PI3K inhib 
Welcome,         Profile    Billing    Logout  
 67 Companies  59 Products   59 Products   344 Diseases   342 Trials   12240 News 


«12...979899100101102103104105106107...229230»
  • ||||||||||  Journal:  Morroniside promotes the osteogenesis by activating PI3K/Akt/mTOR signaling. (Pubmed Central) -  Jul 4, 2021   
    In vivo assays showed that in bone tissue of ovariectomized mice, Morroniside-enhanced osteoblast formation was reversed by the pharmacological inhibition of PI3K or mTOR. In conclusion, Morroniside can promote the osteogenesis through PI3K/Akt/mTOR signaling, which provides a novel clue for the strategy of Morroniside in treating osteoporosis.
  • ||||||||||  5-fluorouracil / Generic mfg.
    Journal, PD(L)-1 Biomarker, IO biomarker:  MM-129 as a Novel Inhibitor Targeting PI3K/AKT/mTOR and PD-L1 in Colorectal Cancer. (Pubmed Central) -  Jul 4, 2021   
    Factor interactions indicated the complex interplay in the elicitation of different negative valence system's items and the fine-tuning of PI3K/Akt signaling pathway intensity by genotype-load and sex. A novel 1,2,4-triazine derivative with a dual mechanism of antitumor activity-MM-129, may act as a chemosensitizer, overcoming chemoresistance against 5-FU, the first-line agent in the chemotherapy of colon cancer.
  • ||||||||||  Journal:  Integrative cBioPortal Analysis Revealed Molecular Mechanisms That Regulate EGFR-PI3K-AKT-mTOR Pathway in Diffuse Gliomas of the Brain. (Pubmed Central) -  Jul 3, 2021   
    Comprehensive statistical analyses show how genomics and epigenomics affect the expression of examined genes differently across various pathohistological types and grades, suggesting that genes AKT3, CHUK and PTEN behave like tumor suppressors, while AKT1, AKT2, EGFR, and PIK3AP1 show oncogenic behavior and are involved in enhanced activity of the EGFR-PI3K-AKT-mTOR signaling pathway. Our findings contribute to the knowledge of the molecular differences between pathohistological types and ultimately offer the possibility of new treatment targets and personalized therapies in patients with diffuse gliomas.
  • ||||||||||  Journal:  Identification of MALT1 Feedback Mechanisms Enables Rational Design of Potent Anti-Lymphoma Regimens for ABC-DLBCL. (Pubmed Central) -  Jul 3, 2021   
    In contrast, simultaneous inhibition of MALT1 and MTORC1 prevented S6 phosphorylation, yielded potent activity against DLBCL cell lines and primary patient specimens, and resulted in more profound tumor regression and significantly improved survival of ABC-DLBCLs in vivo as compared to PI3K inhibitors. These findings provide a basis for maximal therapeutic impact of MALT1 inhibitors in the clinic, by disrupting feedback mechanisms that might otherwise limit their efficacy.
  • ||||||||||  Journal:  RP11-462C24.1 suppresses proliferation and invasion of colorectal carcinoma cells by regulating HSP70 through PI3K/AKT signaling pathway. (Pubmed Central) -  Jul 3, 2021   
    From the results, we found that RP11-462C24.1 was significantly decreased in CRC tumor tissues and the CRC cell lines, which were most significant in SW480 and HT-29 cell lines; moreover, transient overexpression of RP11-462C24.1 suppressed the growth and migration while promoted apoptosis of SW480 and HT-29 cells, while knockdown of RP11-462C24.1 has shown the opposite effects; RP11-462C24.1 may also inhibit the growth of CRC tumors in xenograft mice models; additionally, 70 kD heat shock proteins (HSP70) has been identified as one of the most significantly deferentially expressed genes by RNA-seq, and we further confirmed that RP11-462C24.1 may affect the growth and metathesis of CRC cells via regulating HSP70 and PI3K/AKT signaling pathway. In summary, these results indicated that RP11-462C24 may function as a tumor suppressor in the development of CRC.
  • ||||||||||  Preclinical, Journal:  Celastrol slows the progression of early diabetic nephropathy in rats via the PI3K/AKT pathway. (Pubmed Central) -  Jul 3, 2021   
    In summary, these results indicated that RP11-462C24 may function as a tumor suppressor in the development of CRC. Celastrol functions as a potential therapeutic substance, acting via the PI3K/AKT pathway to attenuate renal injury, inhibit glomerular basement membrane thickening, and achieve podocyte homeostasis in diabetic nephropathy.
  • ||||||||||  Journal:  Lacrimal gland budding requires PI3K-dependent suppression of EGF signaling. (Pubmed Central) -  Jul 2, 2021   
    We further show that this suppression of EGF signaling is necessary for induction of lacrimal gland buds. These results reveal that the interplay between PI3K, mitogen-activated protein kinase, and mTOR mediates the cross-talk among FGF, IGF, and EGF signaling in support of lacrimal gland development.
