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p12CDK2-AP1 interacts with CD82 to regulate the proliferation and survival of human oral squamous cell carcinoma

Juan Chai1, Jun Ju1, Shao-Wu Zhang2

  • 1State Key Laboratory of Military Stomatology, Department of Oral and Maxillofacial Surgery, School of Stomatology, The Fourth Military Medical University, Xi'an, Shaanxi 710032, P.R. China.

Oncology Reports
|June 29, 2016
PubMed

Insights

p12 cyclin-dependent kinase 2 (CDK2)-associating protein 1 (p12CDK2-AP1) interacts with CD82 to suppress oral cancer cell growth. Combined overexpression of both proteins shows synergistic antitumor effects in vitro and in vivo.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Biology

Background:

  • p12 cyclin-dependent kinase 2 (CDK2)-associating protein 1 (p12CDK2-AP1) is known to inhibit CDK2 activity, but its precise molecular mechanism and role in cancer are not fully understood.
  • Understanding p12CDK2-AP1's interactions is crucial for elucidating its function in cellular processes relevant to cancer progression.

Purpose of the Study:

  • To identify binding proteins of p12CDK2-AP1.
  • To investigate the role of p12CDK2-AP1 in regulating the proliferation, invasion, and apoptosis of human oral squamous cell carcinoma (OSCC) cells.
  • To evaluate the combined effect of p12CDK2-AP1 and its binding partner on OSCC growth both in vitro and in vivo.

Main Methods:

  • Computational prediction of protein-protein interactions.
  • Overexpression of p12CDK2-AP1 and CD82 in OSCC-15 cells.
  • Co-immunoprecipitation (Co-IP) to confirm protein binding.
  • MTT assay for proliferation, Transwell system for invasion, and Annexin V-FITC/PI staining for apoptosis.
  • In vivo tumor xenograft models in nude mice.

Main Results:

  • Overexpression of p12CDK2-AP1 or CD82 individually suppressed OSCC cell proliferation and invasion while promoting apoptosis.
  • Combined overexpression of p12CDK2-AP1 and CD82 demonstrated synergistic antitumor activity compared to single protein overexpression.
  • Simultaneous overexpression of p12CDK2-AP1 and CD82 significantly inhibited in vivo tumor growth in nude mice.

Conclusions:

  • p12CDK2-AP1 interacts with CD82.
  • This interaction plays a significant role in suppressing the in vitro and in vivo growth of human oral squamous cell carcinoma cells.
  • The combined overexpression of p12CDK2-AP1 and CD82 exhibits potent synergistic antitumor effects, suggesting therapeutic potential.

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