Functional characterization of the atypical member of the IkappaB inhibitor Bcl-3 in pancreatic ductal adenocarcinoma (P04)

蛋白质B细胞CLL/淋巴瘤3（Bcl-3）的kappa-B（IkappaB）家族的抑制剂的非典型成员是血液恶性肿瘤中确定的癌基因。在这里，我们首次证明了Bcl-3在人类和小鼠PDAC中的过度磷酸化。使用各种遗传工具，我们报告，过度磷酸化Bcl-3负调控胰腺癌的发生和转移。我们将详细阐述Bcl-3及其磷酸化位点在PDAC中以前未被认识的作用，并强调Bcl-3在这种疾病中的新方面。

The atypical member of the Inhibitor of kappa-B (IkappaB) family of proteins B-cell CLL/lymphoma 3 (Bcl-3) is an established oncogene in hematologic malignancies. Here we demonstrate for the first-time hyperphosphorylation of Bcl-3 in human and murine PDAC. Using various genetic tools we report that hyperphosphorylated Bcl-3 negatively regulates pancreatic carcinogenesis and metastasis. We will elaborate the previously unrecognized role for Bcl-3 and its phosphorylated sites in PDAC and highlight new aspects of Bcl-3 in this disease.