Protein salvador homolog 1 acts as a tumor suppressor and is modulated by hypermethylation in pancreatic ductal adenocarcinoma

// Lei Wang 1, * , Mei Wang 2, * , Chenxi Hu 2, * , Pengping Li 3 , Yun Qiao 1 , Youyou Xia 1 , Liang Liu 1 and Xiaodong Jiang 4 1 Department of Radiation Oncology, Lianyungang First People’s Hospital, Jiangsu, People’s Republic of China 2 Tumor Laboratory, Department of Radiation Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Jiangsu, People’s Republic of China 3 Department of Bioinformatics, School of Basic Medical Sciences, Nanjing Medical University, Nanjing, People’s Republic of China 4 Department of Radiation Oncology, The Affiliated Lianyungang Hospital of Xuzhou Medical University, Jiangsu, People’s Republic of China * These authors have contributed equally to this work Correspondence to: Xiaodong Jiang, email: bingliyuxuan@sina.com Keywords: SAV1, tumor suppressor, pancreatic ductal adenocarcinoma, hypermethylation Received: January 13, 2017      Accepted: April 11, 2017      Published: May 18, 2017 ABSTRACT Salvador (SAV) is a gene product that contains two protein-protein interaction modules known as WW domains and is believed to act as a scaffolding protein for Hippo and Warts. SAV1 is the human homolog of Salvador, which is the most well characterized upstream signaling component of Hippo pathway. Although its role in some tumors is known, SAV1 function in other types of tumors, including pancreatic tumor, is still obscure. Here, we determined the role of SAV1 in pancreatic ductal adenocarcinoma (PDAC) development and progression. Our results revealed that SAV1 suppressed expression promoted PDAC invasion and migration, and repressed pancreatic cancer cells apoptosis. Moreover, SAV1 was silenced by hypermethylation. Thus, SAV1 worked as a cancer suppressor and it might be considered as a target for pancreatic cancer therapy.