DLC-1 is deleted in primary hepatocellular carcinoma and exerts inhibitory effects on the proliferation of hepatoma cell lines with deleted DLC-1

We investigated the expression and deletion of DLC-1 (frequently deleted in liver cancer gene), first reported in 1998 and having a high homology with rat p122RhoGAP in hepatocellular carcinoma (HCC). Six (20%) of 30 human HCC samples and 2 (40%) of 5 HCC cell lines were found to have no detectable...

Full description

Saved in:
Bibliographic Details
Published inCancer research (Chicago, Ill.) Vol. 60; no. 23; pp. 6581 - 6584
Main Authors NG, Irene Oi-Lin, LIANG, Zheng-Dong, LIANG CAO, LEE, Terence Kin-Wah
Format Journal Article
LanguageEnglish
Published Philadelphia, PA American Association for Cancer Research 01.12.2000
Subjects
Biological and medical sciences
Blotting, Southern
Carcinoma, Hepatocellular - genetics
Carcinoma, Hepatocellular - pathology
Cell Division - genetics
Gastroenterology. Liver. Pancreas. Abdomen
Gene Deletion
Gene Expression
GTPase-Activating Proteins
Homozygote
Humans
Liver Neoplasms - genetics
Liver Neoplasms - pathology
Liver. Biliary tract. Portal circulation. Exocrine pancreas
Medical sciences
Protein Biosynthesis
Proteins - genetics
Reverse Transcriptase Polymerase Chain Reaction
Tumor Cells, Cultured
Tumor Suppressor Proteins
Tumors
Chromosomal aberration
Human
Multiplication
Tumoral tissue
Hepatic disease
Hepatocellular carcinoma
Malignant tumor
Gene expression
Carcinogenesis
Chromosome C8
In vitro
Gene
Established cell line
Deletion
Digestive diseases
Abnormal chromosome
Tumor cell
Online AccessGet full text

Cover

More Information
Summary:We investigated the expression and deletion of DLC-1 (frequently deleted in liver cancer gene), first reported in 1998 and having a high homology with rat p122RhoGAP in hepatocellular carcinoma (HCC). Six (20%) of 30 human HCC samples and 2 (40%) of 5 HCC cell lines were found to have no detectable DLC-1 expression by reverse transcription-PCR. Homozygous DLC-1 deletion was detected by Southern blotting in two of six HCC samples and in both HCC cell lines with no DLC-1 expression. Transfection of DLC-1 into 5 HCC cell lines (two with DLC-1 deletion and three with intact DLC-1) showed significant growth inhibition in these two HCC cell lines with deleted DLC-1 with both 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation assays but not in three other HCC cell lines with intact DLC-1. Our findings suggest that DLC-1 may play an important role in hepatocarcinogenesis.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0008-5472
1538-7445