  • ||||||||||  Journal:  Mito-Tempo suppresses autophagic flux via the PI3K/Akt/mTOR signaling pathway in neuroblastoma SH-SY5Y cells. (Pubmed Central) -  Jul 2, 2021   
    Moreover, Mito-Tempo treatment altered the autophagy process resulting in the decline in the ratio of the autophagy markers LC3-I/-II and p62 (SQSTM1). We propose that Mito-Tempo can improve neuronal properties against glutamate cytotoxicity through its direct free radical scavenging activity and inhibit excessive autophagy signaling pathway, therefore, allow for further studies to investigate the therapeutic potentials of Mito-Tempo in animal disease models and human.
  • ||||||||||  Journal:  MiR-506 alleviates myocardial ischemia-reperfusion injury via targeting PI3K/AKT. (Pubmed Central) -  Jul 2, 2021   
    Additionally, miR-217 can increase the viability of AECs through the TLR4/PI3K/Akt/ NF-κB signal transduction pathway, and inhibit their apoptosis, inflammatory response, and EndMT. MiR-506 is associated with myocardial injury in rats, which can alleviate myocardial injury through the PI3K/AKT signaling pathway.
  • ||||||||||  sevoflurane / Generic mfg., doxorubicin hydrochloride / Generic mfg.
    Preclinical, Journal:  Sevoflurane ameliorates adriamycin-induced myocardial injury in rats through the PI3K/Akt/GSK-3β pathway. (Pubmed Central) -  Jul 2, 2021   
    SEV pretreatment significantly alleviated the effect of ADR, manifested as significantly lowered content of AST, LDH and CK in the serum (p<0.01), distinctly elevated protein expression levels of p-GSK-3β, p-PI3K and p-Akt (p<0.01), notably reduced apoptosis rate (p<0.01), and relieved myocardial injury. LY294002 remarkably inhibited the protective effect of SEV against myocardial injury (p<0.01) SEV is able to prominently ameliorate ADR-induced myocardial injury by regulating the phosphorylation level of the PI3K/Akt/GSK-3β signaling pathway.
  • ||||||||||  Journal:  MicroRNA-107 Ameliorates Damage in a Cell Model of Alzheimer's Disease by Mediating the FGF7/FGFR2/PI3K/Akt Pathway. (Pubmed Central) -  Jul 1, 2021   
    Furthermore, using bioinformatic prediction, dual-luciferase reporter assay (DLRA), quantitative polymerase chain reaction (qPCR), and Western blot (WB), miR-107 was confirmed to reduce the expression level of FGF7, and it subsequently deactivated the FGFR2/PI3K/Akt pathway. Moreover, FGF7 overexpression counteracted the role of miR-107 in the viability, proliferation, inflammation, and apoptosis of Aβ-induced SH-SY5Y cells.
  • ||||||||||  Review, Journal:  The emerging role of BET inhibitors in breast cancer. (Pubmed Central) -  Jul 1, 2021   
    Consistently, BET inhibition sensitized breast tumors to chemotherapy drugs, hormone therapy and PI3K inhibitors in vitro. This article aims to review all existing preclinical and clinical evidence regarding BET inhibitors in breast cancer.
  • ||||||||||  Journal:  Targeted PI3K/AKT-hyperactivation induces cell death in chronic lymphocytic leukemia. (Pubmed Central) -  Jul 1, 2021   
    Our mechanistic studies reveal that increased AKT activity upon inhibition of SHIP1 leads to increased mitochondrial respiration and causes excessive accumulation of reactive oxygen species (ROS), resulting in cell death in CLL with immunogenic features. Our results demonstrate that CLL cells critically depend on mechanisms to fine-tune PI3K/AKT activity, allowing sustained proliferation and survival but avoid ROS-induced cell death and suggest transient SHIP1-inhibition as an unexpectedly promising concept for CLL therapy.
  • ||||||||||  aspirin / Generic mfg.
    Journal, IO biomarker:  Aspirin has a better effect on PIK3CA mutant colorectal cancer cells by PI3K/Akt/Raptor pathway. (Pubmed Central) -  Jun 30, 2021   
    Thus, our results demonstrate that activation of Wnt/β-catenin pathway involves an ATM/Chk2- independent PI3K/Akt/GSK-3 cascade in TMZ treated cells and further provides mechanistic basis for the chemoresistance of glioma to TMZ. Aspirin can regulate the proliferation, apoptosis and autophagy of CRC cells through the PI3K/Akt/Raptor pathway, affecting PIK3CA-mutant CRC.
  • ||||||||||  Journal:  Editorial: Human Disorders of PI3K Biology. (Pubmed Central) -  Jun 30, 2021   
    The validated HPLC method was successfully applied to a pharmacokinetic study in rats. No abstract available