RGD Reference Report - Changes in polypeptide pattern of rat liver cells during chemical hepatocarcinogenesis. - Rat Genome Database

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Changes in polypeptide pattern of rat liver cells during chemical hepatocarcinogenesis.

Authors: Sugioka, Y  Fujii-Kuriyama, Y  Kitagawa, T  Muramatsu, M 
Citation: Sugioka Y, etal., Cancer Res. 1985 Jan;45(1):365-78.
RGD ID: 152998958
Pubmed: PMID:3965145   (View Abstract at PubMed)

Administration of 2-acetylaminofluorene to rats for 12 weeks induces hyperplastic nodules (HPNs) and later well-differentiated hepatocellular carcinomas (HCCs) in the liver. Total cellular proteins from normal liver, HPN, and HCC were analyzed by two-dimensional gel electrophoresis with a high resolution. Several hundred polypeptides were well resolved as seen by Coomassie blue staining, forming a reproducible and characteristic pattern for each tissue. The polypeptide patterns were very similar among normal liver, HPN, and HCC. Especially the proteins of HPN and HCC were almost indistinguishable. These neoplastic lesions, however, were clearly different from control liver in that a new spot p35-6.6 (designated by molecular weight X 10(-3) and pl) appeared, and five polypeptides, p57-6.9, p57-6.7, p26-6.9, p26-6.6, p26-6.4, increased dramatically in amount as compared with normal liver. These last three spots were found to be a new type of glutathione S-transferase as judged from the specific binding to the antibody. The same changes in polypeptide pattern were found in HCCs induced by other chemical carcinogens, diethylnitrosamine and 3'-methyl-4-dimethylaminoazobenzene, but not in regenerating and neonatal livers. Fetal liver showed a rather different pattern than adult liver, but only p26-6.6 was increased among the spots characteristic of HPN and HCC. Protein phosphorylation was also examined for these cells by incubating tissue slices with 32PO4. After alkali treatment of the gels to eliminate serines phosphorylation, several dozens of phosphoproteins were clearly detected. The patterns of the labeled spots were again very similar among control liver, HPN, and HCC. Only the intensity of a spot designated p57-6.6 increased markedly in both HPN and HCC. This spot was further resolved by an expanded pH gradient into four distinct spots, the major one of which contained phosphothreonine. Similar changes in phosphorylation were noted in hepatomas induced by diethylnitrosamine and 3'-methyl-4-dimethylaminoazobenzene but not in regenerating, fetal, and neonatal livers. These changes are discussed in terms of gene expression relevant to malignant transformation of hepatic cells.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Experimental Liver Neoplasms  ISOCdkn1c (Rattus norvegicus)152998958; 152998958protein:increased expression:liver (rat)RGD 
Experimental Liver Neoplasms  IEP 152998958; 152998958protein:increased expression:liver (rat)RGD 
Experimental Liver Neoplasms  ISOGstp1 (Rattus norvegicus)152998958; 152998958protein:increased expression:liver (rat)RGD 
Focal Nodular Hyperplasia  ISOCdkn1c (Rattus norvegicus)152998958; 152998958protein:increased expression:liver (rat)RGD 
Focal Nodular Hyperplasia  IEP 152998958; 152998958protein:increased expression:liver (rat)RGD 
Focal Nodular Hyperplasia  ISOGstp1 (Rattus norvegicus)152998958; 152998958protein:increased expression:liver (rat)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Cdkn1c  (cyclin-dependent kinase inhibitor 1C)
Gstp1  (glutathione S-transferase pi 1)

Genes (Mus musculus)
Cdkn1c  (cyclin dependent kinase inhibitor 1C)
Gstp1  (glutathione S-transferase, pi 1)

Genes (Homo sapiens)
CDKN1C  (cyclin dependent kinase inhibitor 1C)
GSTP1  (glutathione S-transferase pi 1)


Additional Information