LY294002

Conversely, LY294002 inhibited the glycolytic enhancement and aggressive phenotypes induced by UCHL5 overexpression (P < 0.01)...UCHL5 activates the PI3K/AKT/mTOR cascade, which enhances the glycolysis of RCC cells and promotes the development of renal cancer. This study provides insights into the molecular mechanisms underlying the oncogenic role of UCHL5 in RCC.

Esketamine, a GRIN2D inhibitor, and LY294002, a PI3K inhibitor, either alone or in combination, could suppress the tumor growth induced by high GRIN2D levels both in vitro and in vivo. This study is the first to identify the involvement of GRIN2D in lung cancer and to clarify the underlying mechanism of its effect; the findings further suggest that ketamine in cancer treatment may extend beyond relieving pain and depression.

The present study investigated the mechanism by which Que regulates ATP‑binding cassette (ABC) transporter expression in MCF‑7 cells using a PTEN overexpression plasmid and the PI3K inhibitor LY294002...The results of the present study demonstrated that Que suppresses cell viability and induces apoptosis in MCF‑7 cells. Moreover, it enhances intracellular drug accumulation and downregulates ABC transporter expression by modulating the PTEN/PI3K/AKT signaling pathway.

Pharmacological inhibition of PI3K via LY294002 reversed MICALL2-induced angiogenesis. Therefore, MICALL2 facilitates CRC angiogenesis through the EGFR/PI3K/AKT/KLF5/VEGFA axis and may serve as a promising target for anti-angiogenic therapy.

Overexpression of IL7R was shown to alleviate CIRI by suppressing apoptosis. These findings indicate IL7R as a novel target for IS treatment.

EA at Foot Shaoyang meridian acupoints can alleviate inflammatory responses and bone loss in postmenopausal osteoporosis rats, and its mechanism may be related to the activation of the PI3K/AKT pathway.

Functional validation used a single OPCML small interfering RNA (siRNA) with a non-targeting siRNA control (siNC) in U87 and U251 cells with Transwell invasion, wound healing, colony formation, CCK-8 proliferation, and Western blotting for p-AKT and p-mTOR, with LY294002 rescue...Loss of OPCML aligns with proliferative programs and a GBM-specific immune pattern. These data nominate OPCML as a prognostic marker and a surface-level modulator that could be leveraged alongside RTK/PI3K axis inhibitors in GBM.

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.