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Overexpression of FXYD-3 is involved in the tumorigenesis and development of esophageal squamous cell carcinoma.

ABSTRACT: OBJECTIVE: To investigate the association of FXYD-3 expression with clinicopathological variables and PINCH in patients with ESCC. PATIENTS AND METHODS: Expression of FXYD-3 protein was immunohistochemically examined in normal esophageal mucous (n = 20) and ESCC (n = 64). RESULTS: Expression of FXYD-3 in the cytoplasm markedly increased from normal esophageal epithelial cells to primary ESCC (P = 0.001). The expression of FXYD-3 was correlated with TNM stages and depth of tumor invasion. Furthermore, the cases with lymph node metastasis tended to show a higher frequency of positive expression than those without metastasis (P = 0.086), and FXYD-3 expression tended to be positively related to the expression of PINCH (P = 0.063). Moreover, the cases positive for both proteins had the highest frequency of lymph node metastasis (P = 0.001). However, FXYD-3 expression was not correlated with patient's gender (P = 0.847), age (P = 0.876), tumor location (P = 0.279), size (P = 0.771), grade of differentiation (P = 0.279), and survival (P = 0.113). CONCLUSION: Overexpression of FXYD-3 in the cytoplasm may play an important role in the tumorigenesis and development in the human ESCC, particularly in combination with PINCH expression.

SUBMITTER: Zhu ZL

PROVIDER: S-EPMC3774971 | biostudies-literature | 2013

REPOSITORIES: biostudies-literature

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Overexpression of FXYD-3 is involved in the tumorigenesis and development of esophageal squamous cell carcinoma.

Zhu Zhen-Long ZL Yan Bao-Yong BY Zhang Yu Y Yang Yan-Hong YH Wang Ming-Wei MW Zentgraf Hanswalter H Zhang Xiang-Hong XH Sun Xiao-Feng XF

Disease markers 20130827 3

<h4>Objective</h4>To investigate the association of FXYD-3 expression with clinicopathological variables and PINCH in patients with ESCC.<h4>Patients and methods</h4>Expression of FXYD-3 protein was immunohistochemically examined in normal esophageal mucous (n = 20) and ESCC (n = 64).<h4>Results</h4>Expression of FXYD-3 in the cytoplasm markedly increased from normal esophageal epithelial cells to primary ESCC (P = 0.001). The expression of FXYD-3 was correlated with TNM stages and depth of tumo ...[more]

PMID: 24167366

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Project description:Esophageal cancer occurs as either squamous cell carcinoma (ESCC) or adenocarcinoma. ESCCs comprise almost 90% of cases worldwide, and recur with a less than 15% five-year survival rate despite available treatments. The identification of new ESCC drivers and therapeutic targets is critical for improving outcomes. Here we report that expression of the human DEK oncogene is strongly upregulated in esophageal SCC based on data in the cancer genome atlas (TCGA). DEK is a chromatin-associated protein with important roles in several nuclear processes including gene transcription, epigenetics, and DNA repair. Our previous data have utilized a murine knockout model to demonstrate that Dek expression is required for oral and esophageal SCC growth. Also, DEK overexpression in human keratinocytes, the cell of origin for SCC, was sufficient to cause hyperplasia in 3D organotypic raft cultures that mimic human skin, thus linking high DEK expression in keratinocytes to oncogenic phenotypes. However, the role of DEK over-expression in ESCC development remains unknown in human cells or genetic mouse models. To define the consequences of Dek overexpression in vivo, we generated and validated a tetracycline responsive Dek transgenic mouse model referred to as Bi-L-Dek. Dek overexpression was induced in the basal keratinocytes of stratified squamous epithelium by crossing Bi-L-Dek mice to keratin 5 tetracycline transactivator (K5-tTA) mice. Conditional transgene expression was validated in the resulting Bi-L-Dek_K5-tTA mice and was suppressed with doxycycline treatment in the tetracycline-off system. The mice were subjected to an established HNSCC and esophageal carcinogenesis protocol using the chemical carcinogen 4-nitroquinoline 1-oxide (4NQO). Dek overexpression stimulated gross esophageal tumor development, when compared to doxycycline treated control mice. Furthermore, high Dek expression caused a trend toward esophageal hyperplasia in 4NQO treated mice. Taken together, these data demonstrate that Dek overexpression in the cell of origin for SCC is sufficient to promote esophageal SCC development in vivo.

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Overexpression of FXYD-3 is involved in the tumorigenesis and development of esophageal squamous cell carcinoma.

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Overexpression of FXYD-3 is involved in the tumorigenesis and development of esophageal squamous cell carcinoma.

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