PMID- 8772229
OWN - NLM
STAT- MEDLINE
DCOM- 19961023
LR  - 20081121
IS  - 0340-6245 (Print)
IS  - 0340-6245 (Linking)
VI  - 74
IP  - 6
DP  - 1995 Dec
TI  - Modulation of urokinase-type plasminogen activator gene expression by 
      inflammatory cytokines in human pre-B lymphoma cell line RC-K8.
PG  - 1511-5
AB  - We examined the effects of inflammatory cytokines, such as interleukin-1 alpha 
      (IL-1 alpha), interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6), tumor 
      necrosis factor-alpha (TNF alpha), transforming growth factor-beta (TGF beta) and 
      lipopolysaccharide (LPS), on the urokinase-type plasminogen activator (uPA) gene 
      expression in RC-K8 human pre-B lymphoma cells. Recombinant IL-1 alpha, 
      recombinant IL-1 beta and LPS but not recombinant IL-6, recombinant TNF alpha and 
      TGF beta dose-dependently increased uPA accumulation in the conditioned medium. 
      Northern blot analysis revealed that uPA mRNA levels rapidly increased with a 
      peak induction at 2 h after stimulation with IL-1 alpha and IL- 1 beta, but uPA 
      mRNA increase by LPS began at 9 h after stimulation and the increase was 
      maintained until the experiment ended at 24 h. These responses were independent 
      of de novo synthesis, rather amplified in the presence of a protein synthesis 
      inhibitor. The effects by IL-1 alpha and Il-1 beta were prevented by addition of 
      anti-IL-1 alpha and anti-IL-1 beta neutralizing antibodies, respectively. In 
      contrast, both antibodies did not prevent LPS-induced uPA gene expression. 
      Therefore, it is unlikely that the effect by LPS is through induction of IL-1. 
      Both IL-1 alpha and IL- 1 beta rapidly activated uPA gene transcription, but not 
      increased stability of uPA mRNA. These results suggest that both IL-1 alpha and 
      IL-1 beta cause a rapid activation of uPA gene transcription in which de novo 
      protein synthesis is not required and that LPS induces uPA gene expression 
      independently of the IL-1 pathway. These modulations of uPA production by 
      inflammatory mediators may be implicated in tumor growth and metastasis.
FAU - Niiya, K
AU  - Niiya K
AD  - Department of Clinical Laboratory Medicine, Faculty of Medicine, Toyama Medical 
      and Pharmaceutical University, Japan.
FAU - Shinbo, M
AU  - Shinbo M
FAU - Ozawa, T
AU  - Ozawa T
FAU - Hayakawa, Y
AU  - Hayakawa Y
FAU - Sakuragawa, N
AU  - Sakuragawa N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Germany
TA  - Thromb Haemost
JT  - Thrombosis and haemostasis
JID - 7608063
RN  - 0 (Cytokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator)
SB  - IM
MH  - Antigen-Antibody Reactions
MH  - Cells, Cultured
MH  - Cytokines/*pharmacology
MH  - Gene Expression Regulation, Enzymologic/*drug effects
MH  - Gene Expression Regulation, Neoplastic/*drug effects
MH  - Humans
MH  - Interleukin-1/pharmacology
MH  - Interleukin-6/pharmacology
MH  - Lipopolysaccharides/pharmacology
MH  - Lymphoma, B-Cell/*metabolism
MH  - Precancerous Conditions/*metabolism
MH  - Transforming Growth Factor beta/pharmacology
MH  - Tumor Cells, Cultured
MH  - Tumor Necrosis Factor-alpha/pharmacology
MH  - Urokinase-Type Plasminogen Activator/*genetics
EDAT- 1995/12/01 00:00
MHDA- 1995/12/01 00:01
CRDT- 1995/12/01 00:00
PHST- 1995/12/01 00:00 [pubmed]
PHST- 1995/12/01 00:01 [medline]
PHST- 1995/12/01 00:00 [entrez]
PST - ppublish
SO  - Thromb Haemost. 1995 Dec;74(6):1511-5.