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The expression of p53 and p16 in the course of microcystin-LR inducing of liver tumor

  • Published:
The Chinese-German Journal of Clinical Oncology

Abstract

Objective

To deeply explore the molecular mechanism of MCLR in the course of MCLR promoting liver tumor.

Methods

We applied the two -stage- medium-term theory to set up the animal model, and biochemistry technique to evaluate the model, and then, used RT-PCR technique and image analysis to study the mRNA expression of the p53 and p16 in the course of promoting tumor

Results

(1) MCLR could enhance the positive reaction ratio of γ-Glutamyltransferase(GGT). (2) MCLR could increase the mRNA expression of p53, and had not effect on the mRNA expression of p53.

Conclusion

(1) MC can promote liver tumor strongly. (2) The expression change of p53 may play an important role in the course of MCLR promoting liver tumor.

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References

  1. Yu SZ, Dong CH, Zhang YC. Two biotoxins and liver cancer-aflatoxin and algal toxin. J Hygiene Res (Chinese), 2000, 27: 84.

    Google Scholar 

  2. Sun CS, Chen H, Xue CG, et al. Study of distribution of algal toxin and algal species in Tong-an environment. Chin Public Health (Chinese), 2000, 16: 147–148.

    Google Scholar 

  3. Oh HM, Lee SJ, Jang MH, et al. Microcystin production by microcystis aeruginosa in a phosphorus-limited chemostat. Appl Environ Microbiol, 2000, 66: 176–179.

    Article  PubMed  CAS  Google Scholar 

  4. Rutenberg AM, Kim H, Fischbein JW, et al. Histochemical and ultrastructural demonstration of gamma-glutamyl transpeptidase activity. J Histochem Cytochem, 1969, 17: 517–526.

    Google Scholar 

  5. Ito N, Tamano S, Shirai T. A medium-term rat liver bioassay for rapid in vivo detection of carcinogenic potential of chemicals.Cancer Sci, 2003, 94: 3–8.

    Article  PubMed  CAS  Google Scholar 

  6. Beer DG, Schwarz M, Sawada N, et al. Expression of H-ras and c-myc protooncogenes in isolated gamma-glutamyl transpeptidasepositive rat hepatocytes and in hepatocellular carcinomas induced by diethylnitrosamine. Cancer Res, 1996, 46: 2435–2441.

    Google Scholar 

  7. Petersen BE, Goff JP, Greenberger JS, et al. Hepatic oval cells express the hematopoietic stem cell marker Thy-1 in the rat. Hepatology, 1998, 27: 433–445.

    Article  PubMed  CAS  Google Scholar 

  8. Sheng WD, Huang JF. Progress in specific GGT for diagnosis of liver cancer. World Chin J Digestol (Chinese), 2003, 13: 3–8.

    Google Scholar 

  9. Fawell JK, Mitchell RE, Everett DJ, et al. The toxicity of cyanobacterial toxins in the mouse: I microcystin-LR. Hum Exp Toxicol, 1999, 18: 162–167.

    Article  PubMed  CAS  Google Scholar 

  10. Nakajima H, Nakajima HO, Tsai SC, et al. Expression of mutant p193 and p53 permits cardiomyocyte cell cycle reentry after myocardial infarection in transgenic mice. Circ Res, 2004, 94: 1606–1614.

    Article  PubMed  CAS  Google Scholar 

  11. Offer H, Zurer I, Banfalvi G, et al. p53 modulates base excision repair activity in a cell cycle-specific manner after genotoxic stress. Cancer Res, 2001, 61: 88–96.

    PubMed  CAS  Google Scholar 

  12. Li M, Zhou JY, Ge Y, et al. The phosphatase MKP1 is a transcriptional target of p53 involved in cell cycle regulation. J Biol Chem, 2003, 278: 41059–41068.

    Article  PubMed  CAS  Google Scholar 

  13. Gudas JM, Oka M, Diella F, et al. Expression of wild-type p53 during the cell cycle in normal human mammary epithelial cells. Cell Growth Differ, 1994, 5: 295–304.

    PubMed  CAS  Google Scholar 

  14. Spurgers KB, Gold DL, Coombes KR, et al. Identification of cell cycle regulatory genes as principal targets of p53-mediated transcriptional repression. J Biol Chem, 2006, 281: 25134–25142.

    Article  PubMed  CAS  Google Scholar 

  15. Omura-Minamisawa M, Diccianni MB, Chang RC, et al. p16/p14 (ARF) cell cycle regulatory pathways in primary neuroblastoma: p16 expression is associated with advanced. Clin Cancer Res, 2001, 7: 3481–3490.

    PubMed  CAS  Google Scholar 

Download references

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Authors

Corresponding author

Correspondence to Qiying Lin.

Additional information

Supported by the grants from the Natural Science Foundation of Fujian Province (No. C0210011), and the Science & Technology Program for the Education Department of Fujian Province (No. JA05256).

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Hu, Z., Chen, H., Pang, C. et al. The expression of p53 and p16 in the course of microcystin-LR inducing of liver tumor. Chin. -Ger. J. Clin. Oncol. 7, 690–693 (2008). https://doi.org/10.1007/s10330-008-0137-5

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  • DOI: https://doi.org/10.1007/s10330-008-0137-5

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