Hallmarks of Cancer-Related Newly Prognostic Factors of Oral Squamous Cell Carcinoma

Sasahira, Tomonori; Kirita, Tadaaki

doi:10.3390/ijms19082413

Cited by 204 publications

(197 citation statements)

References 141 publications

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“…Oral squamous cell carcinoma is the sixth most common cancer and increasing rapidly worldwide. [8] The current conventional strategies for the treatment of OSSC include surgical resection, radiotherapy and/or cisplatin based chemotherapy. [9] Even though these multimodal strategies are effective for early stage-oral cavity cancer, 5-years survival rates are significantly lower for the patients with advanced stage-oral squamous cell carcinoma.…”

Section: Discussionmentioning

confidence: 99%

Metformin and Dicholoroacetate Combination Exert a Synergistic Effect on Cell Viability of Oral Squamous Cell Carcinoma

et al. 2019

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Objective: To assess the effects of Metformin, Dichloroacetate (DCA) and their combination on cell viability in oral squamous cell carcinoma, UPCI-SCC-131 cell line. Methods: UPCI-SCC-131 cells were plated in 96 E-plate (1x104 cells/well) and were treated with Metformin (1-16mM) and/or DCA (15-120mM) for 24-48-72h. xCELLigence SP system was used to monitor real time cell viability. In addition, drug combination index was analyzed with CompuSyn software according to Chou-Talalay method. Results: Half-maximal inhibitory concentrations (IC 50) of Met-formin and DCA were found to be 3mM and 23mM, respectively, for 72 hours. CI values (0.76-0.80) in all combination groups below 1 indicated that Metformin/DCA combination had a moderate synergistic effect on cell viability in UPCI-SCC-131 cells. Discussion: Metformin/DCA combination synergistically decreased the cell viability of UPCI-SCC-131 cells. Therefore, a combined application of Metformin and DCA may be considered as a candidate therapy for the "drug repositioning" of the treatment of oral cavity cancer.

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Section: Discussionmentioning

confidence: 99%

Metformin and Dicholoroacetate Combination Exert a Synergistic Effect on Cell Viability of Oral Squamous Cell Carcinoma

et al. 2019

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“…Solid malignant tumors, such as OSCC, have the potential for rapid and unlimited growth due to resistance to apoptosis [3]. Escape from apoptosis allows cancer cells to survive longer and accumulate mutations.…”

Section: Introductionmentioning

confidence: 99%

Dual Targeting of the p38 MAPK-HO-1 Axis and cIAP1/XIAP by Demethoxycurcumin Triggers Caspase-Mediated Apoptotic Cell Death in Oral Squamous Cell Carcinoma Cells

Chien

Yang

et al. 2020

Cancers

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Demethoxycurcumin (DMC) is an curcumin analogue with better stability and higher aqueous solubility than curcumin after oral ingestion and has the potential to treat diverse cancers, including oral squamous cell carcinoma (OSCC). The aim of this study was to investigate the anticancer effects and underlying mechanisms of DMC against OSCC. We found that DMC suppressed cell proliferation via simultaneously inducing G2/M-phase arrest and cell apoptosis. Mechanistic investigations found that the downregulation of cellular IAP 1 (cIAP1)/X-chromosome-linked IAP (XIAP) and upregulation of heme oxygenase-1 (HO-1) were critical for DMC-induced caspase-8/-9/-3 activation and apoptotic cell death. Moreover, p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinase (JNK)1/2 were activated by DMC treatment in OSCC cells, and only the inhibition of p38 MAPK significantly abolished DMC-induced HO-1 expression and caspase-8/-9/-3 activation. The analyses of clinical datasets revealed that patients with head and neck cancers expressing high HO-1 and low cIAP1 had the most favorable prognoses. Furthermore, an combinatorial treatment of DMC with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor, gefitinib, significantly enhanced the inhibitory effect of gefitinib on the proliferation of OSCC cells. Overall, the current study supported an role for DCM as part of an therapeutic approach for OSCC through suppressing IAPs and activating the p38-HO-1 axis.

