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The ING4 Binding with p53 and Induced p53 Acetylation were Attenuated by Human Papillomavirus 16 E6

Yi Guo1, Xiangkai Meng, Qian Wang

  • 1Department of Gynecology, First Affiliated Hospital of China Medical University, Shenyang, China.

Plos One
|August 23, 2013
PubMed

Insights

Human papillomavirus type 16 (HPV16) oncoprotein E6 interferes with the tumor suppressor ING4, hindering its ability to activate p53. This interaction may promote cancer development by disrupting normal cell growth regulation.

Area of Science:

  • Oncology
  • Virology
  • Molecular Biology

Background:

  • High-risk HPV16 oncoprotein E6 drives cell immortalization and transformation.
  • ING4, a tumor suppressor, regulates p53 function.
  • The interaction between HPV16 E6 and ING4 is not well understood.

Purpose of the Study:

  • To investigate the effect and mechanism of HPV16 E6 on ING4 function.
  • To determine if HPV16 E6 interacts with ING4.
  • To elucidate how HPV16 E6 affects ING4-mediated p53 regulation.

Main Methods:

  • In vivo and in vitro binding assays to detect HPV16 E6-ING4 interaction.
  • Assays to measure p53 acetylation and binding to ING4.
  • Assessment of ING4's effect on p53-mediated apoptosis in the presence of HPV16 E6.

Main Results:

  • HPV16 E6 directly binds to ING4 both in vivo and in vitro.
  • HPV16 E6 attenuates ING4-induced p53 acetylation and binding to p53, independent of p53 degradation.
  • The pro-apoptotic function of ING4 on p53 is diminished by HPV16 E6.

Conclusions:

  • ING4 is a target of HPV16 E6.
  • HPV16 E6 disrupts ING4's tumor-suppressive functions by inhibiting p53 acetylation and apoptosis.
  • ING4 may be a common target for oncogenic viruses in driving host cell carcinogenesis.

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