Hypoxia reduces the E-cadherin expression and increases OSCC cell migration regardless of the E-cadherin methylation profile

Domingos, Patrícia Luciana Batista; Souza, Marcela Gonçalves de; Guimarães, Talita Antunes; Santos, Eliane Sobrinho; Farias, Lucyana Conceição; Fraga, Carlos Alberto de Carvalho; Jones, Kimberly Marie; Santos, Sérgio Henrique Souza; Paula, Alfredo Maurício Batista de; Guimarães, André Luiz Sena

doi:10.1016/j.prp.2017.02.003

Cited by 19 publications

(11 citation statements)

References 41 publications

(52 reference statements)

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“…In OSCC cells, reduced E-cadherin was associated with HIF expression (136), which is congruent with the finding that lymph node metastasis and tumour recurrence in OSCC patients was associated with HIF-1a and VEGF (137,138). Similarly, the COX-2/PGE2 pathway, along with hypoxia, has been reported to contribute to OSCC metastases by increasing tumour cell migration and upregulation of intercellular adhesion molecule-1 (ICAM-1) (98,139,140).…”

Section: Mechanisms Linking Inflammation and Hypoxia In Progression Of Osccsupporting

confidence: 87%

Intersecting Mechanisms of Hypoxia and Prostaglandin E2-Mediated Inflammation in the Comparative Biology of Oral Squamous Cell Carcinoma

Nasry

Martin

2021

Front. Oncol.

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The importance of inflammation in the pathogenesis of cancer was first proposed by Rudolph Virchow over 150 years ago, and our understanding of its significance has grown over decades of biomedical research. The arachidonic acid pathway of inflammation, including cyclooxygenase (COX) enzymes, PGE2 synthase enzymes, prostaglandin E2 (PGE2) and PGE2 receptors has been extensively studied and has been associated with different diseases and different types of cancers, including oral squamous cell carcinoma (OSCC). In addition to inflammation in the tumour microenvironment, low oxygen levels (hypoxia) within tumours have also been shown to contribute to tumour progression. Understandably, most of our OSCC knowledge comes from study of this aggressive cancer in human patients and in experimental rodent models. However, domestic animals develop OSCC spontaneously and this is an important, and difficult to treat, form of cancer in veterinary medicine. The primary goal of this review article is to explore the available evidence regarding interaction between hypoxia and the arachidonic acid pathway of inflammation during malignant behaviour of OSCC. Overlapping mechanisms in hypoxia and inflammation can contribute to tumour growth, angiogenesis, and, importantly, resistance to therapy. The benefits and controversies of anti-inflammatory and anti-angiogenic therapies for human and animal OSCC patients will be discussed, including conventional pharmaceutical agents as well as natural products.

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Section: Mechanisms Linking Inflammation and Hypoxia In Progression Of Osccsupporting

confidence: 87%

Intersecting Mechanisms of Hypoxia and Prostaglandin E2-Mediated Inflammation in the Comparative Biology of Oral Squamous Cell Carcinoma

Nasry

Martin

2021

Front. Oncol.

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“…Total protein was extracted after BMSCs were treated with different concentrations of CoCl 2 for various time durations. Treatment duration was chosen based on previous studies (Domingos et al, ). Protein was also extracted 2 h after the medium with CoCl 2 was replaced with fresh medium.…”

Section: Methodsmentioning

confidence: 99%

CoCl₂, a mimic of hypoxia, enhances bone marrow mesenchymal stem cells migration and osteogenic differentiation via STAT3 signaling pathway

