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Corrigendum Free access | 10.1172/JCI71241

Loss of SPARC in bladder cancer enhances carcinogenesis and progression

Neveen Said, Henry F. Frierson, Marta Sanchez-Carbayo, Rolf A. Brekken, and Dan Theodorescu

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Published September 3, 2013 - More info

Published in Volume 123, Issue 9 on September 3, 2013
J Clin Invest. 2013;123(9):4089–4089. https://doi.org/10.1172/JCI71241.
© 2013 The American Society for Clinical Investigation
Published September 3, 2013 - Version history
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Related article:

Loss of SPARC in bladder cancer enhances carcinogenesis and progression
Neveen Said, … , Rolf A. Brekken, Dan Theodorescu
Neveen Said, … , Rolf A. Brekken, Dan Theodorescu
Research Article Oncology

Loss of SPARC in bladder cancer enhances carcinogenesis and progression

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Abstract

Secreted protein acidic and rich in cysteine (SPARC) has been implicated in multiple aspects of human cancer. However, its role in bladder carcinogenesis and metastasis are unclear,with some studies suggesting it may be a promoter and others arguing the opposite. Using a chemical carcinogenesis model in Sparc-deficient mice and their wild-type littermates, we found that loss of SPARC accelerated the development of urothelial preneoplasia (atypia and dysplasia), neoplasia, and metastasis and was associated with decreased survival. SPARC reduced carcinogen-induced inflammation and accumulation of reactive oxygen species as well as urothelial cell proliferation. Loss of SPARC was associated with an inflammatory phenotype of tumor-associated macrophages and fibroblasts, with concomitant increased activation of urothelial and stromal NF-κB and AP1 in vivo and in vitro. Syngeneic spontaneous and experimental metastasis models revealed that tumor- and stroma-derived SPARC reduced tumor growth and metastasis through inhibition of cancer-associated inflammation and lung colonization. In human bladder tumor tissues, the frequency and intensity of SPARC expression were inversely correlated with disease-specific survival. These results indicate that SPARC is produced by benign and malignant compartments of bladder carcinomas where it functions to suppress bladder carcinogenesis, progression, and metastasis.

Authors

Neveen Said, Henry F. Frierson, Marta Sanchez-Carbayo, Rolf A. Brekken, Dan Theodorescu

×

Original citation: J Clin Invest. 2013;123(2):751–766. doi:10.1172/JCI64782.

Citation for this corrigendum: J Clin Invest. 2013;123(9):4089. doi:10.1172/JCI71241.

For Figure 4D, the authors inadvertently included the wrong tubulin blot. The correct tubulin blot is shown below. For Figure 6C, the authors mistakenly included a duplicate of the panel shown in Figure 6B of normal urothelium from a Sparc–/– mouse. Figure 6C below shows an independent replicate.

Figure 4

Figure 6

The authors regret the error.

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