Metastatic colorectal cancer cells maintain the TGF? program and use TGFBI to fuel angiogenesis
نویسندگان
چکیده
Colorectal cancer (CRC) cells are traditionally considered unresponsive to TGF? due mutations in the receptors and/or downstream signaling molecules. influences CRC only indirectly via stromal cells, such as cancer-associated fibroblasts. However, cell ability directly respond currently remains unexplored. This represents a missed opportunity for diagnostic and therapeutic interventions. Methods: We examined whether from primary liver metastases by inducing TGF?-induced protein ig-h3 (TGFBI) expression, contribution of canonical non-canonical pathways this effect. then investigated vitro vivo TGFBI impact on metastasis formation angiogenesis. Using patient serum samples an orthotopic mouse model we assessed diagnostic/tumor targeting value novel antibodies against TGFBI. Results: Metastatic circulating tumor TGF?. These were characterized absence receptor frequent presence p53 mutations. The pro-tumorigenic program orchestrated was mediated through TGFBI, expression which positively regulated cascades. inhibition sufficient significantly reduce vivo. Moreover, function linked its stimulate levels higher untreated patients with than who receiving chemotherapy. A radiolabeled anti-TGFBI antibody selectively targeted metastatic lesions vivo, underscoring potential. Conclusions: contributes their potential cell-independence. Proteins activated TGF?, represent targets more specific anti-metastatic therapies.
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ژورنال
عنوان ژورنال: Theranostics
سال: 2021
ISSN: ['1838-7640']
DOI: https://doi.org/10.7150/thno.51507