Cell Proliferation, RNA and Protein Synthesis During Carcinogenesis in the Rat Liver

Stöcker, E.; Wullstein, H. K.; Friederichs, Kerstin; Friederichs, Christa

doi:10.1016/s0005-8165(73)80017-4

Cited by 2 publications

(2 citation statements)

References 12 publications

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“…The alteration of cellular components is closely related to cell carcinogenesis [19,20]. To further investigate the effects of apoptosis inducer ESC‐3 on the protein expression of human cholangiocarcinoma cancer cells, proteomic analysis was employed to screen for the aberrant proteins of human cholangiocarcinoma cells before and after treatment.…”

Section: Discussionmentioning

confidence: 99%

The aberrant expression and localization of prohibitin during apoptosis of human cholangiocarcinoma Mz‐ChA‐1 cells

Song

Tian

et al. 2013

FEBS Letters

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a b s t r a c tIn this study, we aimed to investigate the aberrant expression and shift in localization of prohibitin (PHB) during apoptosis of human cholangiocarcinoma cells. Our study demonstrated that PHB was expressed primarily in the cytoplasm and only a little in the nucleus. However, PHB expression significantly decreased, and its localization shifted from the cytoplasm to the nucleus during apoptosis. PHB co-localized with AIF, Rb, p53, and c-Fos, but the region of co-localization was altered after treatment. Meanwhile, we detected a direct interaction between PHB and both p53 and Rb in Mz-ChA-1 cells. These results suggest that the altered localization and expression of PHB, as well as its co-localization with related oncogenes and tumor suppressor genes, can affect the apoptosis of Mz-ChA-1 cells. Structured summary of protein interactions:AIF and PHB colocalize by fluorescence microscopy (View interaction) Rb and PHB colocalize by fluorescence microscopy (View interaction) c-Fos and PHB colocalize by fluorescence microscopy (View interaction) PHB and p53 colocalize by fluorescence microscopy (View interaction)

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Section: Discussionmentioning

confidence: 99%

The aberrant expression and localization of prohibitin during apoptosis of human cholangiocarcinoma Mz‐ChA‐1 cells

Song

Tian

et al. 2013

FEBS Letters

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“…In normal rat liver, most hepatocytes are in the quiescent state (Fabrikant, 1968;Stocker et al, 1973). Since these hepatocytes can be induced to re-enter the cell cycle traverse, synthesize DNA and undergo mitosis after partial hepatectomy (Fabrikant, 1968), rat liver is an excellent tissue model system to study control mechanisms involved in growth arrest.…”

Section: Discussionmentioning

confidence: 99%

Characterization of 57 kDa statin as a true marker for growth arrest in tissue by its disappearance from regenerating liver

Sandig

Bissonnette

Liu

et al. 1994

Journal Cellular Physiology

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Statin, a 57 kDa nuclear protein, is lost from quiescent fibroblasts in culture when they are induced to enter the cell cycle by feeding with growth factors, or by removal of contact inhibition. In order to investigate changes in statin expression during the transition from a quiescent to a cycling state in situ, we performed 70% partial hepatectomy on rats and analyzed the regenerating liver by immunofluorescence microscopy with antistatin monoclonal antibodies (S44 mAb), and by immunoblotting of liver proteins in cytoplasmic and enriched nuclear/cytoskeletal fractions. Western blot analysis showed that rat hepatocytes in situ contain a nuclear 57 kDa form of statin, as seen in cultured fibroblasts; however additional S44-immunoreactive polypeptides with molecular weights of 53 and 110 kDa are also present in both cytoplasmic and nuclear/cytoskeletal fractions. Immunofluorescence microscopy indicates that the proportion of S44-positive hepatocyte nuclei drops to approximately 60% within 24 hours after hepatectomy, a time period when re-entry of hepatocytes into the cell cycle is first observed. On Western blots of hepatocyte nuclear/cytoskeletal proteins obtained 24 hours after hepatectomy, the 57 kDa form of statin is markedly reduced. These results suggest that, although in liver the S44 antibody recognizes three proteins (53 kDa, 57 kDa, and 110 kDa), the 57 kDa in intact liver, similar to cultured fibroblasts, is the only polypeptide recognized by the statin antibody that disappears when hepatocytes are induced to re-enter the cell cycle from a quiescent state.

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Cell Proliferation, RNA and Protein Synthesis During Carcinogenesis in the Rat Liver

Cited by 2 publications

References 12 publications

The aberrant expression and localization of prohibitin during apoptosis of human cholangiocarcinoma Mz‐ChA‐1 cells

The aberrant expression and localization of prohibitin during apoptosis of human cholangiocarcinoma Mz‐ChA‐1 cells

Characterization of 57 kDa statin as a true marker for growth arrest in tissue by its disappearance from regenerating liver

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