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“…HER2(also known as C-erbB-2/ERBB2/ErbB2) plays a critical role in the cell proliferation, survival, migration, angiogenesis, and metastasis through a variety of intracellular signaling cascades such as MAPK/ERK1/2 and Pi3K/Akt (18,19).An imbalance in these pathways can lead to permanent activation (20,21). Studies have established a marked correlation between HER2 expression and the poor survival of OSCC patients (22).It has been reported that the SPINKs protein family share 50% of homology to EGF moleculeand can interact by binding to EGFR, activating EGFR downstream AKT signaling pathway, inducing epithelial mesenchymal transition (23). The SPINK6 protein is secreted and act as a functional regulator of nasopharyngeal carcinoma cells metastasis through the bound to EGFR extracellular domain (23).…”

Section: Introductionmentioning

confidence: 99%

SPINK7 Expression Changes Accompanied by HER2, P53 and RB1 may be Potential Biomarkers to Predict Oral Squamous Cell Carcinoma at Molecular Level

Penachiotti

Valdez

González‐Arriagada

et al. 2020

Preprint

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Background. The oral squamous cell carcinoma (OSCC) affects more than 300,000 patients annually worldwide with a high morbidity rate (37.8%). Several tumor biomarkers have been suggested to anticipate outcome but results were poor. Changes of SPINK7 and associated proteins in precancerous oral lesions could lead to genomic instability and promote oncogenesis. Our aim was to evaluate SPINK7as apotential molecular biomarkerpredictive of OSCC stages, compared with well-known molecules altered in cancer: HER2,TP53, RB1, NFKB and CYP4B1. Methods.Oral biopsies from patientswith dysplasia (n=33), less invasive(n=28) andhighly invasiveOSCC (n=18) were collected. 20 cases with a clinical suspicion but normal mucosa confirmedwere included ascontrol. Gene expression of SPINK7, P53,RB, NFKBand CYP4B1 were quantified by qPCR.SPINK7 levels were correlated with a cohort of 330 patients from the TCGA. Also,SPINK7, HER2, TP53, and RB1, were evaluated by immunohistofluorescence. One-way Kruskal-Wallis test and Dunn's post-hocwith a p<0.05 significance were used to data analyze.Results.In OSCC, SPINK7wasdown regulated andP53, RB, NFKB and CYP4B1were up regulatedrespect tothe others groups (p<0.001). Also,SPINK7 expressionwasdiminished in patients of TCGA(p=2.10e-6). In less invasive OSCC,SPINK7 and HER2 proteinswere decreasedandTP53 and RB1 significantly increasedrespect todysplasia and highly invasivegroups (p<0.05).Conclusion. Our results suggest that SPINK7changes accompanied of HER2, P53 and RB1 can be used to classify the molecular stage of epithelial oral lesion inthe OSCC, allowing a more accuratediagnosis to molecular and histopathological level.

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Hallmarks of Cancer-Related Newly Prognostic Factors of Oral Squamous Cell Carcinoma

Cited by 204 publications

References 141 publications

Metformin and Dicholoroacetate Combination Exert a Synergistic Effect on Cell Viability of Oral Squamous Cell Carcinoma

Metformin and Dicholoroacetate Combination Exert a Synergistic Effect on Cell Viability of Oral Squamous Cell Carcinoma

Dual Targeting of the p38 MAPK-HO-1 Axis and cIAP1/XIAP by Demethoxycurcumin Triggers Caspase-Mediated Apoptotic Cell Death in Oral Squamous Cell Carcinoma Cells

SPINK7 Expression Changes Accompanied by HER2, P53 and RB1 may be Potential Biomarkers to Predict Oral Squamous Cell Carcinoma at Molecular Level

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