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Int J Biol Sci. 2019 Jan 1;15(3):636-646. doi: 10.7150/ijbs.29562. eCollection 2019.

SMARCAD1 Promotes Pancreatic Cancer Cell Growth and Metastasis through Wnt/β-catenin-Mediated EMT.

Liu F1,2, Xia Z3, Zhang M1,2, Ding J1,2, Feng Y1,2, Wu J1,2, Dong Y1,2, Gao W1,2, Han Z1,2, Liu Y4, Yao Y1,2, Li D1,2.

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Department of Radiation Oncology, Hainan West Central Hospital (Shanghai Ninth People's Hospital, Hainan Branch), Shanghai Jiaotong University School of Medicine, Hainan, China.
Department of Radiation Oncology, Shanghai Ninth People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Department of General Surgery, DaHua Hospital, Xuhui, Shanghai, China.
Department of Chemotherapy, Nanjing Medical University Affiliated Cancer Hospital, Cancer Institute of Jiangsu Province, Nanjing, Jiangsu, China.


Pancreatic cancer (PC) is one of the most lethal diseases, characterized by early metastasis and high mortality. Subunits of the SWI/SNF complex have been identified in many studies as the regulators of tumor progression, but the role of SMARCAD1, one member of the SWI/SNF family, in pancreatic cancer has not been elucidated. Based on analysis of GEO database and immunohistochemical detection of patient-derived pancreatic cancer tissues, we found that SMARCAD1 is more highly expressed in pancreatic cancer tissues and that its expression level negatively correlates with patients' survival time. With further investigation, it shows that SMARCAD1 promotes the proliferation, migration, invasion of pancreatic cancer cells. Mechanistically, we first demonstrate that SMARCAD1 induces EMT via activating Wnt/β-catenin signaling pathway in pancreatic cancer. Our results provide the role and potential mechanism of SMARCAD1 in pancreatic cancer, which may prove useful marker for diagnostic or therapeutic applications of PC disease.


EMT; SMARCAD1; Wnt/β-catenin; metastasis

Conflict of interest statement

Competing Interests: The authors have declared that no competing interest exists.

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