PurposeThe aim of this study was to confirm the expression profile of cytokeratin (CK)17 in comparison with that of CK13 in oral squamous cell carcinoma (OSCC) and leukoplakia and to clarify an association of CK17 with the OSCC differentiation.MaterialsThe expression of CK17 and CK13 was immunohistochemically examined in 105 patients with OSCC and 108 patients with leukoplakia. A correlation of CK expression with clinicopathological variables was carried out. The over-expression levels of CK17 mRNA were analyzed by real-time RT-PCR in 5 OSCC cell lines (HSC-2, HSC-3, SAS, SQUU-A, SQUU-B).ResultsCK17 and CK13 were detected in 101 (96.2 %) and three (2.9 %) of the 105 OSCCs, respectively. CK17 was significantly expressed in well-differentiated OSCC compared to moderately/poorly differentiated OSCC (p < 0.01). As detected in 19 of the 34 dysplastic leukoplakias (55.9 %) and 36 of the 74 hyperplastic leukoplakias (48.6 %), CK17 was significantly expressed in dysplastic leukoplakias (p < 0.01). As detected in 11 of the 34 dysplastic (32.4 %) and 52 of the 74 hyperplastic leukoplakias (70.3 %), CK13 was significantly expressed in hyperplastic leukoplakias (p < 0.01). The relative expression of CK17 mRNA in HSC-2 was significantly higher than in HSC-3 and SAS (p < 0.05). Moreover, the relative expression of CK17 mRNA in SQUU-A was significantly higher than in SQUU-B (p < 0.05).ConclusionCK17 expression could be associated with the differentiation and the malignancy of OSCC. A combination pattern of CK17/CK13 might be a suitable marker of malignant transformation.

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In this ex vivo model, the hybrid implant demonstrated promising primary stability compared with the cylindrical implant. The improved stability of the hybrid implant was especially evident in cancellous bone. The influence of the cortical layer should be recognized when selecting implants for primary stability.

These results suggest that p75NTR is expressed in undifferentiated cell populations in OL and OSCC. Furthermore, p75NTR is possibly involved in invasion and poor prognosis in OSCC.

Epithelial-to-mesenchymal transition (EMT), an essential developmental program, is involved in tumor progression. ΔNp63, a homolog of p53, is associated with the EMT program, but the detailed mechanism remains to be elucidated. In this study, we investigated the role of ΔNp63 in EMT during progression of oral squamous cell carcinoma (OSCC). Five OSCC cell lines and specimens from 78 patients with OSCC were used. The expressions of ΔNp63, p63α, p63β and epithelial markers (cytokeratins 5 and 14) was detected in the OSCC cells, but not in SQUU-B cells (high metastatic potential). E-cadherin was expressed in all OSCC cells. Mesenchymal markers were strongly expressed in the SQUU-B cells. Knockdown of endogenous ΔNp63 in HSC-2 cells induced morphological changes to the spindle shape, decreased the expression of epithelial markers, increased the expression of mesenchymal markers, increased migration and reduced proliferation. By contrast, SQUU-B cells overexpressing ΔNp63β showed changed their morphology from stromal cell-like to epithelial cells. However, E-cadherin expression was not affected by ΔNp63 knockdown or overexpression. Immunohistochemical staining revealed that cancer cells expressing vimentin were found at the invasive front in the OSCC specimens. The intensity of ΔNp63 expression was also decreased in these cells. Interestingly, the vimentin positivity or decreased intensity of ΔNp63 was positively associated with metastases and poor prognosis in the OSCC patients. These results indicated that ΔNp63 downregulation in cancer cells induces a mesenchymal phenotype that is related to tumor progression of OSCC.