Cysteine-rich intestinal protein 2 (CRIP2) acts as a repressor of NF-κB–mediated proangiogenic cytokine transcription to suppress tumorigenesis and angiogenesis

摘要: Chromosome 14 was transferred into tumorigenic nasopharyngeal carcinoma and esophageal cell lines by a microcell-mediated chromosome transfer approach. Functional complementation of defects present in the cancer cells suppressed tumor formation. A candidate tumor-suppressor gene, cysteine-rich intestinal protein 2 (CRIP2), located hot spot for chromosomal loss at 14q32.3, identified as an important gene capable functionally suppressing Previous studies have shown that CRIP2 is associated with development. To date, no report has provided functional evidence supporting role The study provides unequivocal can suppress tumorigenesis. significantly down-regulated tumors. reexpression suppresses vivo tumorigenesis angiogenesis; these effects are induced its transcription-repressor capability. It interacts NF-κB/p65 to inhibit DNA-binding ability promoter regions major proangiogenesis cytokines critical progression, including IL6, IL8, VEGF. In conclusion, we provide compelling acts transcription repressor NF-κB–mediated proangiogenic cytokine expression thus inhibits formation angiogenesis.