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Fontanini, G., De Laurentiis, M., Silvana Vignati, S., Chinè, S., Lucchi, M., Silvestri, V., Mussi, A., De Placido, S., Tortora, G., Bianco, A.R., Gullick, W., Angeletti, C.A., Bevilacqua, G. and Ciardiello, F. (1998) Evaluation of Epidermal Growth Factor-Related Growth Factors and Receptors and of Neoangiogenesis in Completely Resected Stage I-IIIA Non-Small-Cell Lung Cancer: Amphiregulin and Microvessel Count Are Independent Prognostic Indicators of Survival. Clinical Cancer Research, 4, 241-249.

has been cited by the following article:

• TITLE: Effects of 4-(3-Chloro-Benzyl)-6,7-Dimethoxy-Quinazoline on Kinetics of P120-Catenin and Periplakin in Human Buccal Mucosa Squamous Carcinoma Cell Line

  AUTHORS: Isao Tamura, Aiko Kamada, Seiji Goda, Yoshihiro Yoshikawa, Eisuke Domae, Takashi Ikeo

  KEYWORDS: 4-(3-Chloro-Benzyl)-6, 7-Dimethoxy-Quinazoline, Human Buccal Mucosa Squamous Cancer Cell Line, P120-Catenin, Periplakin

  JOURNAL NAME: Open Journal of Stomatology, Vol.4 No.5, May 15, 2014

  ABSTRACT: In order to detect molecular markers for the epidermal growth factor inhibitor 4-(3-chloro-benzyl)- 6,7-dimethoxy-quinazoline (tyrphostin), we investigated the kinetics of p120-catenin and periplakin in the human buccal mucosa squamous cancer cell line BICR 10 treated with 3 nM tyrphostin. Growth of BICR 10 cells was inhibited by treatment with tyrphostin. Although changes were not observed in the expression of EGFR and p120-catenin, expression of Akt, Src and periplakin in BICR 10 treated with 3 nM tyrphostin tended to decrease. In addition, phosphorylation of EGFR, Akt and Src was inhibited by treatment with tyrphostin. On immunocytochemical staining, immunoreactions with phosphorylated EGFR, phosphorylated Akt and phosphorylated p120-catenin were weak in BICR 10 treated with tyrphostin. There was a slight immunocy to chemical reaction to periplakin in BICR 10 cells induced by tyrphostin. In conclusion, the decrease in phosphorylation in EGFR and p120-catenin by tyrphostin, following the decrease in Src or Akt phosphorylation, may inhibit expression of several growth factors associated with the proliferation and migration of cancer cells.