Clinicopathologic significance of EpCAM expression in squamous cell carcinoma of the tongue and its possibility as a potential target for tongue cancer gene therapy

Yanamoto, Souichi; Kawasaki, Goro; Yoshitomi, Izumi; Iwamoto, Tsutomu; Hirata, K.; Mizuno, Akio

doi:10.1016/j.oraloncology.2006.10.010

Cited by 72 publications

(72 citation statements)

References 39 publications

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“…However, clinicopathological variables and tumour-specific molecular markers that can identify patients with the highest risk of local recurrence have yet to be defined. 16,[18][19][20][21][22][23][42][43][44][45][46][47][48][49] Vimentin, a mesenchymal cell marker, associates with components of the cytoskeleton and membrane adhesions. Studies of human epithelial carcinomas, such as breast cancer, hepatocellular carcinoma, colon carcinoma, and prostatic adenocarcinoma, have shown that vimentin expression can be correlated with tumour invasion and a poor prognosis.…”

Section: Discussionmentioning

confidence: 99%

Upregulation of vimentin and aberrant expression of E-cadherin/β-catenin complex in oral squamous cell carcinomas: correlation with the clinicopathological features and patient outcome

et al. 2010

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Oral squamous cell carcinoma is a challenging oncology problem. A reliable biomarker for metastasis or high-risk prognosis in oral cancer patients remains undefined. Using quantitative immunohistochemistry, we examined the expression of vimentin, E-cadherin, and b-catenin in 83 oral squamous cell carcinoma patients, and the relationships between the expression of these markers and specific clinicopathological features were analysed. The high expression of vimentin was observed in 23 of 43 (53%) tumours from patients who eventually developed a recurrent tumour and was associated with recurrence and death (Po0.001 and o0.001, respectively). The decreased expression of E-cadherin was observed in 36 of 43 (84%) tumours from patients who eventually developed a recurrent tumour and was also associated with recurrence and death (Po0.001 and o0.001, respectively). Although no correlation between b-catenin expression in whole-tumour sections and clinicopathological features was observed, decreased b-catenin expression at the tumour invasive front was closely associated with recurrence and death (P ¼ 0.002 and 0.002, respectively). The expression of vimentin and that of E-cadherin were associated with survival and were independent prognostic factors in univariate and multivariate analyses. Our data show that the overexpression of vimentin was closely associated with recurrence and death in oral squamous cell carcinoma patients. The combination of the upregulation of vimentin and aberrant expression of E-cadherin/b-catenin complexes at the tumour invasive front may provide a useful prognostic marker in oral squamous cell carcinoma. Modern Pathology (2010) 23, 213-224; doi:10.1038/modpathol.2009 published online 13 November 2009 Keywords: vimentin; oral squamous cell carcinoma; immunohistochemistry Oral cancer is the sixth most frequently occurring cancer worldwide, accounting for 3-5% of all malignancies in both sexes.1,2 Over 90% of all oral carcinomas are classified as oral squamous cell carcinoma, which remains a challenging oncology problem.3 Although early-stage oral squamous cell carcinoma can be treated or cured, the prognosis for advanced oral squamous cell carcinoma (stage III and IV) is poor. The treatment of oral squamous cell carcinoma is usually based on surgery or radiation, with or without concomitant chemotherapy. Despite these advanced therapeutic strategies, the 5-year survival rate of oral squamous cell carcinoma (B50%) has not increased over the past four decades.3-5 Local or regional relapse and cervical lymph node metastasis are the most prevalent

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Section: Discussionmentioning

confidence: 99%

Upregulation of vimentin and aberrant expression of E-cadherin/β-catenin complex in oral squamous cell carcinomas: correlation with the clinicopathological features and patient outcome

et al. 2010

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“…53 It was reported that EpCAM expression could be associated with invasiveness in human tongue cancer cell lines. 8 The EpCAM overexpression decreased adhesion mediated by the cadherin-catenin complex. 54,55 In this study, siRNA of cortactin resulted in the downregulation of adhesion molecules such as E-cadherin, β-batenin, and EpCAM levels, in contrast to previous reports.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Cortactin Increases Invasion Potential in Oral Squamous Cell Carcinoma

Yamada

Yanamoto

Kawasaki

et al. 2010

Pathol. Oncol. Res.

