Death Receptor 5 and cellular FLICE-inhibitory protein regulate pemetrexed-induced apoptosis in human lung cancer cells

2011 ◽  
Vol 47 (16) ◽  
pp. 2471-2478 ◽  
Author(s):  
Ling Su ◽  
Guangbo Liu ◽  
Xuexi Hao ◽  
Ning Zhong ◽  
Diansheng Zhong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Death Receptor ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Death Receptor 5 ◽  
Inhibitory Protein ◽  
Human Lung Cancer Cells ◽  
Induced Apoptosis

Cellular FLICE-Inhibitory Protein Down-regulation Contributes to Celecoxib-Induced Apoptosis in Human Lung Cancer Cells

2006 ◽  
Vol 66 (23) ◽  
pp. 11115-11119 ◽  
Author(s):  
Xiangguo Liu ◽  
Ping Yue ◽  
Axel H. Schönthal ◽  
Fadlo R. Khuri ◽  
Shi-Yong Sun
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Human Lung ◽  
Lung Cancer Cells ◽  
Human Lung Cancer ◽  
Inhibitory Protein ◽  
Down Regulation ◽  
Human Lung Cancer Cells ◽  
Induced Apoptosis

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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