PMID- 7835777
OWN - NLM
STAT- MEDLINE
DCOM- 19950224
LR  - 20221207
IS  - 0090-8258 (Print)
IS  - 0090-8258 (Linking)
VI  - 55
IP  - 3 Pt 1
DP  - 1994 Dec
TI  - Differential response of cervical intraepithelial and cervical carcinoma cell 
      lines to transforming growth factor-beta 1.
PG  - 376-85
AB  - Transforming growth factor-beta 1 (TGF-beta 1) is a potent inhibitor of 
      epithelial cell proliferation. It has been proposed that loss of sensitivity to 
      growth inhibition by TGF-beta 1 may be an important step in the development of 
      cervical carcinoma, but it remains unclear whether this represents an early or a 
      late event. We compared the sensitivity to TGF-beta 1 of nontumorigenic human 
      papillomavirus deoxyribonucleic acid (HPV DNA)-positive cell lines derived from 
      cervical intraepithelial neoplasia (CIN), of newly established cervical carcinoma 
      cell lines, of nontumorigenic HPV DNA-transfected cervical cell lines, and of 
      normal ectocervical cells. There is a dose-dependent inhibition of DNA synthesis 
      by TGF-beta 1 in the CIN cell lines and the HPV DNA-transfected cell lines. The 
      carcinoma cell lines are resistant to the growth inhibitory effects of TGF-beta 
      1. The CIN cell lines are significantly more sensitive than the carcinoma cell 
      lines (P < 0.001), but significantly less sensitive than normal cervical cells (P 
      < 0.05). A CIN cell line which contains HPV 31b DNA is more sensitive to TGF-beta 
      1 at early passage than at late passage (P < 0.05). There are no differences in 
      the sensitivity to the growth inhibitory effects of TGF-beta 1 between subclones 
      of this cell line that have different episomal HPV DNA content, 
      population-doubling time, or differentiation characteristics. Both normal and 
      abnormal cervical epithelial cells were able to secrete latent TGF-beta 1 or 
      TGF-beta 2. We conclude that resistance to growth inhibition by TGF-beta 1 is 
      likely to be a late event in the development of cervical carcinoma; it is not the 
      mere consequence of immortalization by HPV genes acquired following transfection 
      in vitro or infection in vivo.
FAU - De Geest, K
AU  - De Geest K
AD  - Department of Obstetrics and Gynecology, Rush Medical College, Chicago, Illinois 
      60612.
FAU - Bergman, C A
AU  - Bergman CA
FAU - Turyk, M E
AU  - Turyk ME
FAU - Frank, B S
AU  - Frank BS
FAU - Wilbanks, G D
AU  - Wilbanks GD
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Gynecol Oncol
JT  - Gynecologic oncology
JID - 0365304
RN  - 0 (DNA, Viral)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Animals
MH  - Carcinoma, Squamous Cell/metabolism/*pathology/virology
MH  - Cell Line, Transformed
MH  - Cells, Cultured
MH  - Cervix Uteri/cytology/virology
MH  - DNA, Viral/genetics
MH  - Female
MH  - Humans
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Mice, Nude
MH  - Papillomaviridae/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Transfection
MH  - Transforming Growth Factor beta/biosynthesis/*pharmacology
MH  - Tumor Cells, Cultured/metabolism/pathology/virology
MH  - Uterine Cervical Neoplasms/metabolism/*pathology/virology
MH  - Uterine Cervical Dysplasia/metabolism/*pathology/virology
EDAT- 1994/12/01 00:00
MHDA- 1994/12/01 00:01
CRDT- 1994/12/01 00:00
PHST- 1994/12/01 00:00 [pubmed]
PHST- 1994/12/01 00:01 [medline]
PHST- 1994/12/01 00:00 [entrez]
AID - S0090-8258(84)71310-2 [pii]
AID - 10.1006/gyno.1994.1310 [doi]
PST - ppublish
SO  - Gynecol Oncol. 1994 Dec;55(3 Pt 1):376-85. doi: 10.1006/gyno.1994.1310.