PMID- 21278918
OWN - NLM
STAT- MEDLINE
DCOM- 20110624
LR  - 20240511
IS  - 1449-2288 (Electronic)
IS  - 1449-2288 (Linking)
VI  - 7
IP  - 1
DP  - 2011 Jan 18
TI  - Lipocalin-2-induced cytokine production enhances endometrial carcinoma cell 
      survival and migration.
PG  - 74-86
AB  - Lipocalin-2 (Lcn-2) is an acute-phase protein that has been implicated in diverse 
      physiological processes in mice, including: apoptosis, ion transport, 
      inflammation, cell survival, and tumorigenesis. This study characterized the 
      biological activity of Lcn-2 in human endometrial carcinoma cells (RL95-2). 
      Exposure of RL95-2 cells to Lcn-2 for >24 h reduced Lcn-2-induced cell apoptosis, 
      changed the cell proliferation and up-regulated cytokine secretions, including: 
      interleukin-8 (IL-8), inteleukin-6 (IL-6), monocyte chemotatic protein-1 (MCP-1) 
      and growth-related oncogene (GRO). However, IL-8 mRNA and protein levels were 
      dramatically increased in Lcn-2-treated RL95-2 cells. To determine the IL-8 
      effect on Lcn-2-treated RL95-2 cells was our major focus. Adding recombinant IL-8 
      (rIL-8) resulted in decreased caspase-3 activity in Lcn-2-treated cells, whereas 
      the addition of IL-8 antibodies resulted in significantly increased caspase-3 
      activity and decreased cell migration. Data indicate that IL-8 plays a crucial 
      role in the induction of cell migration. Interestingly, Lcn-2-induced cytokines, 
      secretion from RL95-2 cells, could not show the potent cell migration ability 
      with the exception of IL-8. We conclude that Lcn-2 triggered cytokine secretions 
      to prevent RL95-2 cells from undergoing apoptosis and subsequently increased cell 
      migration. We hypothesize that Lcn-2 increased cytokine secretion by RL95-2 
      cells, which in turn activated a cellular defense system. This study suggests 
      that Lcn-2 may play a role in the human female reproductive system or in 
      endometrial cancer.
FAU - Lin, Hsiu-Hsia
AU  - Lin HH
AD  - Institute of Biochemical Science, College of Life Science, National Taiwan 
      University, Taiwan.
FAU - Liao, Chi-Jr
AU  - Liao CJ
FAU - Lee, Ying-Chu
AU  - Lee YC
FAU - Hu, Keng-Hsun
AU  - Hu KH
FAU - Meng, Hsien-Wei
AU  - Meng HW
FAU - Chu, Sin-Tak
AU  - Chu ST
LA  - eng
PT  - Journal Article
DEP - 20110118
PL  - Australia
TA  - Int J Biol Sci
JT  - International journal of biological sciences
JID - 101235568
RN  - 0 (Acute-Phase Proteins)
RN  - 0 (Culture Media, Conditioned)
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-8)
RN  - 0 (LCN2 protein, human)
RN  - 0 (Lipocalin-2)
RN  - 0 (Lipocalins)
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (RNA, Messenger)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Acute-Phase Proteins/*pharmacology/physiology
MH  - Apoptosis
MH  - Carcinoma/*metabolism/pathology
MH  - Caspase 3/metabolism
MH  - Cell Line, Tumor
MH  - Cell Movement/drug effects/physiology
MH  - Cell Proliferation
MH  - Cell Survival/drug effects/physiology
MH  - Culture Media, Conditioned
MH  - Cytokines/*biosynthesis
MH  - Endometrial Neoplasms/*metabolism/pathology
MH  - Female
MH  - Humans
MH  - Interleukin-8/metabolism/pharmacology
MH  - Lipocalin-2
MH  - Lipocalins/*pharmacology/physiology
MH  - Proto-Oncogene Proteins/*pharmacology/physiology
MH  - RNA, Messenger/metabolism
PMC - PMC3030144
OTO - NOTNLM
OT  - apoptosis
OT  - cellular defense
OT  - cytokine secretion
OT  - endometrial carcinoma cells
COIS- Conflict of Interests: The authors have declared that no conflict of interest 
      exists.
EDAT- 2011/02/01 06:00
MHDA- 2011/06/28 06:00
PMCR- 2011/01/01
CRDT- 2011/02/01 06:00
PHST- 2010/09/22 00:00 [received]
PHST- 2011/01/11 00:00 [accepted]
PHST- 2011/02/01 06:00 [entrez]
PHST- 2011/02/01 06:00 [pubmed]
PHST- 2011/06/28 06:00 [medline]
PHST- 2011/01/01 00:00 [pmc-release]
AID - ijbsv07p0074 [pii]
AID - 10.7150/ijbs.7.74 [doi]
PST - epublish
SO  - Int J Biol Sci. 2011 Jan 18;7(1):74-86. doi: 10.7150/ijbs.7.74.