Mitogen-activated protein kinase antisense oligonucleotide inhibits the growth of human lung cancer cells.

1999 ◽  
Author(s):  
K Nishio ◽  
K Fukuoka ◽  
H Fukumoto ◽  
T Sunami ◽  
Y Iwamoto ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Antisense Oligonucleotide ◽  
Human Lung ◽  
Mitogen Activated Protein Kinase ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells ◽  
Mitogen Activated Protein

scholarly journals PACAP-27 tyrosine phosphorylates mitogen activated protein kinase and increases VEGF mRNAs in human lung cancer cells

2002 ◽  
Vol 109 (1-3) ◽  
pp. 135-140 ◽  
Author(s):  
Terry W Moody ◽  
Julius Leyton ◽  
Marchessini Casibang ◽  
Joseph Pisegna ◽  
Robert T Jensen
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Human Lung ◽  
Mitogen Activated Protein Kinase ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells ◽  
Mitogen Activated Protein

CIS-diamminedichloroplatinum(II) inhibits p34cdc2 protein kinase in human lung-cancer cells

1993 ◽  
Vol 55 (4) ◽  
pp. 616-622 ◽  
Author(s):  
Kazuto Nishio ◽  
Yasuhiro Fujiwara ◽  
Yuki Miyahara ◽  
Yuichiro Takeda ◽  
Tatsuo Ohira ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells

scholarly journals Atypical Protein Kinase Cι Expression and Aurothiomalate Sensitivity in Human Lung Cancer Cells

2008 ◽  
Vol 68 (14) ◽  
pp. 5888-5895 ◽  
Author(s):  
Roderick P. Regala ◽  
E. Aubrey Thompson ◽  
Alan P. Fields
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Atypical Protein Kinase ◽  
Human Lung Cancer Cells

scholarly journals Survival Function of Protein Kinase Cι as a Novel Nitrosamine 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone-activated Bad Kinase

2005 ◽  
Vol 280 (16) ◽  
pp. 16045-16052 ◽  
Author(s):  
Zhaohui Jin ◽  
Meiguo Xin ◽  
Xingming Deng
Keyword(s):  
Lung Cancer ◽  
Protein Kinase ◽  
Cancer Cells ◽  
Adrenergic Receptor ◽  
Human Lung ◽  
Small Cell ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Small Cell Lung ◽  
Human Lung Cancer Cells

Nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) is formed by nitrosation of nicotine and has been identified as the most potent carcinogen in cigarette smoke. NNK cannot only induce DNA damage but also promotes the survival of human lung cancer cells. Protein kinase C (PKC)ι is an atypical PKC isoform and plays an important role in cell survival, but the downstream survival substrate(s) is not yet identified. Bad, a proapoptotic BH3-only member of Bcl2 family, is co-expressed with PKCι in both small cell lung cancer and non-small cell lung cancer cells. We discovered that NNK potently induces multisite Bad phosphorylation at Ser-112, Ser-136, and Ser-155 via activation of PKCι in association with increased survival of human lung cancer cells. Purified, active PKCι can directly phosphorylate both endogenous and recombinant Bad at these three sites and disrupt Bad/Bcl-XL bindingin vitro. Overexpression of PKCι results in an enhancement of Bad phosphorylation. NNK also stimulates activation of c-Src, which is a known PKCι upstream kinase. Treatment of cells with the PKC inhibitor (staurosporine) or a Src-specific inhibitor (PP2) can block NNK-induced Bad phosphorylation and promote apoptotic cell death. The β-adrenergic receptor inhibitor propranolol blocks both NNK-induced activation of PKCι and Bad phosphorylation, indicating that NNK-induced Bad phosphorylation occurs at least in part through the upstream β-adrenergic receptor. Mechanistically, NNK-induced Bad phosphorylation prevents its interaction with Bcl-XL. Because the specific depletion of PKCι by RNA interference inhibits both NNK-induced Bad phosphorylation and survival, this confirms that PKCι is a necessary component in NNK-mediated survival signaling. Collectively, these findings reveal a novel role for PKCι as an NNK-activated physiological Bad kinase that can directly phosphorylate and inactivate this proapoptotic BH3-only protein, which leads to enhanced survival and chemoresistance of human lung cancer cells.

Anticancer activity of peptide extracted from edible mushroom; Lentinus squarrosulus in human lung cancer cells

Planta Medica ◽  
2016 ◽  
Vol 81 (S 01) ◽  
pp. S1-S381
Author(s):  
S Sumkhemthong ◽  
M Suksomtip ◽  
P Chanvorachote ◽  
C Chaotham
Keyword(s):  
Lung Cancer ◽  
Anticancer Activity ◽  
Cancer Cells ◽  
Human Lung ◽  
Edible Mushroom ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells

Inhibitory effects of Actinidia Chinensis planch root extracts (acRoots) on human lung cancer cells through retinoic acid receptor beta

2017 ◽  
Vol 5 (1) ◽  
Author(s):  
Lingyan Wang ◽  
Jiayun Hou ◽  
Minghuan Zheng ◽  
Lin Shi
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Retinoic Acid Receptor ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Inhibitory Effects ◽  
The Core ◽  
Human Lung Cancer Cells ◽  
Receptor Beta

Actinidia Chinensis Planch roots (acRoots) are used to treat many cancers, although the anti-tumor mechanism by which acRoots inhibit cancer cell growth remains unclear. The present study aims at investigating inhibitory effects of acRoots on human lung cancer cells and potential mechanisms. Our data demonstrate that the inhibitory effects of acRoots on lung cancer cells depend on genetic backgrounds and phenotypes of cells. We furthermore found the expression of metabolism-associated gene profiles varied between acRoots-hypersensitive (H460) or hyposensitive lung cancer cells (H1299) after screening lung cancer cells with different genetic backgrounds. We selected retinoic acid receptor beta (RARB) as the core target within metabolism-associated core gene networks and evaluated RARB changes and roles in cells treated with acRoots at different concentrations and timeframes. Hypersensitive cancer cells with the deletion of RARB expression did not response to the treatment with acRoots, while RARB deletion did not change effects of acRoots on hyposensitive cells. Thus, it seems that RARB as the core target within metabolism-associated networks plays important roles in the regulation of lung cancer cell sensitivity to acRoots.

EFFECTS OF OPIOIDS AND NICOTINE ON APOPTOSIS IN HUMAN LUNG CANCER CELLS

Analgesia ◽  
1995 ◽  
Vol 1 (4) ◽  
pp. 548-552
Author(s):  
Rhoda Maneckjee ◽  
Kathleen Dehen ◽  
John D. Minna
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells

SP1 Mediates MRP1 Upregulation and Multi-Drug Resistance in Human Lung Cancer Cells

2019 ◽  
Author(s):  
Shuli Shao ◽  
Yunjianan Feng ◽  
Yue Xiao ◽  
Yan Li ◽  
Weiwei Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Multi Drug Resistance ◽  
Human Lung Cancer Cells
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