The inhibitory mechanism by curcumin on the Zac1-enhanced cyclin D1 expression in human keratinocytes

J Dermatol Sci. 2015 Sep;79(3):262-7. doi: 10.1016/j.jdermsci.2015.06.006. Epub 2015 Jun 15.

Abstract

Background: ZAC, a zinc finger protein regulating cell cycle arrest and apoptosis, mRNA was found highly expressed in the hyper-proliferative epidermal compartment of psoriatic skin. On the other hand, curcumin has been tried for treatment of psoriasis partly due to its anti-proliferative property.

Objectives: Since cyclin D1 is a positive regulator for cell-cycle progression and its expression can be inhibited by curcumin, we would like to test whether the expression of cyclin D1 can be affected by Zac1. The cross-talk between curcumin and Zac1 upon the regulation of cyclin D1 expression will also be explored in the HaCaT cell line.

Methods: Cyclin D1 promoter luciferase reporter was used to measure the transcriptional activity of Zac1 in the absence or presence of curcumin treatment for HaCaT cells. Likewise, RT-PCR, western blotting and flow cytometry were employed to evaluate the expression of Zac1, cyclin D1 and other negative regulators of S phase entry in cell-cycle.

Results: Zac1 enhances the expression of cyclin D1, but curcumin decreases both the expression of Zac1 and cyclin D1. Interestingly, Zac1-induced cyclin D1 promoter activity is abolished by curcumin. Supportively, curcumin indeed exhibits an inhibitory effect to prevent cultured keratinocytes from entry into S phase in the cell cycle.

Conclusions: These findings revealed that Zac1 modulates not only cell differentiation and apoptosis but also cell proliferation. The experimental results implied that curcumin may inhibit the expression of ZAC, consequently down-regulate the cyclin D1 expression and decelerate cell-cycle progression of psoriatic keratinocytes.

Keywords: Curcumin; Cyclin D1; Keratinocyte; Psoriasis; Zac1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents / pharmacology*
  • Apoptosis
  • Cell Cycle Proteins / drug effects
  • Cell Cycle Proteins / genetics*
  • Cell Cycle Proteins / metabolism*
  • Cell Differentiation
  • Cell Line
  • Cell Proliferation
  • Curcumin / pharmacology*
  • Cyclin D1 / genetics
  • Cyclin D1 / metabolism*
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • G1 Phase Cell Cycle Checkpoints / drug effects*
  • Humans
  • Keratinocytes
  • Promoter Regions, Genetic / drug effects
  • S Phase Cell Cycle Checkpoints / drug effects*
  • Transcription Factor AP-1 / metabolism
  • Transcription Factors / drug effects
  • Transcription Factors / genetics*
  • Transcription Factors / metabolism*
  • Transcription, Genetic / drug effects
  • Tumor Suppressor Proteins / drug effects
  • Tumor Suppressor Proteins / genetics*
  • Tumor Suppressor Proteins / metabolism*

Substances

  • Antineoplastic Agents
  • CDKN1A protein, human
  • Cell Cycle Proteins
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cyclin-Dependent Kinase Inhibitor p21
  • PLAGL1 protein, human
  • Transcription Factor AP-1
  • Transcription Factors
  • Tumor Suppressor Proteins
  • Cyclin D1
  • Curcumin