Nidus vespae protein inhibiting proliferation of HepG2 hepatoma cells through extracellular signal-regulated kinase signaling pathways and inducing G1 cell cycle arrest

  1. Changdong Wang,
  2. Peng Chen,
  3. Hongjuan Jin,
  4. Xu Yan,
  5. Lu Gan,
  6. Yi Li,
  7. Shiyi Zhou,
  8. Junli Chang,
  9. Yuesheng Wang,
  10. Guangxiao Yang,
  11. Guangyuan He*

Article first published online: 1 DEC 2008

DOI: 10.1111/j.1745-7270.2008.00476.x

Issue

Acta Biochimica et Biophysica Sinica

Acta Biochimica et Biophysica Sinica

Volume 40, Issue 11, pages 970–978, November 2008

Additional Information

How to Cite

Wang, C., Chen, P., Jin, H., Yan, X., Gan, L., Li, Y., Zhou, S., Chang, J., Wang, Y., Yang, G. and He, G. (2008), Nidus vespae protein inhibiting proliferation of HepG2 hepatoma cells through extracellular signal-regulated kinase signaling pathways and inducing G1 cell cycle arrest. Acta Biochimica et Biophysica Sinica, 40: 970–978. doi: 10.1111/j.1745-7270.2008.00476.x

Author Information

  1. China-UK HUST-RRes Genetic Engineering and Genomics Joint Laboratory, the Key Laboratory of Molecular Biophysics of Ministry of Education, College of Life Science and Technology, Huazhong University of Science & Technology, Wuhan 430074, China

* *Corresponding author: Tel, 86–27–87792271; Fax, 86–27–87792272; E-mail, guangyuan.he@bbsrc.ac.uk

Publication History

  1. Issue published online: 1 DEC 2008
  2. Article first published online: 1 DEC 2008
  3. Received: July 12, 2008 Accepted: August 5, 2008

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Keywords:

  • Nidus vespae;
  • NVP(1);
  • ERK;
  • cell proliferation

A protein named NVP(1) was isolated from Nidus vespae. T he aim of the present study was to elucidate whether and how NVP(1) modulates the proliferation of HepG2 cells. NVP(1) at a concentration of 6.6 μg/ml could arrest the cell cycle at stage G1 and inhibit the mRNA expression of cyclinB, cyclinD1 and cyclinE. NVP(1) suppressed cdk2 protein expression, but increased p27 and p21 protein expression. However, NVP(1) did not alter p16 protein expression levels. NVP(1) promoted apoptosis in HepG2 cells as indicated by nuclear chromatin condensation, and in addition, the extracellular signal-regulated kinase (ERK) signaling pathway was activated. Moreover, the p-ERK protein expression level was attenuated when the HepG2 cells were pretreated with ERK inhibitor PD98059. These results demonstrate that NVP(1) inhibits proliferation of HepG2 through ERK signaling pathway. NVP(1) could be a potential drug for liver cancer.

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