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Cortactin stimulates cell migration, invasion, and experimental metastasis. However, the underlying mechanism is not still understood. In the present study, we therefore evaluated the possibility that cortactin could be appropriate as a molecular target for cancer gene therapy. In 70 primary oral squamous cell carcinomas and 10 normal oral mucosal specimens, cortactin expression was evaluated by immunological analyses, and the correlations of the overexpression of cortactin with clinicopathologic factors were evaluated. Overexpression of cortactin was detected in 32 of 70 oral squamous cell carcinomas; significantly more frequently than in normal oral mucosa. Cortactin overexpression was more frequent in higher grade cancers according to T classification, N classifications, and invasive pattern. Moreover, RNAi-mediated decrease in cortactin expression reduced invasion. Downregulation of cortactin expression 4 increased the expression levels of E-cadherin, β-catenin, and EpCAM. The siRNA of cortactin also reduced PTHrP expression via EGF signaling. These results consistently indicate that the overexpression of cortactin is strongly associated with an aggressive phenotype of oral squamous cell carcinoma. In conclusion, we propose that cortactin could be a potential molecular target of gene therapy by RNAi targeting in oral squamous cell carcinoma. 5

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“…Moreover, it has been reported that an alteration in the expression of adhesion-related molecules is associated with poor prognosis in OSCC patients [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

Co-overexpression of cortactin and CRKII increases migration and invasive potential in oral squamous cell carcinoma

Yamada

Yanamoto

Rokutanda

et al. 2014

Journal of Oral and Maxillofacial Surgery, Medicine, and Pathol

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Cortactin stimulates cell migration, invasion, and experimental metastasis. Overexpression of cortactin has been reported in several human cancers. CRK was originally identified as an oncogene product of v-CRK in a CT10 chicken retrovirus system. Overexpression of CRKII has been reported in several human cancers. CRKII regulates cell migration, morphogenesis, invasion, phagocytosis, and survival; however, the underlying mechanisms are not well understood. We evaluated the possibility of the combination of cortactin and CRKII as an appropriate molecular target for cancer gene therapy. The expression of cortactin and CRKII in 70 primary oral squamous cell carcinomas and 10 normal oral mucosal specimens was determined immunohistochemically, and the correlation of cortactin and CRKII co-overexpression with clinicopathological factors was evaluated. Co-overexpression of cortactin and CRKII was detected in 31 of 70 oral squamous cell carcinomas, the frequency being significantly greater than in normal oral mucosa. In addition, cortactin and CRKII co-overexpression was more frequent in higher-grade cancers according to 3 the T classification, N classification, and invasive pattern. RNAi-mediated co-suppression of cortactin and CRKII expression reduced the migration and invasion potential of an oral squamous cell carcinoma cell line, OSC20. Downregulation of cortactin and CRKII expression also reduced the expression of vimentin, fibronectin, and N-cadherin. These results indicate that the co-overexpression of cortactin and CRKII may be tightly associated with an aggressive phenotype of oral squamous cell carcinoma. Therefore, we propose that the combination of cortactin and CRKII could be a potential molecular target of gene therapy by RNAi-targeting in oral squamous cell carcinoma. 4 1.IntroductionOral squamous cell carcinoma (OSCC) is the most common malignant tumor of the head and neck region and accounts for more than 90% of cancers of the oral cavity [1]. The primary therapeutic modality for OSCC is surgery. Although recent advances in surgical techniques and anticancer agents have improved tumor regression and survival for patients with OSCC, wide surgical resection of OSCC inevitably causes various oral dysfunctions. Therefore, new treatment strategies are urgently needed.The presence of neck lymph node metastasis is strongly related to a poor prognosis in squamous cell carcinoma of the head and neck [2][3][4]. Moreover, it has been reported that an alteration in the expression of adhesion-related molecules is associated with poor prognosis in OSCC patients [5][6][7][8].Chromosomal band 11q13 is a frequently amplified genomic segment in a large number of malignant neoplasms, and is thought of as a potential biomarker for diagnosis and prognosis [9,10]. In head and neck squamous cell carcinoma, this amplification is one of the most frequently observed genetic alterations [11][12][13][14][15][16][17][18][19][20] and is reportedly correlated with aggressive tumor growth [9,13,19], the presence of lymph node ...

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Clinicopathologic significance of EpCAM expression in squamous cell carcinoma of the tongue and its possibility as a potential target for tongue cancer gene therapy

Cited by 72 publications

References 39 publications

Upregulation of vimentin and aberrant expression of E-cadherin/β-catenin complex in oral squamous cell carcinomas: correlation with the clinicopathological features and patient outcome

Upregulation of vimentin and aberrant expression of E-cadherin/β-catenin complex in oral squamous cell carcinomas: correlation with the clinicopathological features and patient outcome

Overexpression of Cortactin Increases Invasion Potential in Oral Squamous Cell Carcinoma

Co-overexpression of cortactin and CRKII increases migration and invasive potential in oral squamous cell carcinoma

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