title: Oral cancer cells with different potential of lymphatic metastasis displayed distinct biologic behaviors and gene expression profiles.
abstract: OBJECTIVE
  Oral squamous cell carcinoma (OSCC) often spreads from the primary tumor to regional lymph nodes in the early stage. Better understanding of the biology of lymphatic spread of oral cancer cells is important for improving the survival rate of cancer patients.
  
  
  METHODS
  We established the cell line LNMTca8113 by repeated injections in foot pads of nude mice, which had a much higher lymphatic metastasis rate than its parental cell line Tca8113. Then, we compared the biologic behaviors of cancer cells between them. Moreover, microarray-based expression profiles between them were also compared, and a panel of differential genes was validated using real-time-PCR.
  
  
  RESULTS
  In contrast to Tca8113 cells, LNMTca8113 cells were more proliferative and resistant to apoptosis in the absence of serum, and had enhanced ability of inducing capillary-like structures. Moreover, microarray-based expression profiles between them identified 1341 genes involved in cell cycle, cell adhesion, lymphangiogenesis, regulation of apoptosis, and so on. Some genes dedicating to the metastatic potential, including JAM2, TNC, CTSC, LAMB1, VEGFC, HAPLN1, ACPP, GDF9 and FGF11, were upregulated in LNMTca8113 cells.
  
  
  CONCLUSIONS
  These results suggested that LNMTca8113 and Tca8113 cells were proper models for lymphatic metastasis study because there were differences in biologic behaviors and metastasis-related genes between them. Additionally, the differentially expressed gene profiles in cancer progression may be helpful in exploring therapeutic targets and provide the foundation for further functional validation of these specific candidate genes for OSCC.
authors.affiliation: State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu.
authors.forename: Zhang
authors.initials: Z
authors.lastname: Zhuang
authors.forename: Pan
authors.initials: P
authors.lastname: Jian
authors.forename: Li
authors.initials: L
authors.lastname: Longjiang
authors.forename: Han
authors.initials: H
authors.lastname: Bo
authors.forename: Xiao
authors.initials: X
authors.lastname: Wenlin
mesh_terms: D000135:Acid Phosphatase; D000818:Animals; D017209:Apoptosis / Q000235:genetics; D002294:Carcinoma, Squamous Cell / Q000235:genetics / Q000473:pathology* / Q000556:secondary; D020789:Cathepsin C / Q000235:genetics; D002448:Cell Adhesion / Q000235:genetics; D015815:Cell Adhesion Molecules / Q000235:genetics; D002453:Cell Cycle / Q000235:genetics; D045744:Cell Line, Tumor; D049109:Cell Proliferation; D016326:Extracellular Matrix Proteins / Q000235:genetics; D005260:Female; D005346:Fibroblast Growth Factors / Q000235:genetics; D020869:Gene Expression Profiling; D055429:Growth Differentiation Factor 9 / Q000235:genetics; D007797:Laminin / Q000235:genetics; D008207:Lymphatic Metastasis / Q000235:genetics / Q000473:pathology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008819:Mice, Nude; D009062:Mouth Neoplasms / Q000235:genetics / Q000473:pathology*; D009857:Oncogenes / Q000235:genetics; D017027:Protein Tyrosine Phosphatases / Q000235:genetics; D011509:Proteoglycans / Q000235:genetics; D015854:Up-Regulation / Q000235:genetics; D042582:Vascular Endothelial Growth Factor C / Q000235:genetics; D000099249:Proteoglycan Link Protein; D062765:Junctional Adhesion Molecule B
chemical_list: D000135:Acid Phosphatase; D020789:Cathepsin C; D015815:Cell Adhesion Molecules; D016326:Extracellular Matrix Proteins; D005346:Fibroblast Growth Factors; D055429:Growth Differentiation Factor 9; D007797:Laminin; D017027:Protein Tyrosine Phosphatases; D011509:Proteoglycans; D042582:Vascular Endothelial Growth Factor C; D000099249:Proteoglycan Link Protein; C525897:GDF9 protein, human; C411887:JAM2 protein, human; D062765:Junctional Adhesion Molecule B; C478221:LAMB1 protein, human; C428439:prostatic acid phosphatase; C533918:CTSC protein, human