PMID- 22836062
OWN - NLM
STAT- MEDLINE
DCOM- 20130107
LR  - 20211203
IS  - 1879-355X (Electronic)
IS  - 0360-3016 (Linking)
VI  - 84
IP  - 4
DP  - 2012 Nov 15
TI  - Expression of hPNAS-4 radiosensitizes Lewis lung cancer.
PG  - e533-40
LID - S0360-3016(12)00854-1 [pii]
LID - 10.1016/j.ijrobp.2012.06.028 [doi]
AB  - PURPOSE: This study aimed to transfer the hPNAS-4 gene, a novel apoptosis-related 
      human gene, into Lewis lung cancer (LL2) and observe its radiosensitive effect on 
      radiation therapy in vitro and in vivo. METHODS AND MATERIALS: The hPNAS-4 gene 
      was transfected into LL2 cells, and its expression was detected via western blot. 
      Colony formation assay and flow cytometry were used to detect the growth and 
      apoptosis of cells treated with irradiation/PNAS-4 in vitro. The hPNAS-4 gene was 
      transferred into LL2-bearing mice through tail vein injection of the 
      liposome/gene complex. The tumor volumes were recorded after radiation therapy. 
      Proliferating cell nuclear antigen (PCNA) immunohistochemistry staining and 
      terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) 
      assay were performed to detect the tumor cell growth and apoptosis in vivo. 
      RESULTS: The hPNAS-4 gene was successfully transferred into LL2 cells and tumor 
      tissue, and its overexpressions were confirmed via western blot analysis. 
      Compared with the control, empty plasmid, hPNAS-4, radiation, and empty plasmid 
      plus radiation groups, the hPNAS-4 plus radiation group more significantly 
      inhibited growth and enhanced apoptosis of LL2 cells in vitro and in vivo 
      (P<.05). CONCLUSIONS: The hPNAS-4 gene was successfully transferred into LL2 
      cells and tumor tissue and was expressed in both LL2 cell and tumor tissue. The 
      hPNAS-4 gene therapy significantly enhanced growth inhibition and apoptosis of 
      LL2 tumor cells by radiation therapy in vitro and in vivo. Therefore, it may be a 
      potential radiosensitive treatment of radiation therapy for lung cancer.
CI  - Copyright (c) 2012 Elsevier Inc. All rights reserved.
FAU - Zeng, Hui
AU  - Zeng H
AD  - Department of Radiation Oncology, Cancer Center, West China Hospital, Sichuan 
      University, Chengdu, Sichuan Province, China.
FAU - Yuan, Zhu
AU  - Yuan Z
FAU - Zhu, Hong
AU  - Zhu H
FAU - Li, Lei
AU  - Li L
FAU - Shi, Huashan
AU  - Shi H
FAU - Wang, Zi
AU  - Wang Z
FAU - Fan, Yu
AU  - Fan Y
FAU - Deng, Qian
AU  - Deng Q
FAU - Zeng, Jianshuang
AU  - Zeng J
FAU - He, Yinbo
AU  - He Y
FAU - Xiao, Jianghong
AU  - Xiao J
FAU - Li, Zhiping
AU  - Li Z
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120724
PL  - United States
TA  - Int J Radiat Oncol Biol Phys
JT  - International journal of radiation oncology, biology, physics
JID - 7603616
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Neoplasm Proteins)
RN  - 0 (RNA, Small Interfering)
RN  - EC 4.3.- (Carbon-Nitrogen Lyases)
RN  - EC 4.3.- (DESI2 protein, human)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Apoptosis Regulatory Proteins/genetics/*metabolism
MH  - Carbon-Nitrogen Lyases
MH  - Carcinoma, Lewis Lung/*metabolism/pathology/*therapy
MH  - Cell Line, Tumor
MH  - Female
MH  - Flow Cytometry
MH  - Humans
MH  - In Situ Nick-End Labeling/methods
MH  - Lung Neoplasms/*metabolism/pathology/*therapy
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neoplasm Proteins/genetics/*metabolism
MH  - RNA, Small Interfering/pharmacology
MH  - Random Allocation
MH  - Transfection/methods
MH  - Tumor Burden
MH  - Tumor Stem Cell Assay
EDAT- 2012/07/28 06:00
MHDA- 2013/01/08 06:00
CRDT- 2012/07/28 06:00
PHST- 2011/12/21 00:00 [received]
PHST- 2012/06/01 00:00 [revised]
PHST- 2012/06/15 00:00 [accepted]
PHST- 2012/07/28 06:00 [entrez]
PHST- 2012/07/28 06:00 [pubmed]
PHST- 2013/01/08 06:00 [medline]
AID - S0360-3016(12)00854-1 [pii]
AID - 10.1016/j.ijrobp.2012.06.028 [doi]
PST - ppublish
SO  - Int J Radiat Oncol Biol Phys. 2012 Nov 15;84(4):e533-40. doi: 
      10.1016/j.ijrobp.2012.06.028. Epub 2012 Jul 24.