PMID- 7925100
OWN - NLM
STAT- MEDLINE
DCOM- 19941024
LR  - 20041117
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 135
IP  - 4
DP  - 1994 Oct
TI  - Correlation between suppression of c-myc and antiproliferative effect of 
      transforming growth factor-beta 1 in thyroid carcinoma cell growth.
PG  - 1378-84
AB  - The growth regulatory activity of transforming growth factor-beta 1 (TGF beta 1) 
      was studied in a clonal strain of thyroid papillary carcinoma cell (NPA). Despite 
      the presence of TGF beta 1 and its receptor messenger RNA in thyroid carcinoma, 
      the molecular mechanism of TGF beta 1 action on cell growth of thyroid carcinoma 
      has not yet been elucidated. Exogenously added TGF beta 1 inhibited DNA synthesis 
      and cell growth in a dose- and time-dependent manner at concentrations of 0.1-10 
      ng/ml. TGF beta 1 inhibited not only basal but also fetal bovine serum-stimulated 
      cell proliferation. Steady state levels of c-myc messenger RNA transcripts were 
      inhibited by TGF beta 1 after 0.5-h treatment. Antisense, but not sense, c-myc 
      oligodeoxynucleotides also caused suppression of NPA cell growth in a 
      dose-responsive manner. Transfection studies of the 5'-up-stream flanking region 
      (UFR) of c-myc/chloramphenicol acetyltransferase chimera genes suggest the 
      presence of a TGF beta 1-responsive DNA element in the 2.3-kilobase c-myc 5'-UFR. 
      Deletion mutant studies indicate the element lies between -106 to 70 relative to 
      the P1 transcription start site. Studies with the gel mobility shift assay using 
      23-basepair double strand DNA showed the presence of at least two nuclear factors 
      in NPA cell. TGF beta 1 treatment did not cause any alteration in TGF beta 
      1-induced mobility; however, the reduction of a positive band was selectively 
      observed during 30 min to 2 h after treatment with TGF beta 1. In contrast, the 
      position and intensity of another band were not altered by TGF beta 1 treatment. 
      These results demonstrate that the inhibition of a nuclear factor binding to the 
      c-myc 5'-UFR and subsequent suppression of c-myc gene expression are directly 
      involved in the antiproliferative action of TGF beta 1 in NPA cell growth.
FAU - Usa, T
AU  - Usa T
AD  - Department of Cell Physiology, Nagasaki University School of Medicine, Japan.
FAU - Tsukazaki, T
AU  - Tsukazaki T
FAU - Namba, H
AU  - Namba H
FAU - Ohtsuru, A
AU  - Ohtsuru A
FAU - Kimura, H
AU  - Kimura H
FAU - Villadolid, M C
AU  - Villadolid MC
FAU - Nagataki, S
AU  - Nagataki S
FAU - Yamashita, S
AU  - Yamashita S
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Cytokines)
RN  - 0 (DNA, Neoplasm)
RN  - 0 (Oligonucleotides, Antisense)
RN  - 0 (RNA, Messenger)
RN  - 0 (Transforming Growth Factor beta)
RN  - 9002-71-5 (Thyrotropin)
RN  - EC 2.3.1.28 (Chloramphenicol O-Acetyltransferase)
SB  - IM
GS  - c-myc
MH  - Base Sequence
MH  - Blotting, Northern
MH  - Carcinoma, Papillary/*genetics/*pathology/physiopathology
MH  - Cell Count
MH  - Cell Division/drug effects
MH  - Chloramphenicol O-Acetyltransferase/metabolism
MH  - Cytokines/physiology
MH  - DNA, Neoplasm/analysis/genetics
MH  - Dose-Response Relationship, Drug
MH  - Down-Regulation/drug effects/physiology
MH  - Enzyme Activation/drug effects/physiology
MH  - Genes, myc/*genetics
MH  - Humans
MH  - Molecular Sequence Data
MH  - Oligonucleotides, Antisense/pharmacology
MH  - RNA, Messenger/analysis/genetics
MH  - Suppression, Genetic/*drug effects/physiology
MH  - Thyroid Neoplasms/*genetics/*pathology/physiopathology
MH  - Thyrotropin/physiology
MH  - Time Factors
MH  - Transfection
MH  - Transforming Growth Factor beta/*pharmacology
MH  - Tumor Cells, Cultured
EDAT- 1994/10/01 00:00
MHDA- 1994/10/01 00:01
CRDT- 1994/10/01 00:00
PHST- 1994/10/01 00:00 [pubmed]
PHST- 1994/10/01 00:01 [medline]
PHST- 1994/10/01 00:00 [entrez]
AID - 10.1210/endo.135.4.7925100 [doi]
PST - ppublish
SO  - Endocrinology. 1994 Oct;135(4):1378-84. doi: 10.1210/endo.135.4.7925100.