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. 2001 Feb;7(1):33-6.
doi: 10.3748/wjg.v7.i1.33.

Effect of phosphorylation of MAPK and Stat3 and expression of c-fos and c-jun proteins on hepatocarcinogenesis and their clinical significance

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Effect of phosphorylation of MAPK and Stat3 and expression of c-fos and c-jun proteins on hepatocarcinogenesis and their clinical significance

D Y Feng et al. World J Gastroenterol. 2001 Feb.

Abstract

Aim: To study the effect of phosphorylation of MAPK and Stat3 and the expression of c-fos and c-jun proteins on hepatocellular carcinogenesis and their clinical significance.

Methods: SP immunohistochemistry was used to detect the expression of p42/44(MAPK), p-Stat3, c-fos and c-jun proteins in 55 hepatocellular carcinomas (HCC) and their surrounding liver tissues.

Results: The positive rates and expression levels of p42/44(MAPK), p-Stat3, c-fos and c-jun proteins in HCCs were significantly higher than those in pericarcinomatous liver tissues (PCLT). A positive correlation was observed between the expression of p42/44(MAPK) and c-fos proteins,and between p-Stat3 and c-jun but there was no significant correlation between p42/44(MAPK) and p-Stat3 in HCCs and their surrounding liver tissues.

Conclusion: The abnormalities of Ras/Raf/MAPK and JAKs/Stat3 cascade reaction may contribute to malignant transformation of hepatocytes. Hepatocytes which are positive for p42/44(MAPK), c-fos or c-jun proteins may be potential malignant pre-cancerous cells. Activation of MAPK and Stat3 proteins may be an early event in hepatocellular carcinogenesis.

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Figures

Figure 1
Figure 1
The positive rates of p42/44MAPK, p-Stat3, c-fos and c-jun proteins in HCCs and PCLTs.
Figure 2
Figure 2
Localization of positive signal and distribution of positive cells for p42/44MAPK protein in HCC. SP × 400
Figure 3
Figure 3
Localization of positive signal and distribution of positive cells for Stat3 protein in HCC. SP × 400
Figure 4
Figure 4
Positive expression of c-fos protein in HCC. SP × 400
Figure 5
Figure 5
Positive expression of c-jun protein in HCC. SP × 400

References

    1. Ito Y, Sasaki Y, Horimoto M, Wada S, Tanaka Y, Kasahara A, Ueki T, Hirano T, Yamamoto H, Fujimoto J, et al. Activation of mitogen-activated protein kinases/extracellular signal-regulated kinases in human hepatocellular carcinoma. Hepatology. 1998;27:951–958. - PubMed
    1. Schmidt CM, McKillop IH, Cahill PA, Sitzmann JV. Increased MAPK expression and activity in primary human hepatocellular carcinoma. Biochem Biophys Res Commun. 1997;236:54–58. - PubMed
    1. Gu SQ, Liang YY, Fan LR, Li BY, Wang DS. Co-regulative effects of the cAMP/PKA and DAG/PKC signal pathways on human gas-tric cancer cells during differentiation induced by traditional Chi-nese medicines. China Natl J New Gastroen terol. 1997;3:50–53. - PMC - PubMed
    1. Hill CS, Treisman R. Transcriptional regulation by extracellular signals: mechanisms and specificity. Cell. 1995;80:199–211. - PubMed
    1. Kim H, Baumann H. Dual signaling role of the protein tyrosine phosphatase SHP-2 in regulating expression of acute-phase plasma proteins by interleukin-6 cytokine receptors in hepatic cells. Mol Cell Biol. 1999;19:5326–5338. - PMC - PubMed

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