scholarly journals Expression and clinical significance of the phosphatidylinositol 3-kinase/protein kinase B signal transduction pathway in non-small cell lung carcinoma

2014 ◽  
Vol 8 (2) ◽  
pp. 601-607 ◽  
Author(s):  
AI-GUI JIANG ◽  
HONG YU ◽  
JIAN-AN HUANG
Keyword(s):  
Signal Transduction ◽  
Protein Kinase ◽  
Protein Kinase B ◽  
Small Cell Lung Carcinoma ◽  
Signal Transduction Pathway ◽  
Small Cell ◽  
Transduction Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma

Delivery of Gefitinib in synergism with Thymoquinone via Transferrin Conjugated Nanoparticle Sensitizes Gefitinib Resistant Non-Small Cell Lung Carcinoma to Control Metastasis and Stemness

2021 ◽  
Author(s):  
Priyanka Upadhyay ◽  
Avijit Ghosh ◽  
Arijita Basu ◽  
P. A. Pranati ◽  
Payal Gupta ◽  
...  
Keyword(s):  
Small Cell Lung Carcinoma ◽  
Growth Factor Receptor ◽  
Signal Transduction Pathway ◽  
Small Cell ◽  
Transduction Pathway ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Cellular Signal ◽  
Cellular Signal Transduction Pathway ◽  
Epidermal Growth

Epidermal growth factor receptor (EGFR) normally over-express in non-small cell lung cancer (NSCLC) and its mutations act as oncogenic drivers in the cellular signal transduction pathway and induce downstream activation...

scholarly journals Calcium-dependent growth regulation of small cell lung cancer cells by neuropeptides

2006 ◽  
Vol 13 (4) ◽  
pp. 1069-1084 ◽  
Author(s):  
Thomas Gudermann ◽  
Susanne Roelle
Keyword(s):  
Protein Kinase ◽  
Growth Regulation ◽  
Hormone Receptors ◽  
Apoptotic Cell ◽  
Small Cell Lung Carcinoma ◽  
Small Cell ◽  
Mitogen Activated Protein Kinase ◽  
Small Cell Lung ◽  
Cell Lung Carcinoma ◽  
Mitogenic Signal

Approximately 15–25% of all primary cancers of the lung are classified histologically as small cell lung carcinoma (SCLC), a subtype characterized by rapid growth and a poor prognosis. Neuropeptide hormones like bombesin/gastrin-releasing peptide, bradykinin or galanin are the principal mitogenic stimuli of this tumour entity. The mitogenic signal is transmitted into the cell via heptahelical neuropeptide hormone receptors, which couple to the heterotrimeric G proteins of the Gq/11 familiy. Subsequent activation of phospholipase Cβ (PLCβ) entails the activation of protein kinase C and the elevation of the intracellular calcium concentration. There is mounting evidence to support the notion that calcium mobilization is the key event that initiates different mitogen-activated protein kinase cascades. Neuropeptide-dependent proliferation of SCLC cells relies on parallel activation of the Gq/11/PLCβ/Ras/extracellular signal-regulated kinase and the c-jun N-terminal kinase pathways, while selective engagement of either signalling cascade alone results in growth arrest and differentiation or apoptotic cell death. Basic experimental research has the potential to identify and validate novel therapeutic targets located at critical points of convergence of different mitogenic signal transduction pathways. In the case of SCLC, targeting the distinct components of the Ca2+ influx pathway as well as critical Ca2+-dependent cellular effectors may be rewarding in this regard.

scholarly journals Lactosylceramide-enriched glycosphingolipid signaling domain mediates superoxide generation from human neutrophils

Blood ◽  
2002 ◽  
Vol 100 (4) ◽  
pp. 1454-1464 ◽  
Author(s):  
Kazuhisa Iwabuchi ◽  
Isao Nagaoka
Keyword(s):  
Signal Transduction ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Kinase Inhibitor ◽  
Signal Transduction Pathway ◽  
Transduction Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Superoxide Generation ◽  
Kinase C ◽  
Signaling Domain

This study is focused on the functional significance of neutrophil lactosylceramide (LacCer)–enriched microdomains, which are involved in the initiation of a signal transduction pathway leading to superoxide generation. Treatment of neutrophils with anti-LacCer antibody, T5A7 or Huly-m13, induced superoxide generation from the cells, which was blocked by PP1, a Src kinase inhibitor; wortmannin, a phosphatidylinositol-3 kinase inhibitor; SB203580, a p38 mitogen-activated protein kinase (MAPK) inhibitor; and H7, an inhibitor for protein kinase C. When promyelocytic leukemia HL-60 cells were differentiated into neutrophilic lineage by dimethyl sulfoxide (DMSO) treatment, they acquired superoxide-generating activity but did not respond to anti-LacCer antibodies. Density gradient centrifugation revealed that LacCer and Lyn were recovered in detergent-insoluble membrane (DIM) of neutrophils and DMSO-treated HL-60 cells. However, immunoprecipitation experiments indicated that LacCer was associated with Lyn in neutrophils but not in DMSO-treated HL-60 cells. Interestingly, T5A7 induced the phosphorylation of Lyn in neutrophils but not in DMSO-treated HL-60 cells. Moreover, T5A7 induced the phosphorylation of p38 MAPK in neutrophils. T5A7-induced Lyn phosphorylation in neutrophil DIM fraction was significantly enhanced by cholesterol depletion or sequestration with methyl-β-cyclodextrin or nystatin. Collectively, these data suggest that neutrophils are characterized by the presence of cell surface LacCer-enriched glycosphingolipid signaling domain coupled with Lyn and that the ligand binding to LacCer induces the activation of Lyn, which may be suppressibly regulated by cholesterol, leading to superoxide generation through the phosphatidylinositol-3 kinase–, p38 MAPK–, and protein kinase C–dependent signal transduction pathway.

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