PMID- 10210318
OWN - NLM
STAT- MEDLINE
DCOM- 19990614
LR  - 20191024
IS  - 0301-472X (Print)
IS  - 0301-472X (Linking)
VI  - 27
IP  - 4
DP  - 1999 Apr
TI  - Transforming growth factor beta inhibits growth of more differentiated myeloid
      leukemia cells and retinoblastoma protein phosphorylation at serine 795.
PG  - 605-14
AB  - Transforming growth factor beta (TGF-beta) has been shown to be a specific
      inhibitor of early human myeloid progenitors. We show here that TGF-beta1
      potentially inhibited not only the growth of primitive but also more mature
      myeloid leukemic cells. Surprisingly, those apparently more mature progenitor
      cells, such as MV4-11 and Mo7e cells, are very sensitive to the action of
      TGF-beta. The addition of TGF-beta1 to liquid cultures of these cells
      significantly inhibited their proliferation, with as much as 72% inhibition of
      growth of MV4-11 cells. The suppressive effect by TGF-beta1 was not reversed or
      prevented by granulocyte-macrophage colony-stimulating factor or interleukin 3
      used to promote cell growth in TF-1a and MV4-11 cells. TGF-beta1 completely
      abolished the clonal growth of MV4-11 cells in soft agar and inhibited Mo7e,
      KG-1, K562, TF-1, and TF-1a colony growth by 99%, 90%, 63%, 53%, and 43%,
      respectively. The cells treated with TGF-beta1 showed progressive accumulation in
      the G1 phase of cell cycle. Maximal G1 arrest (93%) was observed in MV4-11 cells.
      Using anti-retinoblastoma protein (pRb) and anti-specific phosphorylated-pRb
      antibodies, we demonstrated that TGF-beta1 greatly inhibited pRb phosphorylation 
      at serine 795 in MV4-11 and Mo7e cells. Taken together, our data suggest that the
      sensitivity of myeloid leukemic progenitor cells to growth inhibition by TGF-beta
      may not be inversely correlated with their maturation stage, and the inhibition
      of the cells appeared to be linked to the suppression of pRb phosphorylation at
      serine 795.
FAU - Hu, X
AU  - Hu X
AD  - Department of Internal Medicine, University of South Florida, and H. Lee Moffitt 
      Cancer Center, and Research Institute, Tampa 33612, USA. hu@moffitt.usf.edu
FAU - Moscinski, L C
AU  - Moscinski LC
FAU - Zuckerman, K S
AU  - Zuckerman KS
LA  - eng
GR  - CA56072/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Netherlands
TA  - Exp Hematol
JT  - Experimental hematology
JID - 0402313
RN  - 0 (Proto-Oncogene Proteins)
RN  - 0 (Retinoblastoma Protein)
RN  - 0 (Transforming Growth Factor beta)
RN  - 452VLY9402 (Serine)
RN  - EC 2.7.11.22 (CDK4 protein, human)
RN  - EC 2.7.11.22 (Cyclin-Dependent Kinase 4)
RN  - EC 2.7.11.22 (Cyclin-Dependent Kinases)
SB  - IM
MH  - Cell Differentiation
MH  - Cell Division/drug effects
MH  - Cyclin-Dependent Kinase 4
MH  - Cyclin-Dependent Kinases/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Humans
MH  - Leukemia, Myeloid/*pathology
MH  - Phosphorylation/drug effects
MH  - *Proto-Oncogene Proteins
MH  - Retinoblastoma Protein/*metabolism
MH  - S Phase/drug effects
MH  - Serine/*metabolism
MH  - Time Factors
MH  - Transforming Growth Factor beta/*metabolism/*pharmacology
MH  - Tumor Cells, Cultured
MH  - Tumor Stem Cell Assay
EDAT- 1999/04/21 00:00
MHDA- 1999/04/21 00:01
CRDT- 1999/04/21 00:00
PHST- 1999/04/21 00:00 [pubmed]
PHST- 1999/04/21 00:01 [medline]
PHST- 1999/04/21 00:00 [entrez]
AID - S0301-472X(99)00004-1 [pii]
AID - 10.1016/s0301-472x(99)00004-1 [doi]
PST - ppublish
SO  - Exp Hematol. 1999 Apr;27(4):605-14. doi: 10.1016/s0301-472x(99)00004-1.