EFFECT OF UV-INDUCED APOPTOSIS ON HeLa CELL SURFACE PROTEASE ACTIVITY

1996 ◽  
Vol 24 (4) ◽  
pp. 560S-560S
Author(s):  
T.J. Piva ◽  
D.R. Krause ◽  
G.M. Chojnowski ◽  
K.A.O. Ellem
Keyword(s):  
Cell Surface ◽  
Hela Cell ◽  
Protease Activity ◽  
Induced Apoptosis ◽  
Cell Surface Protease

Effect of UV irradiation on cell surface protease activity and amino acid uptake

1998 ◽  
Vol 422 (1) ◽  
pp. 55-67 ◽  
Author(s):  
Terrence J. Piva ◽  
Kari G. Francis ◽  
Darren R. Krause ◽  
Grace M. Chojnowski ◽  
Kay A.O. Ellem
Keyword(s):  
Amino Acid ◽  
Cell Surface ◽  
Uv Irradiation ◽  
Protease Activity ◽  
Amino Acid Uptake ◽  
Acid Uptake ◽  
Cell Surface Protease

Degradation of Insulin by Isolated Mouse Pancreatic Acini: Evidence for Cell Surface Protease Activity

Diabetes ◽  
1984 ◽  
Vol 33 (1) ◽  
pp. 64-72 ◽  
Author(s):  
I. D. Goldfine ◽  
J. A. Williams ◽  
A. C. Bailey ◽  
K. Y. Wong ◽  
Y. Iwamoto ◽  
...  
Keyword(s):  
Cell Surface ◽  
Protease Activity ◽  
Pancreatic Acini ◽  
Cell Surface Protease

Degradation of insulin by isolated mouse pancreatic acini. Evidence for cell surface protease activity

Diabetes ◽  
1984 ◽  
Vol 33 (1) ◽  
pp. 64-72 ◽  
Author(s):  
I. D. Goldfine ◽  
J. A. Williams ◽  
A. C. Bailey ◽  
K. Y. Wong ◽  
Y. Iwamoto ◽  
...  
Keyword(s):  
Cell Surface ◽  
Protease Activity ◽  
Pancreatic Acini ◽  
Cell Surface Protease

Increased cell surface protease activity in UV-irradiated cells undergoing apoptosis

Redox Report ◽  
2000 ◽  
Vol 5 (2-3) ◽  
pp. 133-136
Author(s):  
T.J. Piva ◽  
C.M. Davern ◽  
C.M. Winterford ◽  
K.A.O. Ellem
Keyword(s):  
Cell Surface ◽  
Protease Activity ◽  
Cell Surface Protease

Relationship between cell surface protease activity and doubling time in various normal and transformed cells

1976 ◽  
Vol 451 (2) ◽  
pp. 499-510 ◽  
Author(s):  
Victor B. Hatcher ◽  
Michael S. Wertheim ◽  
Choo Y. Rhee ◽  
Grace Tsien ◽  
Peter G. Burk
Keyword(s):  
Cell Surface ◽  
Protease Activity ◽  
Doubling Time ◽  
Transformed Cells ◽  
Cell Surface Protease

scholarly journals Up-regulation of FLIP in cisplatin-selected HeLa cells causes cross-resistance to CD95/Fas death signalling

2003 ◽  
Vol 376 (1) ◽  
pp. 253-260 ◽  
Author(s):  
Pachiyappan KAMARAJAN ◽  
Nian-Kang SUN ◽  
Chuck C.-K. CHAO
Keyword(s):  
Cell Surface ◽  
Hela Cell ◽  
Cell Lines ◽  
Antisense Oligonucleotides ◽  
Cross Resistance ◽  
Caspase 8 ◽  
Cervix Carcinoma ◽  
Hela Cell Lines ◽  
Induced Apoptosis ◽  
Resistant Cells

Cisplatin-selected cervix carcinoma HeLa cell lines induced less apoptosis, and weaker activation by cisplatin or Fas-activating antibody, of mitochondrial-associated caspase-9 and death receptor-mediated caspase-8 than did parental cells. Furthermore, less DISC (death-inducing signalling complex) was formed in cisplatin-selected cell lines than in parental cells. Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines. These results imply that cell-surface death signalling is inducible by cisplatin; that reduction of this pathway is associated with drug resistance, and that cisplatin-selected cells acquire cross-resistance to cell-surface death signalling. Sequential up-regulation of FLIP (FLICE-like inhibitory protein), but not Bcl-2, Bcl-xL or inhibitors of apoptosis protein (IAPs), was observed in resistant cells but not in parental cells. The inhibition of FLIP by FLIP antisense oligonucleotides promotes cisplatin and Fas-antibody-induced apoptosis. However, the modulation of apoptosis by FLIP antisense oligonucleotides in resistant cells is greater than that in parental cells. The presented data reveal that the up-regulation of FLIP may contribute to the suppression of apoptosis and thereby change cells that are resistant to cisplatin and Fas-mediated death signals. The results also show that cancer cells that have undergone long-term chemotherapy and become chemoresistant may change the FLIP level, becoming cross-resistant to death factors such as Fas.

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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