Wan

Cheng

et al. 2018

Cell Biology International

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Mesenchymal stem cells homing and migration is a crucial step during bone fracture healing. Hypoxic environment in fracture site induces bone marrow mesenchymal stem cells (BMSCs) migration, but its mechanism remains unclear. Our previous study and studies by other groups have reported the involvement of signal transducer and activator of transcription 3 (STAT3) pathway in cell migration. However, the role of STAT3 pathway in hypoxia-induced cell migration is still unknown. In this study, we investigated the role of STAT3 signaling in hypoxia-induced BMSCs migration and osteogenic differentiation. BMSCs isolated from C57BL/6 male mice were cultured in the presence of cobalt chloride (CoCl ) to simulate intracellular hypoxia. Hypoxia enhanced BMSCs migration, and upregulated cell migration related gene expression, that is, metalloproteinase (MMP) 7, MMP9, and C-X-C motif chemokine receptor 4. Hypoxia enhanced the phosphorylation of STAT3, and cell migration related proteins: c-jun n-terminal kinase (JNK), focal of adhesion kinase (FAK), extracellular regulated protein kinases, and protein kinase B 1/2 (ERK1/2). Moreover, hypoxia enhanced expression of osteogenic differentiation marker. Inhibition of STAT3 suppressed the hypoxia-induced BMSCs migration, cell migration related signaling molecules phosphorylation, and osteogenic differentiation related gene expression. In conclusion, our result indicates that hypoxia-induced BMSCs migration and osteogenic differentiation is via STAT3 phosphorylation and involves the cooperative activity of the JNK, FAK, and MMP9 signaling pathways.

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“…Biochemical Genetics (2020) 58:213-244 with lower expression of E-cadherin protein in OSCC patients (Pannone et al 2014). In contrast, Domingos et al (2017) showed no differences in the methylation level of CDH1 promoter between groups of patients with potentially malignant oral lesions, OSCC, and healthy controls; moreover, in most samples the CDH1 gene promoter was unmethylated and in the OSCC group the level of methylation was not associated with clinicopathological features.…”

mentioning

confidence: 89%

Epigenetic Modifications in Head and Neck Cancer

et al. 2019

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Head and neck squamous cell carcinoma (HNSCC) is the sixth most common human malignancy in the world, with high mortality and poor prognosis for patients. Among the risk factors are tobacco and alcohol intake, human papilloma virus, and also genetic and epigenetic modifications. Many studies show that epigenetic events play an important role in HNSCC development and progression, including DNA methylation, chromatin remodeling, histone posttranslational covalent modifications, and effects of non-coding RNA. Epigenetic modifications may influence silencing of tumor suppressor genes by promoter hypermethylation, regulate transcription by microRNAs and changes in chromatin structure, or induce genome instability through hypomethylation. Moreover, getting to better understand aberrant patterns of methylation may provide biomarkers for early detection and diagnosis, while knowledge about target genes of microRNAs may improve the therapy of HNSCC and extend overall survival. The aim of this review is to present recent studies which demonstrate the role of epigenetic regulation in the development of HNSCC.

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Hypoxia reduces the E-cadherin expression and increases OSCC cell migration regardless of the E-cadherin methylation profile

Cited by 19 publications

References 41 publications

Intersecting Mechanisms of Hypoxia and Prostaglandin E2-Mediated Inflammation in the Comparative Biology of Oral Squamous Cell Carcinoma

Intersecting Mechanisms of Hypoxia and Prostaglandin E2-Mediated Inflammation in the Comparative Biology of Oral Squamous Cell Carcinoma

CoCl₂, a mimic of hypoxia, enhances bone marrow mesenchymal stem cells migration and osteogenic differentiation via STAT3 signaling pathway

Epigenetic Modifications in Head and Neck Cancer

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Hypoxia reduces the E-cadherin expression and increases OSCC cell migration regardless of the E-cadherin methylation profile

Cited by 19 publications

References 41 publications

Intersecting Mechanisms of Hypoxia and Prostaglandin E2-Mediated Inflammation in the Comparative Biology of Oral Squamous Cell Carcinoma

Intersecting Mechanisms of Hypoxia and Prostaglandin E2-Mediated Inflammation in the Comparative Biology of Oral Squamous Cell Carcinoma

CoCl2, a mimic of hypoxia, enhances bone marrow mesenchymal stem cells migration and osteogenic differentiation via STAT3 signaling pathway

Epigenetic Modifications in Head and Neck Cancer

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CoCl₂, a mimic of hypoxia, enhances bone marrow mesenchymal stem cells migration and osteogenic differentiation via STAT3 signaling pathway