Immunolocalization of vimentin, keratin 17, Ki-67, involucrin, ß-catenin and E-cadherin in cutaneous squamous cell carcinoma.

Skin squamous cell carcinoma (SCC) is a subtype of very aggressive skin cancers. To investigate if epithelial-mesenchymal transition (EMT), a process for epitheloid cells losing their polarity and cohesiveness and transform into spindle-shaped cells, occurs in skin SCC. By using immunofluorescence, we defined the immunolocalization of vimentin, Keratin 17, ß-catenin, E-cadherin, Ki-67 and involucrin, in SCC samples. Our results show reduced activity of involucrin and E-cadherin, and increased expression of Ki-67, ß-catenin, Keratin 17 and vimentin in SCC. These data propose that EMT really occurs in poorly differentiated SCC and keratin 17 and involucrin may be another two biomarkers for EMT.

Phospholipase D participates in H(2)O(2)-induced A549 alveolar epithelial cell migration.

To investigate the effects of phospholipase D (PLD) on low-concentration hydrogen peroxide (H(2)O(2))-induced growth and migration in alveolar epithelial A549 cells, the cells were exposed to H(2)O(2) (3-100 µM) for 12-48 hours, cell proliferation was determined by MTT assay and cell migration was tested by a modified epithelial wound healing assay. We found that one bolus of H(2)O(2) (10-100 µM) did not affect proliferation, but significantly stimulated migration (143-161% of control) after a 12-hour exposure. Pretreatment with the antioxidants catalase (1000 U/ml), N-acetyl-cysteine (2 mM), or edaravone (10 µM) abolished the migration induced by 30 µM H(2)O(2); the PLD inhibitor 1-butanol (0.5%) also attenuated H(2)O(2)-induced migration to the control level; while exogenous phosphatidic acid (PA) (10(-7)-10(-4) M) mimicked the effects of PLD activation and induced migration in a dose-dependent manner. We suggest that the alveolar epithelial cell migration induced by exposure to low concentrations of H(2)O(2) benefits tissue repair during acute lung injury (ALI) and PLD is involved in the underlying mechanism.