- |||||||||| quercetin (LY294002) / Eli Lilly
Journal: Phloretin Suppresses Bone Morphogenetic Protein-2-Induced Osteoblastogenesis and Mineralization via Inhibition of Phosphatidylinositol 3-kinases/Akt Pathway. (Pubmed Central) - Nov 14, 2019 In addition, treatment with a phosphatidylinositol 3-kinase (PI3K)/Akt inhibitor, LY294002, suppressed the mineralization and the expression of osteoblast differentiation markers other than ALP...The effects of GLUT1 silencing on osteoblast differentiation markers and mineralization were inconsistent with those of phloretin. Taken together, these findings suggest that phloretin suppressed osteoblastogenesis of ST2 and MC3T3-E1 cells by inhibiting the PI3K/Akt pathway, suggesting that the effects of phloretin may not be associated with glucose uptake inhibition.
- |||||||||| Journal: miR-424 protects PC-12 cells from OGD-induced injury by negatively regulating MKP-1. (Pubmed Central) - Nov 11, 2019
Our findings provide a rational to further evaluate Axitinib alone and in combination with other therapeutic agents for the treatment of most aggressive medulloblastoma subtypes. miR-424 protected PC-12 cells from OGD-induced injury through direct suppression of MKP-1 expression, as MKP-1 promoted OGD-induced cell injury by inhibiting the expression of HIF-1α and PI3K/AKT/mTOR pathways.
- |||||||||| Journal: Requirement of GSK-3 for PUMA induction upon loss of pro-survival PI3K signaling. (Pubmed Central) - Nov 11, 2019
A constitutively active mutant of FOXO3A, which cannot be controlled by AKT directly, still required active GSK-3 for the full transcriptional induction of Puma and cell death upon IL-3 withdrawal. Thus, the suppression of GSK-3 is the key function of PI3K signaling in order to prevent the induction of Puma by FOXO3A and p53 and thereby apoptosis upon growth factor withdrawal.
- |||||||||| Preclinical, Journal, PARP Biomarker, IO Biomarker: Loss of Tctn3 causes neuronal apoptosis and neural tube defects in mice. (Pubmed Central) - Nov 11, 2019
Finally, NPHP1, a protein with anti-apoptotic ability, was found to form a complex with Tctn3, and its levels were decreased in Tctn3 KO mice. In conclusion, our results show that Tctn3 KO disrupts the Shh signaling pathway and neural tube patterning, resulting in abnormal embryonic development, cellular apoptosis, and prenatal death in mice.
- |||||||||| Journal: PI3K-Mediated Blimp-1 Activation Controls B Cell Selection and Homeostasis. (Pubmed Central) - Nov 11, 2019
Interestingly, Blimp-1 also acts at early stages of B cell development to regulate B cell selection, as Blimp-1 deficiency results in an increased proportion of autoreactive B cells. Together, our data suggest that the combined requirement of deregulated PI3K signaling in addition to defective terminal differentiation represents the basis for proper selection and expansion of developing B cells.
- |||||||||| Journal: Phosphatidyl Inositol 3-Kinase (PI3K)-mTOR Inhibitor PKI-402 Inhibits Breast Cancer Induced Osteolysis. (Pubmed Central) - Nov 10, 2019
Importantly, as evidenced by the observation that the administration of PKI-402 inhibited MDA-MB-231-induced osteolysis in vivo, PKI-402 exerted an inhibitory effect on osteoclast formation and bone resorption, critical for cancer cells-induced bone destruction. These results strongly suggest that PKI-402 might have a therapeutic potential to inhibit breast cancer induced osteolysis.
- |||||||||| Ibrance (palbociclib) / Pfizer
Clinical, Journal: Genome-wide discovery of somatic coding and non-coding mutations in pediatric endemic and sporadic Burkitt lymphoma. (Pubmed Central) - Nov 10, 2019 Our results suggest that tumor EBV status defines a specific BL phenotype irrespective of geographic origin with particular molecular properties and distinct pathogenic mechanisms. The novel mutation patterns identified here imply rational use of DNA-damaging chemotherapy in some BL patients and targeted agents such as the CDK4/6 inhibitor palbociclib in others, whereas the importance of BCR signaling in BL strengthens the potential benefit of inhibitors for PI3K, Syk and Src family kinases among these patients.
- |||||||||| Journal: Monitoring flux in signalling pathways through measurements of 4EBP1-mediated eIF4F complex assembly. (Pubmed Central) - Nov 10, 2019
We show that 4EBP1 is a critical regulator of the mitogen responsive RAS/ERK and PI3K/AKT pathways and a key transducer of resistance mechanisms that affect small molecule inhibition of these pathways, principally by attenuating their effects on cap-dependent translation. These findings highlight the importance of highly efficacious direct inhibitors of eIF4E and eIF4F assembly, which could potentially target a wide spectrum of tumours containing differing mutations that effect these pathways and which confer chemo-resistance.
- |||||||||| Journal: An update on PTEN modulators - A patent review. (Pubmed Central) - Nov 10, 2019
Thus, novel treatment strategies that can regulate PTEN alone, or combinational treatment approaches that can induce PTEN and simultaneously affect downstream mediators in the PI3K/Akt pathway, are needed, which were not investigated in detail. Commercial interests associated with molecules that regulate PTEN are discussed here, along with limitations and new possibilities to improve them.
