Scutellarin inhibits cell migration by regulating production of αvβ6 integrin and E-cadherin in human tongue cancer cells.
To examine the effect of scutellarin on adhesion and migration of oral squamous cell carcinoma (OSCC), the HSC-4 and SAS human OSCC cells were treated with various concentrations of scutellarin. Scutellarin cytotoxicity was evaluated by MTT assays; migration of tongue cancer cells was assessed by wound healing and Transwell chemotaxis; αvβ6 integrin and E-cadherin expression was assessed by immunofluorescence and reverse transcription polymerase chain reaction. Scutellarin at 75 nM significantly inhibited tongue cancer cell proliferation and at 15 nM, significantly reduced HSC-4 and SAS cell motility by 46.3% and 44%, respectively. Scutellarin inhibited SAS cell adhesion to fibronectin in a dose-dependent manner. However, it had no significant effect on HSC-4 cell adhesion to fibronectin; at the same concentration, HSC-4 cells adhered more strongly to fibronectin than SAS cells. Following treatment with scutellarin, E-cadherin and desmoplakin protein levels were increased, whereas E-cadherin mRNA expression was unchanged; protein levels of αvβ6 integrin were decreased-consistent with the change in αvβ6 integrin mRNA. After a 3 nM scutellarin treatment, levels of desmoplakin in HSC-4 and SAS cells increased by 79.9% and 74.5%, respectively. Scutellarin (3 nM) increased expression of E-cadherin in HSC-4 and SAS cells by 37.9% and 52%, respectively, and decreased the expression of αvβ6 integrin by 45.4% and 47.2%, respectively. This study shows that scutellarin inhibits tumor cell proliferation and migration and regulates cell adhesion in OSCC cells; this may be closely related to up-regulation of E-cadherin and down-regulation of αvβ6 integrin.
Li
Haixia
H
Department of Anatomy, Basic Medical Science College, The Second Clinical College, Harbin Medical University, Harbin 150081, PR China.
Huang
Dayong
D
Gao
Zhongxiuzi
Z
Lv
Yanhong
Y
Zhang
Lina
L
Cui
Haidong
H
Zheng
Jinhua
J
D000951:Antigens, Neoplasm / Q000096:biosynthesis* / Q000235:genetics; D047310:Apigenin / Q000494:pharmacology*; D015820:Cadherins / Q000096:biosynthesis* / Q000235:genetics; D002294:Carcinoma, Squamous Cell / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D002448:Cell Adhesion / Q000187:drug effects / Q000502:physiology; D045744:Cell Line, Tumor; D002465:Cell Movement / Q000187:drug effects* / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects; D005965:Glucuronates / Q000494:pharmacology*; D006801:Humans; D016023:Integrins / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D014062:Tongue Neoplasms / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism / Q000473:pathology*
D000951:Antigens, Neoplasm; D015820:Cadherins; D005965:Glucuronates; D016023:Integrins; D012333:RNA, Messenger; C073878:integrin alphavbeta6; C484876:scutellarin; D047310:Apigenin