PMID- 7850789
OWN - NLM
STAT- MEDLINE
DCOM- 19950314
LR  - 20131121
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 55
IP  - 4
DP  - 1995 Feb 15
TI  - Beta-2 microglobulin is mitogenic to PC-3 prostatic carcinoma cells and 
      antagonistic to transforming growth factor beta 1 action.
PG  - 781-6
AB  - Previous studies have identified a M(r) 12,000 protein in rat prostatic stromal 
      cell-conditioned medium with growth stimulatory activity to human prostatic 
      carcinoma cells as a direct match with beta 2-microglobulin (beta 2-m). The 
      present study was conducted to characterize the activities of human beta 2-m 
      directly, using commercially available, purified human beta 2-m. Beta 2-m was 
      assayed for growth stimulatory activity to human PC-3 prostatic carcinoma cells 
      and rat PS-1 prostatic stromal cells and for antagonistic activity to 
      transforming growth factor beta 1 (TGF-beta 1)-induced growth inhibitory actions. 
      Beta 2-m acted to stimulate [3H]thymidine incorporation in PC-3 cells in a 
      linear, concentration-dependent and saturable manner in serum-free medium. Beta 
      2-m stimulated cell proliferation and significantly decreased population doubling 
      times in both PC-3 and PS-1 cell lines. At half-maximal concentrations of 
      TGF-beta 1 and lower, beta 2-m acted in a concentration-dependent, antagonistic 
      manner, acting to stimulate growth-inhibited PC-3 cells to fully neutralize 
      TGF-B1 activity. In contrast, cells exposed to maximum activity TGF-beta 1 
      concentrations were refractory to beta 2-m action, regardless of the 
      concentration tested. This represents the first report to demonstrate a 
      growth-stimulatory activity of B2-m with carcinoma/epithelial cells and to show 
      beta 2-m antagonistic activity to TGF-B1 growth-induced inhibition. Beta 2-m has 
      been shown previously to associate with hormone/growth factor receptors. 
      Together, these data suggest that beta 2-m may play a role in modulating cell 
      proliferation, possibly through modification of ligand/receptor kinetics. Owing 
      to the elevation of both beta 2-m and TGF-beta 1 in many dysplastic-neoplastic 
      conditions, beta 2-m may be relevant to mechanisms of abnormal proliferation 
      disorders and in modulating TGF-beta 1 mechanisms of actions.
FAU - Rowley, D R
AU  - Rowley DR
AD  - Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030.
FAU - Dang, T D
AU  - Dang TD
FAU - McBride, L
AU  - McBride L
FAU - Gerdes, M J
AU  - Gerdes MJ
FAU - Lu, B
AU  - Lu B
FAU - Larsen, M
AU  - Larsen M
LA  - eng
GR  - CA58093/CA/NCI NIH HHS/United States
GR  - DK45909/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Cancer Res
JT  - Cancer research
JID - 2984705R
RN  - 0 (Culture Media)
RN  - 0 (Mitogens)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (beta 2-Microglobulin)
RN  - 10028-17-8 (Tritium)
RN  - VC2W18DGKR (Thymidine)
SB  - IM
MH  - Cell Division/drug effects
MH  - Culture Media
MH  - Humans
MH  - Kinetics
MH  - Male
MH  - Mitogens/*pharmacology
MH  - Prostate/cytology/drug effects
MH  - Prostatic Neoplasms/*pathology
MH  - Stimulation, Chemical
MH  - Stromal Cells/cytology/drug effects
MH  - Thymidine/metabolism
MH  - Transforming Growth Factor beta/*antagonists & inhibitors/pharmacology/physiology
MH  - Tritium
MH  - Tumor Cells, Cultured/drug effects
MH  - beta 2-Microglobulin/*pharmacology
EDAT- 1995/02/15 00:00
MHDA- 1995/02/15 00:01
CRDT- 1995/02/15 00:00
PHST- 1995/02/15 00:00 [pubmed]
PHST- 1995/02/15 00:01 [medline]
PHST- 1995/02/15 00:00 [entrez]
PST - ppublish
SO  - Cancer Res. 1995 Feb 15;55(4):781-6.