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Enhanced growth of tumors in SPARC null mice is associated with changes in the ECM

Rolf A Brekken1, Pauli Puolakkainen, David C Graves

  • 1Department of Vascular Biology, The Hope Heart Institute, Seattle, Washington 98104-2046, USA.

The Journal of Clinical Investigation
|February 18, 2003
PubMed

Insights

Secreted acidic rich protein (SPARC) is crucial for regulating the tumor microenvironment. Mice lacking SPARC showed faster tumor growth, indicating SPARC

Area of Science:

  • Biochemistry
  • Oncology
  • Extracellular Matrix Biology

Background:

  • Secreted acidic rich protein (SPARC) is a glycoprotein involved in cell-matrix interactions, morphogenesis, and differentiation.
  • SPARC exhibits de-adhesion and anti-proliferative functions in vitro and is expressed in remodeling tissues, including tumors.
  • The role of endogenous SPARC in tumor progression remains largely unknown.

Purpose of the Study:

  • To investigate the function of endogenous SPARC in tumor growth and progression using a mouse model.
  • To determine the impact of SPARC deficiency on the tumor microenvironment, including extracellular matrix (ECM) organization and immune cell infiltration.

Main Methods:

  • Implantation of tumors into SPARC-null and wild-type mice.
  • Analysis of ECM component production and organization within tumors.
  • Assessment of macrophage infiltration and angiogenic growth factor levels.
  • Evaluation of tumor cell proliferation and apoptosis in vivo and in vitro.

Main Results:

  • Tumors implanted in SPARC-null mice exhibited significantly accelerated growth compared to wild-type controls.
  • SPARC deficiency led to altered ECM production and organization and reduced macrophage infiltration in tumors.
  • No significant changes in angiogenic growth factor levels were observed, but total vascular area differed.
  • SPARC inhibited tumor cell growth in vitro but showed no demonstrable effect on proliferation or apoptosis in vivo.

Conclusions:

  • Host-derived SPARC plays a critical role in organizing the tumor microenvironment, particularly the ECM, in response to tumor implantation.
  • The ECM, regulated by SPARC, is a key factor influencing tumor growth.
  • These findings highlight SPARC's importance in modulating the tumor microenvironment and suggest potential therapeutic strategies targeting ECM remodeling.

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