- |||||||||| fimepinostat (CUDC-907) / Curis, Farydak (panobinostat) / Novartis, Istodax (romidepsin) / Celgene, Astellas
Preclinical, Journal: Fimepinostat, a novel dual inhibitor of HDAC and PI3K, effectively reverses HIV-1 latency ex vivo without T cell activation. (Pubmed Central) - Nov 9, 2019 Latently HIV-1-infected J-lat Tat-GFP and ACH-2 cell lines were stimulated with clinically relevant concentrations of fimepinostat using the HDAC inhibitors (HDACi) panobinostat and romidepsin for comparison...At therapeutic concentration, the dual HDAC and PI3K inhibitor fimepinostat was a potent HIV-1 latency-reversing agent and it did not induce T cell activation and proliferation. The potential of fimepinostat as a latency-reversing agent warrants further investigation.
- |||||||||| fimepinostat (CUDC-907) / Curis, Farydak (panobinostat) / Novartis, Istodax (romidepsin) / Celgene, Astellas
Preclinical, Journal: Fimepinostat, a novel dual inhibitor of HDAC and PI3K, effectively reverses HIV-1 latency ex vivo without T cell activation. (Pubmed Central) - Nov 9, 2019 Latently HIV-1-infected J-lat Tat-GFP and ACH-2 cell lines were stimulated with clinically relevant concentrations of fimepinostat using the HDAC inhibitors (HDACi) panobinostat and romidepsin for comparison...At therapeutic concentration, the dual HDAC and PI3K inhibitor fimepinostat was a potent HIV-1 latency-reversing agent and it did not induce T cell activation and proliferation. The potential of fimepinostat as a latency-reversing agent warrants further investigation.
- |||||||||| Rituxan (rituximab) / Roche, Biogen
ACTIVATED PHOSPHOINOSITIDE 3-KINASE DELTA SYNDROME: A CASE SERIES (Monitor 4) - Nov 9, 2019 - Abstract #ACAAI2019ACAAI_732; Discussion Given the low prevalence of “PI3K” patients, there are no standardized guidelines for management and treatment at this time. Based on our experience, we have arrived at the following multidisciplinary approach: engagement of local genetics to look for underlying primary immunodeficiency; concurrent medical management between immunology and hematology-oncology with immunoglobulin replacement, rituximab, sirolimus, and prophylactic antimicrobials; early referral for bone marrow transplant evaluation, discussion, and HLA typing; and referral to NIH for evaluation and consideration of PIK3 inhibitor leniolisib.
- |||||||||| Journal: Linc-ROR promotes endometrial cell proliferation by activating the PI3K-Akt pathway. (Pubmed Central) - Nov 8, 2019
Based on our experience, we have arrived at the following multidisciplinary approach: engagement of local genetics to look for underlying primary immunodeficiency; concurrent medical management between immunology and hematology-oncology with immunoglobulin replacement, rituximab, sirolimus, and prophylactic antimicrobials; early referral for bone marrow transplant evaluation, discussion, and HLA typing; and referral to NIH for evaluation and consideration of PIK3 inhibitor leniolisib. Linc-ROR is highly expressed in the ectopic endometrium of adenomyosis, and it can promote the proliferative activity of endometrial cells by activating the PI3K-Akt pathway.
- |||||||||| Journal: Hirsutine induces mPTP-dependent apoptosis through ROCK1/PTEN/PI3K/GSK3β pathway in human lung cancer cells. (Pubmed Central) - Nov 8, 2019
Collectively, these findings suggest a hierarchical model in which induction of apoptosis by hirsutine stems primarily from activation of ROCK1 and PTEN, inactivation of PI3K/Akt, leading in turn to GSK3β dephosphorylation and mPTP opening, and culminating in caspase-3 activation and apoptosis. These findings could provide a novel mechanistic basis for the application of hirsutine in the treatment of human lung cancer.
- |||||||||| Journal: Exercise activates the PI3K-AKT signal pathway by decreasing the expression of 5α-reductase type 1 in PCOS rats. (Pubmed Central) - Nov 8, 2019
The PCOS non-exercise group and the PE + RI group displayed significantly lower phosphorylation of Akt, PI3K p85 and GLUT4 expression, while in the PE + R2I group, the level of Akt phosphorylation and PI3K p85 expression was significantly higher than that of the PCOS non-exercise group and the PE + RI group. In summary, our study demonstrated that exercise can activate the PI3K/AKT signal pathway of PCOS rats by decreasing the expression of 5αR1.
- |||||||||| Zydelig (idelalisib) / Gilead
Journal: PI3K p110δ inactivation antagonizes chronic lymphocytic leukemia and reverses T cell immune suppression. (Pubmed Central) - Nov 8, 2019 Targeted therapy with small molecules directed at essential survival pathways in leukemia represents a major advance, including the phosphatidylinositol-3'-kinase (PI3K) p110δ inhibitor idelalisib...Reconstitution of p110δD910A/D910A mice with p110δWT/WT Tregs reversed leukemia resistance. Our findings suggest that p110δ inhibitors may have direct antileukemic and indirect immune-activating effects, further supporting that p110δ blockade may have a broader immune-modulatory role in types of leukemia that are not sensitive to p110δ inhibition.
- |||||||||| Journal: Pin1 inhibition potently suppresses gastric cancer growth and blocks PI3K/AKT and Wnt/β-catenin oncogenic pathways. (Pubmed Central) - Nov 8, 2019
Furthermore, whereas Pin1 overexpression promoted the transformed phenotype in immortalized and nontransformed human gastric cells, either genetic or chemical Pin1 inhibition in multiple human gastric cancer cells potently suppressed cell growth, G1/S transition and colony formation in vitro, as well as tumor growth in xenograft tumor models in vivo, which were further supported by downregulation of multiple key oncoproteins in PI3K/AKT and Wnt/β-catenin signaling pathways. These results not only provide the first evidence for a critical role of Pin1 in the tumorigenesis of gastric cancer but also suggest that targeting Pin1 using ATRA or other inhibitors offers an effective new therapeutic approach for treating advanced gastric cancer.
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