Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Enzyme
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Query: UMLS:C1864663 (
HCC
)
2,985
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Recent data suggest that Bin1, a novel C-MYC interacting protein, is a suppressor gene whose loss of expression is a frequent aberration associated with several malignancies. The mechanism responsible for loss of
BIN1
expression is not understood. The purpose of this study is to investigate DNA profile of the
BIN1
gene in human hepatoma Hep G2 cells, previously documented with lack of
BIN1
expression. Chromosome and molecular analyses of Hep G2 cells were initiated to exclude the possibility of genetic alterations as a factor affecting
BIN1
gene expression in these cells. We used Hep G2 cell line and its hepatitis B virus (HBV) transfected variants--Hep G2T14.1 and Hep G2215 cell lines. The cytogenetic localization of
BIN1
was identified in the 2q14 region. Fluorescence in situ hybridization (FISH) with the chromosome 2 whole chromosome painting probe (WCP) demonstrated three or four intact copies of chromosome 2 in all three hepatoma cell lines studied. FISH analyses with the
BIN1
-specific probe of the Hep G2, Hep G2T14.1, and Hep G2215 metaphase chromosomes document no rearrangement of the
BIN1
gene on any of the multiple copies of chromosome 2. FISH with the specific HBV probe did not identify the HBV integration site in Hep G2T14.1 and Hep G2215 cells within the
BIN1
locus. Southern blot analyses revealed no genetic rearrangements in the
BIN1
gene in any of the cell lines studied. Our RNA analyses (northern blot and RT-PCR) document lack of
BIN1
message in Hep G2 cells in contrast to the presence of
BIN1
in Hep G2T14.1 and Hep G2215 cells. No difference was identified in other transcripts analyzed, including c-myc. Analyses of
BIN1
expression of Hep G2 cells at different passages were initiated and document low levels of
BIN1
transcript in Hep G2 cells of passage < 85. Furthermore,
BIN1
transcript was identified in additional seven
HCC
cell lines analyzed. Our data indicate that lack of Bin1 expression in HepG2 cells previously documented is a characteristic of cells of passage > 85 and is not due to genetic loss, or rearrangement within the
BIN1
DNA sequence. Loss of the
BIN1
transcript is not a characteristic of HCCs analyzed.
...
PMID:Investigation of the expression of Bin1, a putative suppressor, in human hepatoma cells. 1061 29
