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Upregulation of C/EBP? contributes to colorectal cancer growth, metastasis and indicates poor survival outcome.

ABSTRACT: The function and clinical implication of transcription factor CCAAT/enhancer-binding protein ? (C/EBP?) in colorectal cancer (CRC) still remains undefined. In fact, C/EBP? has long been considered as a tumor suppressor in hematopoietic system and also found lowly expressed in numerous solid tumors. However, our results here for the first time showed that C/EBP? was unexpectedly upregulated and was an independent prognostic marker for patients with CRC. We therefore aimed to explore the detailed role and mechanisms of C/EBP? in CRC. Our investigation demonstrated that C/EBP? promoted tumor growth both in vitro and in vivo. In addition, suppression of C/EBP? inhibited cell proliferation by inducing G1 phase arrest and inducing apoptosis. Also, C/EBP? enhances CRC cells migration and invasion in vitro as well as metastasis in vivo through regulating EMT. Mechanistically, C/EBP? exerts its oncogenic role by targeting c-Myc/cyclin D1 mediated by ?-catenin involved pathway and we provide evidence indicating that cytoplasmic exclusion of C/EBP? might contribute to its oncogenic function in tumor progression. In conclusion, C/EBP? acts as an oncogene in CRC and could be a potential biomarker of colon carcinogenesis.

SUBMITTER: Mi L

PROVIDER: S-EPMC6129490 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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