- |||||||||| sirolimus / Generic mfg.
Journal: Neuroligin 3 Regulates Dendritic Outgrowth by Modulating Akt/mTOR Signaling. (Pubmed Central) - Dec 22, 2019 In conclusion, our results suggest that NL3 regulates neuronal morphology, especially dendritic outgrowth, by modulating the PTEN/Akt/mTOR signaling pathway, probably via MAGI-2. Thereby, this study provides a new link between NL3 and neuronal morphology.
- |||||||||| Journal: Leukemia cells remodel marrow adipocytes via TRPV4-dependent lipolysis. (Pubmed Central) - Dec 22, 2019
In addition, an AML mouse model exhibited smaller BM adipocytes, whereas the TRPV4 activator 4α-phorbol 12,13-didecanoate (4αPDD) partly rescued this process and increased survival. In conclusion, TRPV4 plays a critical role in BM adipocyte remodeling induced by leukemia cells, suggesting that targeting TRPV4 may constitute a novel strategy for AML therapy.
- |||||||||| Xalkori (crizotinib) / Pfizer
Journal: Crizotinib and PARP inhibitors act synergistically by triggering apoptosis in high-grade serous ovarian cancer. (Pubmed Central) - Dec 22, 2019 The FDA has approved the PARP inhibitor olaparib (Lynparza™) as maintenance treatment after first-line platinum-containing chemotherapy and olaparib, niraparib (Zejula™) and rucaparib (Rubraca™) are approved as maintenance therapies in the recurrent, platinum-sensitive setting; nevertheless, development of resistance limits their efficacy...Carboplatin, olaparib, niraparib, the PI3K inhibitor LY294002 and the c-Met inhibitor crizotinib were used for this investigation...Crizotinib together with either of the PARP inhibitors was more strongly synergistic than combinations with a PARP inhibitor and carboplatin or the PI3K inhibitor. Sequential combination of crizotinib and a PARP inhibitor resulted in activation of ATM/CHK2 and inhibition of c-Met pathways, contributing to a decrease in RAD51 levels and induction of caspase-3 dependent apoptotic cell death and suggesting that the combination of crizotinib with a PARP inhibitor may be considered and further explored as a new therapeutic strategy in HGSOC.
- |||||||||| Journal: The cyclohexene derivative MC-3129 exhibits antileukemic activity via RhoA/ROCK1/PTEN/PI3K/Akt pathway-mediated mitochondrial translocation of cofilin. (Pubmed Central) - Dec 21, 2019
Collectively, these findings suggest a hierarchical model, in which the induction of apoptosis by MC-3129 primarily results from the activation of RhoA/ROCK1/PTEN and inactivation of PI3K/Akt, leading to the dephosphorylation and mitochondrial translocation of cofilin, and culminating in cytochrome c release, caspase activation, and apoptosis. Our study reveals a novel role for RhoA/ROCK1/PTEN/PI3K/Akt signaling in the regulation of mitochondrial translocation of cofilin and apoptosis and suggests MC-3129 as a potential drug for the treatment of human leukemia.
- |||||||||| cytarabine / Generic mfg.
Preclinical, Journal: SAMHD1 modulates in vitro proliferation of acute myeloid leukemia-derived THP-1 cells through the PI3K-Akt-p27 axis. (Pubmed Central) - Dec 21, 2019 Sterile alpha motif and HD domain-containing protein 1 (SAMHD1) is a mammalian dNTP hydrolase that acts as a negative regulator in the efficacy of cytarabine treatment against acute myeloid leukemia (AML)...This effect correlated with significantly increased expression of tumor necrosis factor α (TNF-α) in tumors, which may suggest that TNF-α-mediated inflammation could account for the decreased tumorigenicity in vivo. Our findings implicate that SAMHD1 can regulate AML cell proliferation via modulation of the PI3K-Akt-p27 signaling axis, and that SAMHD1 may affect tumorigenicity by downregulating inflammation.
- |||||||||| Journal: Satb1 promotes Schwann cell viability and migration via activation of PI3K/AKT pathway. (Pubmed Central) - Dec 21, 2019
Our findings implicate that SAMHD1 can regulate AML cell proliferation via modulation of the PI3K-Akt-p27 signaling axis, and that SAMHD1 may affect tumorigenicity by downregulating inflammation. Our study demonstrated that the Satb1 knock-out could inhibit the activation of PI3K/AKT pathway by up-regulating SHIP1, thus inhibiting cell viability and migration, and promoting Schwann cell apoptosis.
- |||||||||| Journal, IO Biomarker: Study of EGCG induced apoptosis in lung cancer cells by inhibiting PI3K/Akt signaling pathway. (Pubmed Central) - Dec 21, 2019
Our study demonstrated that the Satb1 knock-out could inhibit the activation of PI3K/AKT pathway by up-regulating SHIP1, thus inhibiting cell viability and migration, and promoting Schwann cell apoptosis. EGCG can inhibit the proliferation and induce apoptosis of H1299 lung cancer cells, and the effect is related to the inhibition of the activation of PI3K/Akt signaling pathway.
