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High SPON2 expression is associated with hepatocellular carcinoma.
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Matricellular protein SPON2 acts as an HCC suppressor and utilizes distinct signaling events to perform dual functions in HCC microenvironment
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spondin-2 might be a novel therapeutic target and prognostic biomarker for squamous cell carcinoma patients
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Egr-1 regulates mindin expression by directly binding to the mindin promoter; mindin suppresses colon cancer progression by blocking angiogenesis.
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Spondin-2 overexpression contributes to tumor aggressiveness and prognosis in gastric cancer.
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SPON2 is a transcriptional target of the metastasis gene MACC1. SPON2 induces cell motility in vitro and CRC metastasis in mice. In patients, SPON2 serves as prognostic indicator for CRC metastasis and survival, and might represent a promising target for therapeutic approaches.
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Data suggest that spondin-2 could be an independent diagnostic and prognostic biomarker of colon cancer.
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Mindin protects against vascular hyperplasia by suppression of abnormal VSMC proliferation, migration and phenotypic switching in an AKT-dependent manner.
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Using tissue microarray by immunohistostaining, we found SPON2 to be over-expressed in prostate cancer (PCa). SPON2 staining was more intense in Gleason score sum 7-8 and in PCa patients with metastasis.
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mindin serves as a novel mediator that protects against cardiac hypertrophy and the transition to heart failure by blocking AKT/GSK3beta and TGF-beta1-Smad signalling.
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High Mindin is associated with diabetic nephropathy in type 2 diabetes.
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Spondin 2, which is regulated by T(3), has an important role in cell invasion, cell migration, and hepatoma tumor progression.
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The structure of the F-spondin domain of mindin was determined at 1.8-A resolution.