moreover, the identified critical regulatory pathways are prospective therapeutic targets for EOC management.

Additionally, Western blot and experiments employing the PI3K inhibitor LY294002 have demonstrated that TCF7L2 activates the PI3K/AKT signaling pathway, thereby facilitating the proliferation of CRC cells...Spearman correlation analysis confirmed a positive relationship between the expressions of TCF7L2 and HIF-1α, while Kaplan-Meier survival analysis demonstrated that their co-expression was predictive of reduced overall survival. Collectively,these findings position TCF7L2 as a critical downstream effector of HIF-1α in hypoxic CRC, and its mechanistic role in promoting malignancy and correlation with poor prognosis provide a theoretical basis for exploring TCF7L2 as a potential therapeutic target in future studies..

Treatment with the PI3K inhibitor LY294002 produced changes consistent with those observed upon YBX1 silencing. In a subcutaneous xenograft mouse model, YBX1 silencing was associated with reduced tumor growth and ferroptosis-related changes, effects that were partially reversed by EGF treatment. These findings suggest that YBX1 is associated with ferroptosis-related changes and altered proliferation and migration in A549 cells, potentially involving PI3K/AKT/mTOR signaling, highlighting YBX1 as a potential therapeutic target.

The proteasome inhibitor MG132 confirmed that fisetin accelerates β-catenin and MITF degradation. Additionally, inhibition of the PI3K/AKT pathway by LY294002 or the ERK pathway by PD98059 reversed fisetin's reduction of tyrosinase activity and melanin synthesis, further verifying the participation of these pathways. Computational docking integrated with deep learning-based CNN scoring revealed that fisetin interacts with PKCα, β-catenin, tyrosinase, and TYRP1. Collectively, these findings suggest that fisetin exerts multi-targeted inhibitory effects on melanogenesis, highlighting its potential as a therapeutic and cosmetic agent for hyperpigmentation.

Critically, the use of a PI3K inhibitor (LY294002) demonstrated that the nicotine-induced downregulation of p53 and upregulation of MMP-2, as well as the enhancement of cellular invasion are dependent on PI3K/AKT pathway activation. These findings conclusively demonstrate that nicotine promotes the malignant transformation of HPV-16 positive cervical cancer cells by altering the expressions of MMP-2, p53, Caspase-3, and p21 via the activation of the PI3K/AKT pathway. This highlights the therapeutic potential of targeting this pathway in cervical cancer treatment.

Interventions utilizing a range of inhibitors at the in vitro level, including the PDGFR-β inhibitor AG1296, the PI3K inhibitor LY294002, the AKT inhibitor MK2206, and the FAK inhibitor Y15, demonstrated that E. multilocularis protoscoleces protein (EmP) induces angiogenesis through PDGFR/PI3K/AKT/FAK signaling pathway. Our findings provide new perspectives on how E. multilocularis infection triggers pathological angiogenesis in the host liver, and may provide a novel anti-angiogenic therapeutic strategy against E. multilocularis infection.

When these cancer cells were treated with doxorubicin (ADM) and 5-fluorouracil (5-FU), cell survival rate was determined by MTT, apoptosis by TUNEL, and colony formation by colony formation assay. The cancer cells were treated with the PI3K/Akt pathway inhibitor LY294002, and the expression of drug resistance-related proteins MDR1, MRP1, BCRP, Livin, cIAP1, XIAP, Akt, p-Akt, p65, and p-p65 was detected by Western blotting...AFP regulates the expression of drug resistance-related genes by activating the PI3K/Akt/NF-κB signaling pathway. AFP plays a pivotal role in MDR of cancer cells, the mechanism may be involved in activating the PI3K/Akt/NF-κB signaling pathway.

Our study reveals for the first time that TAX restores osteogenic-adipogenic equilibrium in OP-BMSCs and promotes bone regeneration through PI3K/AKT/PPARγ activation and mitochondrial protection-mediated suppression of necroptosis. These results position TAX as a promising therapeutic candidate for osteoporosis.