| セッション情報 | The 4th International ForumShort Oral Presentations（Pancreaticobiliary disorders 2） |
|---|---|
| タイトル | IF-SOP-17：Pancreatic Ductal Adenocarcinoma（PDAC）：Identification of compounds that inhibit NUPR1 protein function in cell culture |
| 演者 | Abian Olga（Aragon Health Science Institute, Spain） |
| 共同演者 | Arruebo Maria（Aragon Health Science Institute, Spain）, Iovana Juan（Aragon Health Science Institute, Spain）, Neira Jose Luis（Aragon Health Science Institute, Spain）, Lanas Angel（Aragon Health Science Institute, Spain）, Velazquez-Campoy Adrian（Aragon Health Science Institute, Spain） |
| 抄録 | Because pancreatic cancer is often diagnosed at a late stage, surgical removal of the tumor is often difficult, if not impossible. Pancreatic ductal adenocarcinoma, or PDAC, is by far the most common type of pancreatic malignancy. Patients whose disease is caught at an early stage have a better chance of long-term survival, but the pancreas emits few known clues to signal that the carcinogenic process has begun, so there are currently no early detection tests. Overall, just 6 percent of patients survive 5 years after diagnosis. Protein NUPR1（Nuclear Protein 1）, also known as protein p8, which is overexpressed in several types of human cancers（breast, thyroid, skin...）, but it is especially overexpressed in PDAC. It has been demonstrated in mice studies that, in this kind of tumors, p8 protein is essential in the development and progression of tumor. After blocking its expression in pancreatic cancer cells, the formation of tumors can be prevented, thus, confirming its key role in PDAC. NUPR1 protein is a small basic protein（82 aminoacids）of both nuclear and cytoplasmic localization, which belongs to the group of proteins called intrinsically unstructured or intrinsically disordered proteins（IDPs）. In our group, we have developed a new strategy for identifying compounds that stabilize the native structure of p8 and block NUPR1 intracellular interactions. The in vitro selected compounds inhibited NUPR1 interactions with one of its cellular partners and efficiently blocked NUPR1 function in cell-based studies. |
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