PMID- 7585526
OWN - NLM
STAT- MEDLINE
DCOM- 19951206
LR  - 20211203
IS  - 0008-5472 (Print)
IS  - 0008-5472 (Linking)
VI  - 55
IP  - 21
DP  - 1995 Nov 1
TI  - Reduction in the expression and action of transforming growth factor beta 1 on 
      lactotropes during estrogen-induced tumorigenesis in the anterior pituitary.
PG  - 4892-8
AB  - We have previously shown that transforming growth factor beta 1 (TGF-beta 1) 
      receptor and TGF-beta type II receptor (T beta R-II) are produced in lactotropes, 
      and that TGF-beta 1 inhibits the growth of these anterior pituitary cells by an 
      autocrine mechanism. To study the changes of the expression and function of this 
      growth factor during tumorigenesis, we have measured the levels of TGF-beta 1 and 
      T beta R-II mRNAs and proteins in the normal and tumor anterior pituitary cells 
      in vivo and in vitro and have compared the cell growth responses to TGF-beta 1 in 
      normal and tumor pituitary cells in vitro. Treatment with estradiol-17 beta for 
      1, 2, 4, and 8 weeks caused a time-dependent increase in pituitary protein, 
      prolactin, and prolactin mRNA levels and in plasma prolactin levels, suggesting 
      that estrogen enhanced lactotropic proliferation in anterior pituitary glands. 
      The levels of TGF-beta 1 protein and mRNA in anterior pituitary tissues were 
      reduced over time after estrogen treatment during the development of pituitary 
      tumors. The mRNA and protein levels of T beta R-II decreased markedly during the 
      development of pituitary tumors. In addition, two transformed lactotropes, GH3 
      and PR1 cell lines, showed markedly reduced levels of TGF-beta 1 as well as T 
      beta R-II mRNA. Comparison of the antiproliferative effects of TGF-beta in 
      transformed and normal lactotropes in cultures revealed that the sensitivity of 
      GH3 cells is reduced, and that PR1 cells are virtually resistant to TGF-beta 
      1.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Pastorcic, M
AU  - Pastorcic M
AD  - Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, 
      Washington State University, College of Veterinary Medicine, Pullman 99164-6520, 
      USA.
FAU - De, A
AU  - De A
FAU - Boyadjieva, N
AU  - Boyadjieva N
FAU - Vale, W
AU  - Vale W
FAU - Sarkar, D K
AU  - Sarkar DK
LA  - eng
GR  - CA 56056/CA/NCI NIH HHS/United States
PT  - Comparative Study
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 (RNA, Messenger)
RN  - 0 (Receptors, Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta)
RN  - 4TI98Z838E (Estradiol)
RN  - 9002-62-4 (Prolactin)
RN  - EC 2.7.11.1 (Protein Serine-Threonine Kinases)
RN  - EC 2.7.11.30 (Receptor, Transforming Growth Factor-beta Type II)
SB  - IM
MH  - Animals
MH  - Cell Division/drug effects
MH  - Cell Line, Transformed
MH  - Estradiol/*toxicity
MH  - Female
MH  - Pituitary Gland, Anterior/cytology/*drug effects/*metabolism
MH  - Pituitary Neoplasms/*chemically induced/*metabolism/pathology
MH  - Prolactin/*metabolism/pharmacology
MH  - Protein Serine-Threonine Kinases
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Inbred F344
MH  - Receptor, Transforming Growth Factor-beta Type II
MH  - Receptors, Transforming Growth Factor beta/metabolism
MH  - Transforming Growth Factor beta/biosynthesis/pharmacology/*physiology
MH  - Tumor Cells, Cultured
EDAT- 1995/11/01 00:00
MHDA- 1995/11/01 00:01
CRDT- 1995/11/01 00:00
PHST- 1995/11/01 00:00 [pubmed]
PHST- 1995/11/01 00:01 [medline]
PHST- 1995/11/01 00:00 [entrez]
PST - ppublish
SO  - Cancer Res. 1995 Nov 1;55(21):4892-8.