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Xiao M.,Shanghai JiaoTong University | Xiao M.,Shanghai Research Institute of Stomatology and Shanghai Key Laboratory of Stomatology | Yan M.,Shanghai JiaoTong University | Yan M.,Shanghai Research Institute of Stomatology and Shanghai Key Laboratory of Stomatology | And 9 more authors.
Experimental Cell Research | Year: 2017

Our previous studies have identified that CD166 works as a cancer stem-like cell (CSC) marker in epithelial cancers with a large repertoire of cellular functions. However, the post-translational regulatory mechanisms underlying CD166 turnover remain elusive. Several independent studies have reported that E3 ubiquitin ligase CHIP revealed significant biological effects through ubiquitin proteasome pathway on some kinds of malignant tumors. With analyzing the effects of CHIP expressions on stem-like cell populations, we found that CHIP represses CSC characteristics mainly targeting the CSC related protein CD166 in head and neck cancer (HNC). To investigate the role and relationship between CD166 and CHIP, HNC tissues and cell lines were used in this study. A significant negative correlation was observed between the expression levels of CHIP and CD166 in HNC patient samples. We also found that CHIP directly regulates the stability of CD166 protein through the ubiquitin proteasome system, which was also identified participating in the regulation of CSC behaviors in HNCs. Our findings demonstrate that CHIP-CD166-proteasome axis participates in regulating CSC properties in HNCs, suggesting that the regulation of CD166 by CHIP could provide new options for diagnosing and treating in the patients with HNCs. © 2017 The Authors


Wu X.,Shanghai JiaoTong University | Wu X.,Shanghai Research Institute of Stomatology and Shanghai Key Laboratory of Stomatology | Cao W.,Shanghai JiaoTong University | Cao W.,Shanghai Research Institute of Stomatology and Shanghai Key Laboratory of Stomatology | And 11 more authors.
Molecular Cancer | Year: 2013

Background: In our previous study using oligonucleotide microarrays, we revealed that transglutaminase 3 (TGM3) was remarkably down-regulated in head and neck cancer (HNC). However, the potential of TGM3 as a useful biomarker or molecular target for HNC is unclear. Methods: The transcriptional and post-translational status of TGM3 in HNC cell lines and specimens was detected using real-time PCR and western blot analysis. Bisulfate-treated DNA sequencing was used to analyze the molecular mechanism of TGM3 gene silencing. In addition, the effects of TGM3 on the proliferation, colony formation and induction of apoptosis in vitro and tumorigenicity in vivo were investigated through exogenous expression of TGM3 in HNC cells. Immunohistochemistry was used to evaluate TGM3 expression in large HNC samples. Results: TGM3 was down-regulated in HNC samples and cell lines (P < 0.0001). The hypermethylation of a promoter CpG island was one of the mechanisms of silencing the TGM3 gene in HNC. Exogenous expression of TGM3 in HNC cells could inhibit the proliferation and enhance the apoptosis of HNC cells in vitro and suppress tumor growth in vivo. In addition, TGM3 protein levels were strongly associated with the pathological differentiation of HNC tissues (P = 0.0037). Survival analysis revealed that low TGM3 expression was associated with worse overall survival (P = 0.0002), and TGM3 expression level was an independent predictor in patients with HNC.Conclusions: The studies prove that TGM3, as a candidate tumor suppressor, contributes to the carcinogenesis and development of HNC and may serve as a useful biomarker for patients with HNC. © 2013 Wu et al.; licensee BioMed Central Ltd.


