Identification of chemoresistant factors by protein expression analysis with iTRAQ for head and neck carcinoma

Nishimura, Kunihiro; Tsuchiya, Yoshimasa; Okamoto, Hiroki; Ijichi, Kei; Gosho, Masahiko; Fukayama, Minoru; Yoshikawa, Kazuhiro; Bradford, Carol R.; Carey, Thomas E.; Ogawa, Tetsuya

doi:10.1038/bjc.2014.395

Cited by 15 publications

(14 citation statements)

References 26 publications

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“…Recently, the clinical outcome of OSCC has gradually improved, however, patients with OSCC develop chemoresistance reflecting limits in our understanding of the pathogenesis of this cancer [3,4]. Therefore, a better understanding of the molecular mechanisms for oral cancer carcinogenesis contributes to development of novel diagnostic and therapeutic approaches to improve the treatments and prognosis of OSCC patients.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-143 suppresses oral squamous cell carcinoma cell growth, invasion and glucose metabolism through targeting hexokinase 2

Sun

Zhang

2017

Bioscience Reports

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miRNAs are non-coding RNAs that have functions to regulate gene expression and play essential roles in a variety of biological processes of cancers. In the present study, we report miR-143 acts as a tumor suppressor in human oral squamous cell carcinoma (OSCC). The expressions of miR-143 are down-regulated in both OSCC cell lines and patient samples compared with normal adjacent tissues. We found overexpression of miR-143 in oral cancer cell lines suppresses cell migration, cellular glucose metabolism and proliferation. Moreover, overexpression of miR-143 promoted apoptosis and significantly caused cell cycle arrest at G1 stage. The colony formation of oral cancer cells was also suppressed by miR-143. We identified hexokinase 2 (HK2) as a direct target of miR-143 in oral cancer cells. Our data show that miR-143 complementary pairs to the 3′-UTR of HK2 in oral cancer cells, leading to the inhibition of glycolysis in vitro and in vivo. Moreover, knockdown of HK2 by siRNA in oral cancer cells inhibited glucose metabolism, proliferation and migration. Recovery of glucose metabolism by overexpression of HK2 in miR-143 overexpressing cells restores the cell migration and proliferation, suggesting that the miR-143-mediated cancer suppression is through the direct inhibition of HK2. In summary, the present studies highlight miR-143 as a tumor suppressor in OSCC by the suppression of cell migration, glucose metabolism and proliferation through directly targeting HK2, rendering miR-143 a therapeutic strategy for the treatment of clinical OSCC patients.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-143 suppresses oral squamous cell carcinoma cell growth, invasion and glucose metabolism through targeting hexokinase 2

Sun

Zhang

2017

Bioscience Reports

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“…α-Enolase is a metabolic enzyme and is called as platinum drug chemo-resistant factor and is upregulated in platinum-resistant cells. 46 , 47 The proposed theories for chemotherapy resistance are (a) α-enolase loses its glycolytic activity, which is very essential for the antitumor action of cisplatin; 48 (b) α-enolase–tubulin interactions modulates microtubule network, thereby causing resistance to microtubule-targeted drugs such as paclitaxel; 49 (c) in the cell membrane of apoptotic cells, α-enolase acts as plasminogen receptor promoting cellular metabolism in anaerobic conditions and driving tumor invasion through plasminogen activation and extracellular matrix degradation, activating intracellular survival pathway and controlling cell apoptosis; 50 , 51 and (d) α-enolase also inhibits apoptosis partly. 40 Overexpression of this protein in the tissue of patients not responding to carboplatin further validates and reiterates these studies.…”

Section: Resultsmentioning

confidence: 99%

Comparative Proteomic Analysis of Advanced Ovarian Cancer Tissue to Identify Potential Biomarkers of Responders and Nonresponders to First-Line Chemotherapy of Carboplatin and Paclitaxel

et al. 2016

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Conventional treatment for advanced ovarian cancer is an initial debulking surgery followed by chemotherapy combination of carboplatin and paclitaxel. Despite initial high response, three-fourths of these women experience disease recurrence with a dismal prognosis. Patients with advanced-stage ovarian cancer who underwent cytoreductive surgery were enrolled and tissue samples were collected. Post surgery, these patients were started on chemotherapy and followed up till the end of the cycle. Fluorescence-based differential in-gel expression coupled with mass spectrometric analysis was used for discovery phase of experiments, and real-time polymerase chain reaction, Western blotting, and pathway analysis were performed for expression and functional validation of differentially expressed proteins. While aldehyde reductase, hnRNP, cyclophilin A, heat shock protein-27, and actin are upregulated in responders, prohibitin, enoyl-coA hydratase, peroxiredoxin, and fibrin-β are upregulated in the nonresponders. The expressions of some of these proteins correlated with increased apoptotic activity in responders and decreased apoptotic activity in nonresponders. Therefore, the proteins qualify as potential biomarkers to predict chemotherapy response.

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“…[34] An iTRAQ-based MALDI-MS proteomics study on four human HNSCC cell lines: Cisplatin-sensitive UM-SCC-23, UM-SCC-23-CDDPR with acquired cisplatin resistance, naturally cisplatinresistant UM-SCC-81B and UM-SCC-23/WR with acquired 5-fluorouracil resistance proposed α-Enolase as a true cisplatin chemoresistance factor of 13 proteins which were found to be associated with multidrug resistance. [35] Bortezomib is the first therapeutic FDA approved proteosome inhibitor treating relapsed multiple myeloma and mantle cell lymphoma. In HN cancers, its solitary role has not been quite promising however, combining bortezomib with TRAIL (tumor necrosis factor related apoptosis inducing ligand) receptor agonists produced a synergistic cytotoxic effect in TRAIL-resistant HPVpositive cells [ Table 2].…”

Section: Current Treatment Modalities In Head and Neck Cancer And Promentioning

confidence: 99%

Head and Neck Cancer Stem Cell Proteomics

Saleem

Tariq

2019

J Cancer Allied Spec

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It is critical to identify the cell of origin of cancer and the genes/proteins/transcriptional/epigenetic factors of that cell. Here, we review studies on head and neck cancer stem cells (CSC) in the hope of developing better understanding of their role highlighting their importance as novel drug targets. CSC model has introduced a hierarchical conceptual framework for the interpretation of intratumour heterogeneity within tumour. This, in turn, has culminated in a major paradigm shift in terms of how different types of cancers can be targeted for treatment. Several malignancies conform to the CSC model of tumour growth yet identification of CSC markers remains a profound challenge.Key words: Chemo- and radio-resistance, head and neck cancer stem cells, proteomics, treatment modalities

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Identification of chemoresistant factors by protein expression analysis with iTRAQ for head and neck carcinoma

Cited by 15 publications

References 26 publications

MicroRNA-143 suppresses oral squamous cell carcinoma cell growth, invasion and glucose metabolism through targeting hexokinase 2

MicroRNA-143 suppresses oral squamous cell carcinoma cell growth, invasion and glucose metabolism through targeting hexokinase 2

Comparative Proteomic Analysis of Advanced Ovarian Cancer Tissue to Identify Potential Biomarkers of Responders and Nonresponders to First-Line Chemotherapy of Carboplatin and Paclitaxel

Head and Neck Cancer Stem Cell Proteomics

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