BackgroundAnnexins are calcium and phospholipid binding proteins that form an evolutionary conserved multigene family. Considerable evidence indicates that annexin A10 (ANXA10) is involved in tumoral progression, although little is known about its role in human oral carcinogenesis. In this study, we investigated the involvement of ANXA10 in oral squamous cell carcinoma (OSCC).Methodology/Principal FindingsANXA10 mRNA and protein expressions were assessed by quantitative reverse transcriptase polymerase chain reaction and immunoblotting, and we conducted a proliferation assay and cell-cycle analysis in ANXA10 knockdown cells in vitro. We evaluated the correlation between the ANXA10 expression status in 100 primary OSCCs and the clinicopathological features by immunohistochemistry. ANXA10 mRNA and protein expression levels were up-regulated in all cellular lines examined (n = 7, p<0.05). ANXA10 knockdown cells showed that cellular proliferation decreased by inactivation of extracellular regulated kinase (ERK) (p<0.05), and cell-cycle arrest at the G1 phase resulted from up-regulation of cyclin-dependent kinase inhibitors. ANXA10 protein expression in primary OSCCs was also significantly greater than in normal counterparts (p<0.05), and higher expression was correlated with tumoral size (p = 0.027).Conclusions/SignificanceOur results proposed for the first time that ANXA10 is an indicator of cellular proliferation in OSCCs. Our results suggested that ANXA10 expression might indicate cellular proliferation and ANXA10 might be a potential therapeutic target for the development of new treatments for OSCCs.
Abstract. Heat shock factor 1 (HSF1) is responsible for expression of a large class of heat shock proteins that have been implicated in the malignant phenotype of human cancers. Little is known about the effect of a high level of HSF1 on the behavior of oral squamous cell carcinoma (OSCC). In this study, we assessed the value of HSF1 for predicting clinical outcomes in OSCC. Quantitative reverse transcriptase-polymerase chain reaction and Western blotting showed that the expressions of HSF1 mRNA and protein in OSCC-derived cell lines (HSC-2, HSC-3, HSC-4, Sa3, Ca9-22, KON and Ho-1-u-1) were elevated compared with those in human normal oral keratinocytes (P<0.05). Similar to in vitro data, HSF1 mRNA expression in primary OSCCs (n=50) was significantly greater than in normal counterparts (P<0.05). Since HSF1 was observed in the nucleus and cytoplasm by immunohistochemistry, we investigated the correlation between the HSF1 expression status at each subcellular location and the clinical behavior of OSCCs. Among the clinical classifications, higher nuclear HSF1 expression was closely related to tumor size and histopathologic types (P<0.05). These results showed for the first time that nuclear HSF1 expression may contribute to cancer progression and that HSF1 might be a potential diagnostic biomarker and a therapeutic target for
Our results suggested for the first time that Sec8 might play a specific role in OSCC progression by mediating MMP secretion.
Purpose: Family with sequence similarity 3, member B (FAM3B), also known as PANcreatic DERived factor (PANDER), is an islet‐specific cytokine predominantly expressed in both pancreatic α‐ and β‐cells. FAM3B is known to induce apoptosis in pancreatic cells, and may therefore be able to regulate apoptosis in other cell types, including cancer cells. However, the role of FAM3B in carcinogenesis is unknown. We previously performed global gene screening using DNA microarray analysis to identify crucial molecules in oral squamous cell carcinoma (OSCC). The results showed significant down‐regulation of FAM3B in OSCC‐derived cell lines, as compared with human normal oral keratinocytes (HNOKs). The aim of the present study was to clarify the association between FAM3B and OSCCs. Results: Expression profiles of FAM3B in OSCC‐derived cell lines and human primary OSCCs were examined by real‐time quantitative reverse transcriptase‐polymerase chain reaction and Western blot analysis. Significantly decreased expression of FAM3B mRNA and FAM3B protein were observed in five OSCC‐derived cell lines, as compared with HNOKs. Moreover, immunohistochemical analysis revealed down‐regulated FAM3B protein expression in primary OSCC samples. In order to examine whether microRNA (miRNA) potentially regulates FAM3B expression, miRNA microarray analysis was performed with OSCC‐derived cell lines. miRNA microarray data showed that miR‐181a, miR‐181b, miR‐200b, and miR‐200c, which can induce imperfect base pairing with the 3′‐untranslated region of FAM3B mRNA, were up‐regulated in all cell lines examined. Conclusions: These results indicate that decreased FAM3B expression is able to promote OSCC progression and that certain miRNAs may be correlated with the altered expression of FAM3B.
The human kallikrein-related peptidase family is comprised of 15 serine protease genes on chromosome 19q13.4. Our previous microarray analyses showed that the gene kallikrein-related peptidase 13 (KLK13) was down-regulated in oral squamous cell carcinoma (OSCC) cell lines. We evaluated the expression status of KLK13 in primary OSCCs and performed functional molecular experiments in OSCC cell lines. In 102 primary tumors studied, KLK13 expression significantly (P < 0.05) decreased compared with matched normal counterparts. Interestingly, KLK13-negative cases correlated significantly (P < 0.05) with regional lymph node metastasis. In vitro, cells overexpressing KLK13 (oeKLK13) had decreased invasiveness and motility and up-regulation of adhesion molecules (E-cadherin, α-catenin, β-catenin, junction plakoglobin, plakophilin4, desmocollin2, desmoglein3, and desmoplakin) compared with control cells. A rescue experiment that transfected oeKLK13 cells with siRNA against KLK13 restored invasiveness and migration activities with down-regulated adhesion molecules. Based on our results, we concluded that KLK13 may play an important role in regulating cellular migration and invasiveness, making the loss of KLK13 a potential biomarker for early detection of lymph node metastasis in OSCCs.
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