PMID- 23708314
OWN - NLM
STAT- MEDLINE
DCOM- 20140107
LR  - 20130604
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Linking)
VI  - 8
IP  - 1
DP  - 2013 Jul
TI  - Conditionally replicating adenovirus combined with gene-targeted radiotherapy 
      induces apoptosis via TRAIL death receptors in MDA-MB-231 cells.
PG  - 299-305
LID - 10.3892/mmr.2013.1488 [doi]
AB  - Malignant tumors are usually treated using monotherapies, which are not always 
      effective. Therefore, combination therapies have gained increasing attention. The 
      aims of this study were to investigate the effects of conditionally replicating 
      adenovirus (CRAd) in combination with X-ray irradiation on the proliferation and 
      apoptosis of MDA-MB-231 cells, as well as to determine the molecular mechanisms 
      involved. MDA-MB-231 cells were treated simultaneously with CRAd and X-ray 
      irradiation. Then, cell viability was measured using Cell Counting Kit-8. Cell 
      apoptosis was assessed by flow cytometry with Annexin V and propidium iodide (PI) 
      double-staining. The expression of tumor necrosis factor (TNF)-related apoptosis 
      inducing ligand (TRAIL), death receptor 5 (DR5), caspase-3 and caspase-8 mRNA was 
      detected by quantitative polymerase chain reaction. The expression of TRAIL, DR5, 
      caspase-3 and caspase-8 protein was measured by enzyme-linked immunosorbent assay 
      (ELISA) and western blotting, respectively. The results showed that CRAd, in 
      combination with irradiation, inhibited cell proliferation, promoted cell 
      apoptosis and significantly increased the expression of TRAIL, DR5, caspase-3 and 
      caspase-8 mRNA and proteins in MDA-MB-231 cells. Therefore, three aspects, 
      including the targeted killing effect of CRAd, the apoptosis-promoting role of 
      TRAIL and the direct killing effect of ionizing radiation to MDA-MB-231 cells, 
      contribute to the mechanisms of CRAd in combination with irradiation to inhibit 
      the proliferation of MDA-MB-231 cells. The pro-apoptotic effect may involve the 
      interaction between TRAIL, DR5, caspase-3 and caspase-8.
FAU - Wu, Jia Hui
AU  - Wu JH
AD  - Key Laboratory of Radiobiology, Ministry of Health, School of Public Health, 
      Jilin University, Changchun, Jilin 130021, PR China.
FAU - Wang, Hong Fang
AU  - Wang HF
FAU - Wang, Zhi Cheng
AU  - Wang ZC
FAU - Xu, Kai
AU  - Xu K
FAU - Qi, Ya Li
AU  - Qi YL
FAU - Li, Jin Hua
AU  - Li JH
FAU - Gong, Shou Liang
AU  - Gong SL
FAU - Liu, Yang
AU  - Liu Y
FAU - Liu, Ya
AU  - Liu Y
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130523
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (Early Growth Response Protein 1)
RN  - 0 (Receptors, TNF-Related Apoptosis-Inducing Ligand)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspase 8)
SB  - IM
MH  - Adenoviridae/*genetics
MH  - Apoptosis/*genetics/*radiation effects
MH  - Caspase 3/genetics/metabolism
MH  - Caspase 8/genetics/metabolism
MH  - Cell Line, Tumor
MH  - Early Growth Response Protein 1/genetics
MH  - Gene Expression
MH  - Genetic Therapy
MH  - Genetic Vectors/*genetics
MH  - Humans
MH  - Promoter Regions, Genetic
MH  - Radiation
MH  - Radiotherapy
MH  - Receptors, TNF-Related Apoptosis-Inducing Ligand/*genetics
EDAT- 2013/05/28 06:00
MHDA- 2014/01/08 06:00
CRDT- 2013/05/28 06:00
PHST- 2013/01/16 00:00 [received]
PHST- 2013/05/20 00:00 [accepted]
PHST- 2013/05/28 06:00 [entrez]
PHST- 2013/05/28 06:00 [pubmed]
PHST- 2014/01/08 06:00 [medline]
AID - 10.3892/mmr.2013.1488 [doi]
PST - ppublish
SO  - Mol Med Rep. 2013 Jul;8(1):299-305. doi: 10.3892/mmr.2013.1488. Epub 2013 May 23.