Cisplatin induces expression of drug resistance-related genes through c-jun N-terminal kinase pathway in human lung cancer cells

2017 ◽  
Vol 80 (2) ◽  
pp. 235-242 ◽  
Author(s):  
Li Xu ◽  
Yingya Fu ◽  
Youlun Li ◽  
Xiaoli Han
Keyword(s):  
Lung Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells ◽  
Kinase Pathway

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

Fas Ligand Enhances Apoptosis of Human Lung Cancer Cells Cotreated with RIG-I-like Receptor Agonist and Radiation

2020 ◽  
Vol 20 (5) ◽  
pp. 372-381
Author(s):  
Yoshiaki Sato ◽  
Hironori Yoshino ◽  
Eichi Tsuruga ◽  
Ikuo Kashiwakura
Keyword(s):  
Lung Cancer ◽  
Cell Surface ◽  
Cancer Cells ◽  
Fas Ligand ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Poly I:C ◽  
Human Lung Cancer ◽  
Human Lung Cancer Cells ◽  
Induced Apoptosis

Background: Retinoic acid-inducible gene I (RIG-I)-like receptors (RLRs) play key roles in the antiviral response, but recent works show that RLR activation elicits anticancer activity as well, including apoptosis. Previously, we demonstrated that the anticancer activity of the RLR agonist Poly(I:C)-HMW/LyoVec™ [Poly(I:C)-HMW] against human lung cancer cells was enhanced by cotreatment with ionizing radiation (IR). In addition, cotreatment with Poly(I:C)-HMW and IR induced apoptosis in a Fas-independent manner, and increased Fas expression on the cell surface. Objective: The current study investigated the resultant hypothesis that Fas ligand (FasL) may enhance apoptosis in lung cancer cells cotreated with Poly(I:C)-HMW+IR. Methods: FasL was added into culture medium at 24 h following cotreatment with Poly(I:C)- HMW+IR, after upregulation of cell surface Fas expression on human lung cancer cells A549 and H1299 have already been discussed. Results: FasL enhanced the apoptosis of A549 and H1299 cells treated with Poly(I:C)-HMW+IR. Similarly, IR alone - and not Poly(I:C)-HMW - resulted in the upregulation of cell surface Fas expression followed by a high response to FasL-induced apoptosis, thus suggesting that the high sensitivity of cells treated with Poly(I:C)-HMW+IR to FasL-induced apoptosis resulted from the cellular response to IR. Finally, knockdown of Fas by siRNA confirmed that the high response of treated cells to FasL-induced apoptosis is dependent on Fas expression. Conclusion: In summary, the present study indicates that upregulated Fas expression following cotreatment with Poly(I:C)-HMW and IR is responsive to FasL-induced apoptosis, and a combination of RLR agonist, IR, and FasL could be a potential promising cancer therapy.

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