PMID- 23232551
OWN - NLM
STAT- MEDLINE
DCOM- 20140107
LR  - 20211021
IS  - 1791-2423 (Electronic)
IS  - 1019-6439 (Print)
IS  - 1019-6439 (Linking)
VI  - 42
IP  - 2
DP  - 2013 Feb
TI  - Ligation of CM1 enhances apoptosis of lung cancer cells through different 
      mechanisms in conformity with EGFR mutation.
PG  - 469-77
LID - 10.3892/ijo.2012.1731 [doi]
AB  - Although remarkable developments in lung cancer treatments have been made, lung 
      cancer remains the leading cause of cancer mortality worldwide. Epidermal growth 
      factor receptor (EGFR) is occasionally mutated in non-small cell lung cancer and 
      heterogeneity in treatment response results from different EGFR mutations. In the 
      present study, we found that centrocyte/centroblast marker 1 (CM1), previously 
      reported as a possible apoptosis inducer of B lymphoma cells, is expressed on 
      both A549 with wild‑type EGFR and HCC827 with mutant EGFR lung cancer cells. 
      Ligation of CM1 with anti-CM1 mAb enhanced apoptosis in both lung cancer cell 
      lines through generation of reactive oxygen species (ROS) and disruption of 
      mitochondrial membrane potential, however, the signaling mechanisms differed from 
      each other. Further studies to investigate the signaling mechanisms identified 
      that ligation of CM1‑induced apoptosis in A549 cell involved FasL expression, 
      caspase-8, ERK1/2 and Akt kinase, whereas apoptosis of HCC827 cells was induced 
      through caspase-9, JNK and c-jun‑dependent pathways. Taken together, we suggest 
      that CM1 could be developed as a therapeutic target of lung cancer regardless of 
      EGFR mutation status.
FAU - Lee, Hyun-Kyung
AU  - Lee HK
AD  - Department of Internal Medicine, Inje University Busan Paik Hospital, Busan 
      614-735, Republic of Korea.
FAU - Park, Ga Bin
AU  - Park GB
FAU - Kim, Yeong Seok
AU  - Kim YS
FAU - Song, Hyunkeun
AU  - Song H
FAU - Broaddus, V Courtney
AU  - Broaddus VC
FAU - Hur, Dae Young
AU  - Hur DY
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121207
PL  - Greece
TA  - Int J Oncol
JT  - International journal of oncology
JID - 9306042
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (centrocyte centroblast marker 1 protein, human)
RN  - EC 2.7.10.1 (EGFR protein, human)
RN  - EC 2.7.10.1 (ErbB Receptors)
SB  - IM
MH  - Antibodies, Monoclonal/pharmacology
MH  - Apoptosis/*genetics
MH  - Apoptosis Regulatory Proteins/*genetics
MH  - Carcinoma, Non-Small-Cell Lung
MH  - Cell Line, Tumor
MH  - ErbB Receptors/*genetics/metabolism
MH  - Germinal Center/cytology/metabolism
MH  - Humans
MH  - Lung Neoplasms/*genetics/pathology
MH  - Mutation
MH  - Reactive Oxygen Species/metabolism
PMC - PMC3583643
EDAT- 2012/12/13 06:00
MHDA- 2014/01/08 06:00
PMCR- 2012/12/07
CRDT- 2012/12/13 06:00
PHST- 2012/10/02 00:00 [received]
PHST- 2012/11/23 00:00 [accepted]
PHST- 2012/12/13 06:00 [entrez]
PHST- 2012/12/13 06:00 [pubmed]
PHST- 2014/01/08 06:00 [medline]
PHST- 2012/12/07 00:00 [pmc-release]
AID - ijo-42-02-0469 [pii]
AID - 10.3892/ijo.2012.1731 [doi]
PST - ppublish
SO  - Int J Oncol. 2013 Feb;42(2):469-77. doi: 10.3892/ijo.2012.1731. Epub 2012 Dec 7.