- |||||||||| quercetin (LY294002) / Eli Lilly
Preclinical, Journal: Gastrin-releasing peptide receptor gene silencing inhibits the development of the epithelial-mesenchymal transition and formation of a calcium oxalate crystal in renal tubular epithelial cells in mice with kidney stones via the PI3K/Akt signaling pathway. (Pubmed Central) - Dec 21, 2019 After treatment of shGRPR-1 and shGRPR-1 + LY294002, levels of urinary oxalate and urinary calcium in the serum, as well as positive rate of GRPR, became relatively low, levels of E-cadherin enhanced, whereas levels of Akt, PI3K, GRPR, extents of PI3K and Akt phosphorylation, α-SMA, Vimentin and FSP-1, OPN, MCP-1, and CD44 decreased and a number of crystals reduced. Taken together, we conclude that GRPR gene silencing suppresses the development of the EMT and formation of the calcium oxalate crystal in renal TECs of kidney stones through the inactivation of the PI3K/Akt signaling pathway.
- |||||||||| Preclinical, Journal: Aloe-emodin ameliorates renal fibrosis via inhibiting PI3K/Akt/mTOR signaling pathway in vivo and in vitro. (Pubmed Central) - Dec 21, 2019
Furthermore, both wortmannin, an inhibitor for PI3K, and short hairpin RNAs for PI3K knockdown, abrogated TGF-β1-induced phosphorylation of Akt and mTOR, and decreased the suppression of fibrosis. These findings indicated that AE alleviated fibrosis by inhibiting PI3K/Akt/mTOR pathway in vivo and in vitro, which may provide a potential therapeutic option for CKD.
- |||||||||| Journal: PI3Kβ - a versatile transducer for GPCR, RTK and small GTPase signaling. (Pubmed Central) - Dec 21, 2019
The unusually complex regulation of PI3Kβ by small and trimeric G-proteins and RTKs leads to a rich landscape of signaling responses at the cellular and organismic level. This review will focus first on the regulation of PI3Kβ activity in vitro and in cells, and will summarize the biology of PI3Kβ signaling in distinct tissues and in human disease.
- |||||||||| Journal: A Single Discrete Rab5 Binding Site in PI3Kβ is Required for Tumor Cell Invasion. (Pubmed Central) - Dec 21, 2019
Whereas soluble Rab5 did not affect PI3Kβ activity in vitro, the interaction of these two proteins was critical for chemotaxis, invasion, and gelatin degradation by breast cancer cells. Our results define a single, discrete Rab5-binding site in the p110β helical domain and may be useful for generating inhibitors to better define the physiological role of Rab5-PI3Kβ coupling in vivo.
- |||||||||| Journal: Small molecule SOS1 agonists modulate MAPK and PI3K signaling via independent cellular responses. (Pubmed Central) - Dec 20, 2019
In addition, we used CRISPR/Cas9 gene-editing to generate clonally derived SOS1 knockout cells and identified a potent SOS1 agonist that rapidly elicited on target molecular effects at substantially lower concentrations than those causing off target effects. Our findings will allow us to further define the on-target utility of SOS1 agonists.
- |||||||||| omipalisib (GSK2126458) / GSK, BGT226 / Novartis, dactolisib (RTB101) / Novartis, PureTech
Journal: Chemoproteomic selectivity profiling of PIKK and PI3K kinase inhibitors. (Pubmed Central) - Dec 20, 2019 The results further show that NVP-BEZ235 is not a PI3K inhibitor. Surprisingly, the designated ATM inhibitor CP466722 was found to bind strongly to ALK2, identifying a new chemotype for drug discovery to treat fibrodysplasia ossificans progressiva.
- |||||||||| navitoclax (ABT 263) / AbbVie, Roche
Journal, Combination therapy, IO Biomarker: Dissecting mechanisms of resistance to targeted drug combination therapy in human colorectal cancer. (Pubmed Central) - Dec 20, 2019 ERK inhibitors may have clinical utility in overcoming resistance to MEK inhibitor regimes; however, we find a recurrent active site mutation of ERK2 that drives resistance to ERK inhibitors in mono- or combined regimens, suggesting that resistance will remain a hurdle. Importantly, we find that the addition of low concentrations of the BCL2-family inhibitor navitoclax to the MEK-PI3K inhibitor regimen improves the synergistic interaction and blocks the acquisition of resistance.
- |||||||||| Review, Journal: Histone deacetylases as an epigenetic pillar for the development of hybrid inhibitors in cancer. (Pubmed Central) - Dec 20, 2019
In this regard, because of their multiple anticancer effects, histone deacetylase inhibitors have become a privileged tool for the development of hybrid drugs. The clinical trials of two multi-acting chimeras, HDAC/EGFR/HER2 and HDAC/PI3K inhibitors, encouraged the design of novel hybrids, such as compounds 22a (LSD1/HDAC) and 16a (CDK4/JAK1/HDAC), which showed superior anticancer effects than single-targeting agents or their combination both in cellular and mouse models.
- |||||||||| Journal: Liensinine induces gallbladder cancer apoptosis and G2/M arrest by inhibiting ZFX-induced PI3K/AKT pathway. (Pubmed Central) - Dec 20, 2019
Liensinine also affected GBC cell cycle progression and induced apoptosis by down-regulating phosphorylated protein kinase B (AKT), phosphorylated protein kinase B (p-AKT), phosphatidylinositol 3-kinase (PI3K), and Zinc finger X-chromosomal protein (ZFX) proteins. Liensinine induced G2/M arrest and apoptosis in gallbladder cancer, suggesting that liensinine might represent a novel and effective agent against gallbladder cancer.
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