Ren Z.-H.,Shanghai JiaoTong University | Ren Z.-H.,Shanghai Research Institute of Stomatology and Shanghai Key Laboratory of Stomatology | Lin C.-Z.,Shanghai JiaoTong University | Lin C.-Z.,Shanghai Research Institute of Stomatology and Shanghai Key Laboratory of Stomatology | And 23 more authors.
Oncotarget | Year: 2016

CD73 is a cell surface immunosuppressive enzyme involved in tumor progression and metastasis. While patients whose cancer cells express elevated CD73 are typically associated with an unfavorable outcome, the clinical impact of CD73 expression in patients with Head and neck squamous cell carcinoma (HNSCC) remains unclear. In the present study, we investigated the prognostic significance of CD73 in HNSCC using gene and protein expression analyses. Our results demonstrate that high levels of CD73 are significantly associated with reduced overall survival in patients with HNSCC. We also investigated the functional role of CD73 in vitro and demonstrated that CD73 promotes HNSCC migration and invasion through adenosine A3R stimulation and the activation of EGF/EGFR signaling. Moreover, in vivo xenograft studies demonstrated that CD73 promotes tumorigenesis. In conclusion, our study highlights a role for CD73 as a poor prognostic marker of patient survival and also as a candidate therapeutic target in HNSCCs.


Xiao M.,Shanghai JiaoTong University | Xiao M.,Shanghai Research Institute of Stomatology and Shanghai Key Laboratory of Stomatology | Wang X.,Shanghai JiaoTong University | Wang X.,Shanghai Research Institute of Stomatology and Shanghai Key Laboratory of Stomatology | And 4 more authors.
Expert Review of Molecular Diagnostics | Year: 2016

Introduction: Many basic studies have provided some evidences for the correlations of CD166 to cancer. However, along with the growing studies on the clinical values of CD166 in cancer areas, some controversial and inconclusive results were obtained. Areas covered: An appropriate query and collection of the published articles was conducted through search in PubMed and EMBASE database. A subsequent systematical and quantitative summary of CD166 related expression and cancer was conducted with meta-analysis to clarify its clinical significance for potential translation as cancer biomarkers. Expert commentary: The overall results suggested total CD166 correlated to cancer risk, membrane CD166 correlated to nodal metastasis and cytoplasmic CD166 correlated to TNM stage, and disease-free survival. The membrane CD166, cytoplasmic CD166 and soluble CD166 showed great potential to be used as a panel of markers for predicting cancer overall survival. We might conclude that CD166 functions as a risk factor for cancers, and the alterations of its different functional isoforms were observed to correlate with specific or interplayed clinical outcomes. © 2016 Informa UK Limited, trading as Taylor & Francis Group


Liu J.,Shanghai JiaoTong University | Cao W.,Shanghai JiaoTong University | Chen W.,Shanghai JiaoTong University | Chen W.,Shanghai Research Institute of Stomatology and Shanghai Key Laboratory of Stomatology | And 2 more authors.
Journal of Oral Pathology and Medicine | Year: 2015

Background: Kallmann syndrome 1 sequence gene (KAL1) protein is an extracellular matrix associated protein which plays vital roles in neurons development and cell migration. However, its biological functions and clinical implications have yet not been revealed in oral carcinogenesis. The objective of the study was to evaluate the role of KAL1 in oral cancer and determine clinical significance of KAL1 in oral squamous cell carcinomas (OSCCs). Methods: The expression pattern of KAL1 was examined in a testing cohort including OSCCs (n = 42) and paired adjacent tissues (PATs) (n = 14) by real-time PCR. The result was further validated in a validating cohort of OSCCs (n = 32). Correlation between clinicopathological parameters and KAL1 mRNA levels was analyzed by Kruskal-Wallis test. In vitro, the effects of KAL1 ablation through siRNA-mediated knockdown on the proliferation of OSCC cells were determined by CCK-8, BrdU, and colonies formation assays, respectively. In addition, cell cycle distribution was further evaluated by cytometry. Results: We observed that remarkably decreased expression of KAL1 mRNA in two independent cohorts (P = 0.0002 and P = 0.033, respectively). Furthermore, downregulated KAL1 mRNA was significantly associated with worse pathological grade (P = 0.013 and P = 0.035, respectively). Upon KAL1 silencing, the proliferation and colonies formation potentials of OSCC cells were notably promoted by accelerating G1 to M phase transition. Conclusion: These data indicated that KAL1 plays a potential suppressive role on OSCC initiation and progression, and KAL1 gene may serve as an adjuvant biomarker for the identification of pathological grade. © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

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