PMID- 20623193
OWN - NLM
STAT- MEDLINE
DCOM- 20110309
LR  - 20101201
IS  - 1573-675X (Electronic)
IS  - 1360-8185 (Linking)
VI  - 15
IP  - 12
DP  - 2010 Dec
TI  - Role of elevated pressure in TRAIL-induced apoptosis in human lung carcinoma 
      cells.
PG  - 1517-28
LID - 10.1007/s10495-010-0525-5 [doi]
AB  - TNF-related apoptosis-inducing ligand (TRAIL, Apo2L) is a promising anticancer 
      agent with high specificity for cancer cells. Many strategies have been proposed 
      to enhance the sensitivity of cancer cells to TRAIL-mediated apoptosis, including 
      the use of combination treatment with conventional cancer therapies. However, few 
      reports have evaluated the effects of TRAIL in combination with mechanical 
      stress, which can also cause apoptosis of cancer cells. In the present study, we 
      describe a custom-designed culture system that delivers two atmospheres of 
      elevated pressure (EP) by using compressed air, and which enhances the 
      sensitivity of cancer cells to TRAIL-mediated apoptosis. The combination of TRAIL 
      and EP significantly increased apoptosis of human H460 lung cancer cells more 
      than hyperbaric normoxia or normobaric mild hyperoxia. EP-potentiating 
      TRAIL-mediated apoptosis of H460 cells was accompanied by up-regulated death 
      receptor 5 (DR5), activation of caspases, decreased mitochondrial membrane 
      potential, and reactive oxygen species production. We also observed EP-induced 
      sensitization of TRAIL-mediated apoptosis in other cancer cell types. In 
      contrast, human normal cells showed no DNA damage or cell death when exposed to 
      the combined treatment. In a chicken chorioallantoic membrane model, EP enhanced 
      TRAIL-mediated apoptosis of tumors that developed from transplanted H460 cells. 
      Collectively, EP enhanced TRAIL-induced apoptosis of human lung carcinoma cells 
      in vitro and in vivo. These findings suggest that EP is a mechanical and 
      physiological stimulus that might have utility as a sensitizing tool for cancer 
      therapy.
FAU - Oh, Sangnam
AU  - Oh S
AD  - Cellular and Developmental Biology, Division of Biomedical Science, Seoul, Korea.
FAU - Kwon, Daeho
AU  - Kwon D
FAU - Lee, Hyun Jeong
AU  - Lee HJ
FAU - Kim, Joonhee
AU  - Kim J
FAU - Lee, Eunil
AU  - Lee E
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Apoptosis
JT  - Apoptosis : an international journal on programmed cell death
JID - 9712129
RN  - 0 (Antineoplastic Agents)
RN  - 0 (Intracellular Signaling Peptides and Proteins)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand)
RN  - 0 (Recombinant Proteins)
RN  - 0 (TNF-Related Apoptosis-Inducing Ligand)
RN  - EC 3.4.22.- (Caspases)
SB  - IM
MH  - Animals
MH  - Antineoplastic Agents/*pharmacology/therapeutic use
MH  - *Apoptosis/drug effects/physiology
MH  - Carcinoma, Non-Small-Cell Lung/drug therapy/metabolism/pathology
MH  - Caspases/metabolism
MH  - Cell Line, Tumor
MH  - Chick Embryo
MH  - Combined Modality Therapy
MH  - Female
MH  - Fetus
MH  - Humans
MH  - Intracellular Signaling Peptides and Proteins/metabolism
MH  - Lung Neoplasms/drug therapy/metabolism/pathology
MH  - Membrane Potential, Mitochondrial/*drug effects/physiology
MH  - Oxidative Stress
MH  - Reactive Oxygen Species/metabolism
MH  - Receptors, TNF-Related Apoptosis-Inducing Ligand/*metabolism
MH  - *Recombinant Proteins/genetics/pharmacology/therapeutic use
MH  - Signal Transduction/drug effects/physiology
MH  - Stress, Mechanical
MH  - *TNF-Related Apoptosis-Inducing Ligand/genetics/pharmacology/therapeutic use
EDAT- 2010/07/14 06:00
MHDA- 2011/03/10 06:00
CRDT- 2010/07/13 06:00
PHST- 2010/07/13 06:00 [entrez]
PHST- 2010/07/14 06:00 [pubmed]
PHST- 2011/03/10 06:00 [medline]
AID - 10.1007/s10495-010-0525-5 [doi]
PST - ppublish
SO  - Apoptosis. 2010 Dec;15(12):1517-28. doi: 10.1007/s10495-010-0525-5.