title: KLF2 is downregulated in pancreatic ductal adenocarcinoma and inhibits the growth and migration of cancer cells.
abstract: Members of the Kruppel-like factor (KLF) family have been considered as the tumor suppressors for their inhibitory effects on cell proliferation. Dysregulation of KLF2, a member of KLF family, has been observed in various cancer types. However, its expression pattern and functions in the pancreatic ductal adenocarcinoma (PDAC) are unknown. In this study, we examined the expression of KLF2 in PDAC clinical samples and evaluated the functions of KLF2 in the progression of PDAC. KLF2 is shown to be downregulated in PDAC clinical samples and overexpression of KLF2 inhibits the growth, migration, and metastasis of PDAC cancer cells. KLF2 interacts with beta-catenin and negatively regulates the beta-catenin/TCF signaling. Taken together, this study suggests the suppressive functions of KLF2 in PDAC.
authors.affiliation: General Surgery Department, The Fifth People's Hospital of Shanghai, Fudan University, 128 Ruili Rd., Shanghai, 200240, China.
authors.forename: Dexiang
authors.initials: D
authors.lastname: Zhang
authors.affiliation: Department of Medical Oncology, Cancer Hospital of Fudan University, Minhang Branch, Shanghai, 200240, China.
authors.forename: Yuedi
authors.initials: Y
authors.lastname: Dai
authors.affiliation: General Surgery Department, The Fifth People's Hospital of Shanghai, Fudan University, 128 Ruili Rd., Shanghai, 200240, China.
authors.forename: Yuankun
authors.initials: Y
authors.lastname: Cai
authors.affiliation: General Surgery Department, Zhongshan Hospital, General Surgery Institute, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
authors.forename: Tao
authors.initials: T
authors.lastname: Suo
authors.affiliation: General Surgery Department, Zhongshan Hospital, General Surgery Institute, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
authors.forename: Han
authors.initials: H
authors.lastname: Liu
authors.affiliation: General Surgery Department, Zhongshan Hospital, General Surgery Institute, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China.
authors.forename: Yueqi
authors.initials: Y
authors.lastname: Wang
authors.affiliation: General Surgery Department, The Fifth People's Hospital of Shanghai, Fudan University, 128 Ruili Rd., Shanghai, 200240, China. chengzhijian2015@tom.com.
authors.forename: Zhijian
authors.initials: Z
authors.lastname: Cheng
authors.affiliation: General Surgery Department, Zhongshan Hospital, General Surgery Institute, Fudan University, 180 Fenglin Rd., Shanghai, 200032, China. liuhoubao66@sina.com.
authors.forename: Houbao
authors.initials: H
authors.lastname: Liu
mesh_terms: D000230:Adenocarcinoma / Q000473:pathology*; D021441:Carcinoma, Pancreatic Ductal / Q000473:pathology*; D002465:Cell Movement; D049109:Cell Proliferation; D057809:HEK293 Cells; D006801:Humans; D051741:Kruppel-Like Transcription Factors / Q000032:analysis / Q000502:physiology*; D009362:Neoplasm Metastasis; D010190:Pancreatic Neoplasms / Q000473:pathology*; D015398:Signal Transduction / Q000502:physiology; D051820:TCF Transcription Factors / Q000502:physiology; D051176:beta Catenin / Q000502:physiology
chemical_list: C495270:CTNNB1 protein, human; C096161:KLF2 protein, human; D051741:Kruppel-Like Transcription Factors; D051820:TCF Transcription Factors; D051176:beta Catenin
keywords: Beta-catenin/TCF signaling; Cell growth and migration; KLF2; PDAC