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Development of UV-induced squamous cell carcinomas is suppressed in the absence of SPARC

Ronnie L Aycock1, Amy C Bradshaw, E Helene Sage

  • 1Department of Biochemistry, University of Texas Health Center at Tyler, 11937 US Highway 271, Tyler, TX 75708, USA.

The Journal of Investigative Dermatology
|August 12, 2004
PubMed

Insights

Secreted Protein Acidic and Rich in Cysteine (SPARC) promotes skin tumor development after UV exposure. SPARC-null mice showed significant resistance to UV-induced skin tumors, indicating SPARC

Area of Science:

  • Oncology
  • Dermatology
  • Extracellular Matrix Biology

Background:

  • Secreted Protein Acidic and Rich in Cysteine (SPARC) is a matricellular glycoprotein involved in cell-extracellular matrix interactions.
  • The role of SPARC in UV-induced skin carcinogenesis is not well understood.
  • Understanding SPARC's function is crucial for developing targeted skin cancer therapies.

Purpose of the Study:

  • To investigate the role of SPARC in the development of skin tumors following UV irradiation.
  • To compare UV-induced skin tumor formation and extracellular matrix changes in SPARC-null mice versus wild-type controls.
  • To assess the impact of SPARC on UV-induced immune suppression.

Main Methods:

  • Development of a hairless SPARC-null mouse model.
  • Comparison of tumor induction in SPARC-null mice and control SKH1 hairless mice following chronic UVB exposure (14.5 J/cm² over 23 weeks).
  • Immunohistochemical analysis of SPARC expression in skin tumors.
  • Evaluation of contact hypersensitivity response and UV-induced immune suppression.

Main Results:

  • Wild-type mice developed numerous tumors, including squamous cell carcinomas, after UVB exposure.
  • SPARC-null mice exhibited striking resistance to UV-induced skin tumors, with no squamous cell carcinomas and minimal papilloma formation.
  • SPARC was detected in UV-induced tumor masses but not in non-irradiated skin.
  • SPARC-null mice showed a reduced contact hypersensitivity response and were refractory to UV-induced immune suppression.

Conclusions:

  • SPARC plays a critical role in mediating UV-induced skin tumor formation.
  • The absence of SPARC confers significant resistance to skin carcinogenesis.
  • SPARC may influence skin tumor development through modulation of the immune response and extracellular matrix.

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