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ADAM17 regulates prostate cancer cell proliferation through mediating cell cycle progression by EGFR/PI3K/AKT pathway

Ping Lin1, Xicai Sun, Tian Feng

  • 1Department of Biochemistry and Molecular Biology, College of Basic Medical Science, Harbin Medical University, Harbin, 150081, China.

Molecular and Cellular Biochemistry
|August 13, 2011
PubMed

Insights

A disintegrin and metalloprotease 17 (ADAM17) promotes prostate cancer cell proliferation by upregulating cyclin E/CDK2 and downregulating p21/p27. This occurs via activation of the epidermal growth factor receptor (EGFR)/PI3K/AKT pathway.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • A disintegrin and metalloprotease 17 (ADAM17) is a key enzyme involved in cancer progression.
  • ADAM17's role in prostate cancer proliferation and cell cycle regulation requires further elucidation.

Purpose of the Study:

  • To investigate the functional role of ADAM17 in human prostate cancer cell proliferation and cell cycle distribution.
  • To elucidate the underlying molecular mechanisms by which ADAM17 influences prostate cancer cell growth.

Main Methods:

  • Overexpression and RNA interference (RNAi) strategies were employed in human prostate cancer cells.
  • Cell proliferation was assessed using growth curves, CCK-8, and bromodeoxyuridine (BrdU) incorporation assays.
  • Gene and protein expression changes were analyzed via RT-PCR, Western blotting, and ELISA, alongside cell cycle analysis.

Main Results:

  • ADAM17 overexpression significantly increased prostate cancer cell proliferation and promoted G1 to S phase transition.
  • Upregulation of cyclin E and CDK2, and downregulation of p21 and p27 were observed upon ADAM17 overexpression.
  • ADAM17 increased TGF-α release, activating the EGFR/PI3K/AKT pathway, which was crucial for its proliferative effects.

Conclusions:

  • ADAM17 overexpression drives prostate cancer cell proliferation by modulating cell cycle regulators (cyclin E, CDK2, p21, p27).
  • The EGFR/PI3K/AKT pathway is a critical mediator of ADAM17's pro-proliferative effects in prostate cancer.
  • Targeting ADAM17 or the EGFR/PI3K/AKT pathway may represent a therapeutic strategy for prostate cancer.

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