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Published on: May 8, 2020

XPC silencing in normal human keratinocytes triggers metabolic alterations through NOX-1 activation-mediated reactive

Hamid Reza Rezvani1, Rodrigue Rossignol, Nsrein Ali

  • 1Department of Dermatology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA. hamidreza.rezvani@u-bordeaux2.fr

Biochimica Et Biophysica Acta
|December 21, 2010
PubMed

Insights

Xeroderma pigmentosum C (XPC) knockdown alters cancer cell metabolism via NADPH oxidase-1 (NOX-1) and reactive oxygen species (ROS). Blocking NOX-1 may prevent and treat skin cancers.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Cancer cells exhibit altered bioenergetic properties.
  • Genomic instability plays a role in neoplastic transformation.
  • Xeroderma pigmentosum C (XPC) is crucial for genomic stability.

Purpose of the Study:

  • To investigate the link between genomic instability, reactive oxygen species (ROS), and metabolic alterations in cancer.
  • To explore the role of XPC in neoplastic transformation and its impact on cellular metabolism.

Main Methods:

  • Knockdown of XPC (XPC(KD)) in normal human keratinocytes.
  • Assessed metabolism remodeling through NADPH oxidase-1 (NOX-1) activation.
  • Measured reactive oxygen species (ROS) levels.
  • Investigated the effect of antioxidant enzymes (catalase, CuZnSOD, MnSOD) and NOX-1 inhibition on metabolic changes.

Main Results:

  • XPC knockdown led to metabolism remodeling via NOX-1 activation, increasing ROS levels.
  • Overexpression of antioxidant enzymes did not prevent metabolism remodeling.
  • Impaired NOX-1 activation abrogated ROS level alterations and energy metabolism modifications.
  • NOX-1 activation is present in human squamous cell carcinomas (SCCs).

Conclusions:

  • NOX-1 activation is a key mediator of metabolic alterations and ROS generation linked to XPC deficiency.
  • NOX-1 represents a potential therapeutic target for skin cancer prevention and treatment.

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