PMID- 10484044
OWN - NLM
STAT- MEDLINE
DCOM- 19990928
LR  - 20190725
IS  - 0026-0495 (Print)
IS  - 0026-0495 (Linking)
VI  - 48
IP  - 9
DP  - 1999 Sep
TI  - Transforming growth factor beta-1 and beta-2 and type II receptor functional 
      regulation of ALVA-101 human prostate cancer cells.
PG  - 1075-81
AB  - Transforming growth factor beta-1 (TGFbeta-1) causes apoptosis of many epithelial 
      cells, including the prostate, but other secondary effects of TGFbeta-1 may be 
      important in carcinogenesis. In a human prostate cancer cell line (ALVA-101), we 
      determined the effects of TGFbeta-1 and TGFbeta type I and II receptor antibody 
      on cell proliferation and TGFbeta-1 receptor binding. TGFbeta-1 and -2 and 
      TGFbeta type II receptor mRNA expression levels were determined by polymerase 
      chain reaction (PCR) and Northern blot analysis. A dose-responsive suppression 
      (0.03 to 10 ng/mL) was observed for cells treated with TGFbeta-1 from 3 to 7 days 
      (P < .01). Untreated cells had 1.1 x 10(3) (n = 3) TGFbeta receptors per cell, 
      with a Kd of 0.20 nmol/L (n = 3) as determined by Scatchard analysis; treatment 
      for 3 days with TGFbeta-1 (1 ng/mL) reduced the receptor number (0.9 x 10(3)) and 
      the Kd (0.12 nmol/L). Antibodies to TGFbeta type I and II receptor stimulated 
      proliferation with or without added TGFbeta-1 (50% +/- 5% above control, P < .01, 
      n = 6). TGFbeta-1 and -2 and TGFbeta type II receptor mRNA expression was 
      observed in untreated cells. In cells treated with TGFbeta-1, TGFbeta-1 mRNA was 
      not affected by treatment, but expression levels of the TGFbeta type II receptor 
      and TGFbeta-2 mRNA were moderately suppressed after 72 hours of treatment. 
      Control cells actively produced TGFbeta-1 as measured by radioimmunoassay. The 
      active and inactive forms of TGFbeta-1 were approximately equal, but TGFbeta-2 
      was secreted in smaller quantities than TGFbeta-1 and the inactive form of 
      TGFbeta-2 predominated, with very small amounts of the active form. Our results 
      suggest that the human prostate cancer cell line ALVA-101 retains negative 
      control of proliferation in response to TGFbeta-1. Inhibition of endogenous 
      TGFbeta action by antibodies to its receptor enhances the growth of ALVA-101 
      human prostate cancer cells, suggesting that endogenous TGFbeta exerts an 
      inhibitory control on their growth and cellular function.
FAU - Meikle, A W
AU  - Meikle AW
AD  - Department of Medicine and Pathology, University of Utah School of Medicine, Salt 
      Lake City 84132, USA.
FAU - Swope, R E
AU  - Swope RE
FAU - Yin, D Y
AU  - Yin DY
FAU - Fullmer, D
AU  - Fullmer D
FAU - Loop, S M
AU  - Loop SM
FAU - Murray, D K
AU  - Murray DK
LA  - eng
GR  - DK-43344/DK/NIDDK NIH HHS/United States
GR  - R01 DK-45760/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Metabolism
JT  - Metabolism: clinical and experimental
JID - 0375267
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Cell Division/drug effects
MH  - Gene Expression Regulation, Neoplastic/*drug effects
MH  - Humans
MH  - Male
MH  - Prostatic Neoplasms
MH  - Protein Binding/drug effects
MH  - RNA, Messenger/metabolism
MH  - Receptors, Transforming Growth Factor beta/*metabolism
MH  - Transforming Growth Factor beta/metabolism/*pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1999/09/14 00:00
MHDA- 1999/09/14 00:01
CRDT- 1999/09/14 00:00
PHST- 1999/09/14 00:00 [pubmed]
PHST- 1999/09/14 00:01 [medline]
PHST- 1999/09/14 00:00 [entrez]
AID - S0026-0495(99)90118-X [pii]
AID - 10.1016/s0026-0495(99)90118-x [doi]
PST - ppublish
SO  - Metabolism. 1999 Sep;48(9):1075-81. doi: 10.1016/s0026-0495(99)90118-x.