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Induction of miR-21-PDCD4 signaling by UVB in JB6 cells involves ROS-mediated MAPK pathways

Lichao Hou1, Linda Bowman, Terence G Meighan

  • 1Graduate Center for Toxicology, College of Medicine, The University of Kentucky, Lexington, KY 40503, USA; Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA; Department of Anesthesiology, Xijing Hospital, The Fourth Military Medical University, Xi'an, Shaanxi Province 710032, PR China.

Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Fur Toxikologische Pathologie
|July 30, 2013
PubMed

Insights

UVB irradiation inhibits PDCD4 expression in mouse skin cells, increasing miR-21 levels. This process involves reactive oxygen species (ROS) and MAPK signaling pathways, crucial for skin cancer development.

Area of Science:

  • Dermatology
  • Molecular Biology
  • Cancer Research

Background:

  • Ultraviolet (UV) irradiation, particularly UVB, is a significant factor in human skin carcinogenesis.
  • Understanding the molecular mechanisms underlying UV-induced skin cancer is critical for developing preventative strategies.

Purpose of the Study:

  • To investigate the impact of UVB irradiation on miR-21-PDCD4 signaling in a mouse epidermal cell line (JB6 P(+)).
  • To elucidate the role of reactive oxygen species (ROS) and mitogen-activated protein kinase (MAPK) pathways in UVB-induced PDCD4 inhibition.

Main Methods:

  • Exposure of JB6 P(+) cells to UVB irradiation.
  • Assessment of PDCD4 and miR-21 expression levels.
  • Pharmacological inhibition of ERK and p38 pathways using U0126 and SB203580, respectively.
  • Treatment with the ROS scavenger N-acetyl-l-cysteine (NAC).

Main Results:

  • UVB irradiation significantly inhibited PDCD4 expression in JB6 cells.
  • UVB exposure led to a marked increase in miR-21 expression, an upstream regulator of PDCD4.
  • Inhibition of ERK and p38 pathways, as well as ROS scavenging, partially reversed UVB-induced PDCD4 inhibition.
  • These findings suggest UVB-induced PDCD4 inhibition is mediated by ROS and MAPK signaling (ERK and p38 phosphorylation).

Conclusions:

  • UVB-induced PDCD4 inhibition in mouse epidermal cells is associated with increased miR-21 expression.
  • Reactive oxygen species (ROS), particularly H2O2, and the phosphorylation of ERK and p38 pathways play a role in this inhibitory process.
  • Elucidating these mechanisms offers insights into UVB-induced skin carcinogenesis.
Keywords:
JB6 cellPDCD4Reactive oxygen speciesUltraviolet lightmicroRNA-21

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