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Ibrutinib presents antitumor activity in skin cancer and induces autophagy

F-D Sun1, P-C Wang, J Shang

  • 1Department of Pharmacy, Yantai Yuhuangding Hospital, Yantai, China. zshzqf@163.com.

European Review for Medical and Pharmacological Sciences
|February 10, 2018
PubMed
Abstract

Insights

Ibrutinib, a Bruton's Tyrosine Kinase (BTK) inhibitor, inhibits skin cancer cell proliferation and induces apoptosis and autophagy. Combining ibrutinib with autophagy inhibitors enhances its anti-cancer effects, offering new therapeutic strategies for skin cancer.

Area of Science:

  • Dermatology
  • Oncology
  • Molecular Biology

Background:

  • Skin cancer is a prevalent malignancy with poor patient prognosis.
  • Ibrutinib, a Bruton's Tyrosine Kinase (BTK) inhibitor, shows promise as an anticancer agent.
  • Investigating ibrutinib's efficacy in skin cancer treatment is crucial.

Purpose of the Study:

  • To explore the anti-tumor activity of ibrutinib in skin cancer.
  • To evaluate ibrutinib's effects on skin cancer cell proliferation, apoptosis, and autophagy.
  • To assess the potential of combining ibrutinib with autophagy inhibitors.

Main Methods:

  • Cell Counting Kit-8 (CCK8) and plate cloning assays for proliferation.
  • Flow cytometry for apoptosis analysis.
  • Western blotting for autophagy-related protein expression.

Main Results:

  • Ibrutinib demonstrated dose- and time-dependent inhibition of skin cancer cell proliferation.
  • Ibrutinib treatment induced apoptosis in skin cancer cells.
  • Ibrutinib was found to induce autophagy in skin cancer cells, dependent on concentration and time.
  • Combination therapy with ibrutinib and 3MA significantly increased apoptosis.

Conclusions:

  • Ibrutinib exhibits anti-tumor activity against skin cancer by inducing autophagy.
  • Combining ibrutinib with autophagy inhibitors can enhance its anti-skin cancer efficacy.
  • These findings offer novel therapeutic avenues for skin cancer drug development.

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