scholarly journals PI3 Kinase Pathway and MET Inhibition is Efficacious in Malignant Pleural Mesothelioma

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Rajani Kanteti ◽  
Jacob J. Riehm ◽  
Immanuel Dhanasingh ◽  
Frances E. Lennon ◽  
Tamara Mirzapoiazova ◽  
...  
Keyword(s):  
Malignant Pleural Mesothelioma ◽  
Pi3 Kinase ◽  
Pleural Mesothelioma ◽  
Pi3 Kinase Pathway ◽  
Kinase Pathway

Integration of stimulatory and inhibitory signals in pituitary tumor cells through the PI3 kinase pathway

2006 ◽  
Vol 114 (08) ◽  
Author(s):  
T Colaco ◽  
C Onofri ◽  
M Theodoropoulou ◽  
M Kowarik ◽  
GK Stalla ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Pituitary Tumor ◽  
Pi3 Kinase ◽  
Pi3 Kinase Pathway ◽  
Kinase Pathway

scholarly journals c-Cbl Is Tyrosine-Phosphorylated by Interleukin-4 and Enhances Mitogenic and Survival Signals of Interleukin-4 Receptor by Linking With the Phosphatidylinositol 3′-Kinase Pathway

Blood ◽  
1998 ◽  
Vol 91 (1) ◽  
pp. 46-53 ◽  
Author(s):  
Hiroo Ueno ◽  
Ko Sasaki ◽  
Hiroaki Honda ◽  
Tetsuya Nakamoto ◽  
Tetsuya Yamagata ◽  
...  
Keyword(s):  
Specific Inhibitor ◽  
Pi3 Kinase ◽  
Interleukin 4 ◽  
Phosphatidylinositol 3 Kinase ◽  
Proliferation And Differentiation ◽  
Interleukin 4 Receptor ◽  
Pi3 Kinase Pathway ◽  
Kinase Pathway ◽  
Phosphatidylinositol 3 ◽  
Survival Signals

Interleukin-4 (IL-4) is a cytokine that induces both proliferation and differentiation and suppresses apoptosis of B cells. Although IL-4 has been shown to activate the phosphatidylinositol 3′ (PI3)-kinase pathway, the role of PI3 kinase in the IL-4 receptor (IL-4R) signaling remains unclear. In this study, we demonstrated that c-Cbl proto-oncogene product is inducibly phosphorylated on tyrosine residues and is associated with the p85 subunit of PI3-kinase by IL-4 stimulation. Overexpression of c-Cbl enhances the PI3-kinase activity and, at the same time, mitogenic activity and survival of cells in the presence of IL-4. However, these effects of c-Cbl were abolished by wortmannin, a specific inhibitor for the PI3 kinase pathway, or by a point mutation at tyrosine 731 of c-Cbl, which is a major binding site for p85. These results indicate that c-Cbl plays a role in linking IL-4R with the PI3 kinase pathway and thus enhancing the mitogenic and survival signals.

scholarly journals PI3 kinase pathway regulated miRNome in glioblastoma: identification of miR-326 as a tumour suppressor miRNA

2016 ◽  
Vol 15 (1) ◽  
Author(s):  
Zahid Nawaz ◽  
Vikas Patil ◽  
Yashna Paul ◽  
Alangar S. Hegde ◽  
Arimappamagan Arivazhagan ◽  
...  
Keyword(s):  
Pi3 Kinase ◽  
Tumour Suppressor ◽  
Pi3 Kinase Pathway ◽  
Kinase Pathway

Tonic support of contraction involving the PI3 kinase pathway in ventricular myocytes from failing human heart

2008 ◽  
Vol 44 (4) ◽  
pp. 752-753
Author(s):  
Edwin A. Garcia ◽  
Gaelle Kikonda Kanda ◽  
Alexander Lyon ◽  
Clare E. Gallon ◽  
Andrew E. Messer ◽  
...  
Keyword(s):  
Human Heart ◽  
Ventricular Myocytes ◽  
Pi3 Kinase ◽  
Pi3 Kinase Pathway ◽  
Kinase Pathway

scholarly journals Cooperativity of TMPRSS2-ERG with PI3-kinase pathway activation in prostate oncogenesis

2009 ◽  
Vol 41 (5) ◽  
pp. 524-526 ◽  
Author(s):  
Jennifer C King ◽  
Jin Xu ◽  
John Wongvipat ◽  
Haley Hieronymus ◽  
Brett S Carver ◽  
...  
Keyword(s):  
Pi3 Kinase ◽  
Pathway Activation ◽  
Pi3 Kinase Pathway ◽  
Kinase Pathway

Role of Phosphatidylinositol 3- Kinase/AKT Pathway in Diffuse Large B-Cell Lymphoma Survival.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 4808-4808
Author(s):  
Shahab Uddin ◽  
Azhar R. Hussain ◽  
Prahant Bavi ◽  
Abdul K. Siraj ◽  
Khawla S. Al-Kuraya
Keyword(s):  
B Cell ◽  
Cell Lines ◽  
Cell Lymphoma ◽  
B Cell Lymphoma ◽  
Pi3 Kinase ◽  
Phosphatidylinositol 3 Kinase ◽  
Large B Cell Lymphoma ◽  
Pi3 Kinase Pathway ◽  
Kinase Pathway ◽  
Large B Cell

Abstract Phosphatidylinositol 3-kinase (PI3-kinase) is a key player in cell growth signaling in a number of lymphoid malignancies including myeloma and primary effusion lymphoma. However, its role in diffuse large B-cell lymphoma (DLBCL) has not been elucidated. Therefore, we have studied the PI3-kinase pathway and apoptosis in a panel of DLBCL cell lines (SUDHL4, SUDHL8, SUDHL10 and OCI-LY19). Our data show that inhibition of PI3-kinase by a specific inhibitor, LY294002, induced apoptosis as detected by Annexin V/Propidium Iodide dual staining in the majority of DLBCL cell lines. We then dissected the PI3-kinase pathway by analyzing the downstream targets of phosphorylation by Western blot. We found that AKT/PKB was constitutively phosphorylated, and thus activated, in all DLBCL cell lines. The downstream elements of AKT, ForkHead (FKHR) and GSK3 were also constitutively phosphorylated in all DLBCL cell lines. Similarly, treatment with LY294002 prevented this phenomenon in all the cell lines regardless of their final apoptotic endpoint. Inhibition of PI3-kinase activity further downstream induced cleavage of Bid in all DLBCL cells and subsequently loss of mitochondrial membrane potential and release of cytochrome c from mitochondria in all DLBCL cell lines. The release of cytochrome C led to activation of Caspases 9 and 3 and cleavage of PARP. Finally expression of the inhibitor of apoptosis, XIAP, which is also a downstream target of AKT, was compromised in the all cell lines following LY294002 treatment. Our data demonstrate that the PI3-kinase pathway plays a major role in the survival and growth of DLBCL cells. Altogether, these results suggest that blocking the PI3-kinase pathway may be a potential target for therapeutic intervention in diffuse large B-cell lymphoma.

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