title: Naringenin decreases invasiveness and metastasis by inhibiting TGF-β-induced epithelial to mesenchymal transition in pancreatic cancer cells.
abstract: Epithelial to mesenchymal transition (EMT) promotes cellular motility, invasiveness and metastasis during embryonic development and tumorigenesis. Transforming growth factor-β (TGF-β) signaling pathway is a key regulator of EMT. A lot of evidences suggest that this process is Smad3-dependent. Herein we showed that exposure of aspc-1 and panc-1 pancreatic cancer cells to TGF-β1 resulted in characteristic morphological alterations of EMT, and enhancement of cell motility and gemcitabine (Gem) resistance along with an up-regulation of EMT markers genes such as vimentin, N-cadherin, MMP2 and MMP9. Naringenin (Nar) down-regulated EMT markers expression in both mRNA and protein levels by inhibiting TGF-β1/Smad3 signal pathway in the pancreatic cancer cells. Consequently, Nar suppressed the cells migration and invasion and reversed their resistance to Gem.
authors.affiliation: Department of Gastrointestinal Medical Oncology, The Affiliated Third Hospital of Harbin Medical University, Institute of Prevention and Treatment of Cancer of Heilongjiang Province, Harbin, People's Republic of China.
authors.forename: Changjie
authors.initials: C
authors.lastname: Lou
authors.forename: Fayun
authors.initials: F
authors.lastname: Zhang
authors.forename: Ming
authors.initials: M
authors.lastname: Yang
authors.forename: Juan
authors.initials: J
authors.lastname: Zhao
authors.forename: Wenfeng
authors.initials: W
authors.lastname: Zeng
authors.forename: Xiaocui
authors.initials: X
authors.lastname: Fang
authors.forename: Yanqiao
authors.initials: Y
authors.lastname: Zhang
authors.forename: Chunling
authors.initials: C
authors.lastname: Zhang
authors.forename: Wei
authors.initials: W
authors.lastname: Liang
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D015153:Blotting, Western; D002465:Cell Movement / Q000187:drug effects*; D049109:Cell Proliferation / Q000187:drug effects; D003841:Deoxycytidine / Q000031:analogs & derivatives / Q000494:pharmacology; D019008:Drug Resistance, Neoplasm / Q000187:drug effects; D058750:Epithelial-Mesenchymal Transition / Q000187:drug effects*; D004965:Estrogen Antagonists / Q000494:pharmacology*; D044950:Flavanones / Q000494:pharmacology*; D006801:Humans; D009361:Neoplasm Invasiveness; D010190:Pancreatic Neoplasms / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D010766:Phosphorylation / Q000187:drug effects; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism*; D014407:Tumor Cells, Cultured; D014945:Wound Healing / Q000187:drug effects; D000093542:Gemcitabine
chemical_list: D004965:Estrogen Antagonists; D044950:Flavanones; D012333:RNA, Messenger; D016212:Transforming Growth Factor beta; D003841:Deoxycytidine; C005273:naringenin; D000093542:Gemcitabine