Journal
JOURNAL OF CLINICAL INVESTIGATION
Volume 111, Issue 4, Pages 487-495Publisher
AMER SOC CLINICAL INVESTIGATION INC
DOI: 10.1172/JCI200316804
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Funding
- NHLBI NIH HHS [F32 HL10352, R01 HL59574, F32 HL010352] Funding Source: Medline
- NIGMS NIH HHS [R01 GM040711, R01 GM40711] Funding Source: Medline
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SPARC, a 32-kDa glycoprotein, participates in the regulation of morphogenesis and cellular differentiation through its modulation of cell-matrix interactions. Major functions defined for SPARC in vitro are de-adhesion and antiproliferation. In vivo, SPARC is restricted in its expression to remodeling tissues, including pathologies such as cancer. However, the function of endogenous SPARC in tumor growth and progression is not known. Here, we report that implanted tumors grew more rapidly in mice lacking SPARC. We observed that tumors grown in SPARC null mice showed alterations in the production and organization of ECM components and a decrease in the infiltration of macrophages. However, there was no change in the levels of angiogenic growth factors in comparison to tumors grown in wild-type mice, although there was a statistically significant difference in total vascular area. Whereas SPARC did inhibit the growth of tumor cells in vitro, it did not have a demonstrable effect on the proliferation or apoptosis of tumor cells in vivo. These data indicate that host-derived SPARC is important for the appropriate organization of the ECM in response to implanted tumors and highlight the importance of the ECM in regulating tumor growth.
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