Presentation Category
Research
Introduction/Context/Diagnosis
The epithelial-mesenchymal transition (EMT) is a trans-differentiation process of epithelial cells into motile mesenchymal cells. It plays an integral role in embryonic development, wound healing and cancer progression. During EMT, epithelial cells lose their cellular polarity due to the loss of intercellular adhesion and acquire migratory and invasive characteristics associated with mesenchymal cells. EMT is tightly regulated by a number of distinct molecular processes which allow its initiation and progression to completion. These processes include activation of transcription factors, expression of specific cell-surface proteins, reorganization and expression of cytoskeletal proteins, production of extracellular matrix-degrading enzymes and changes in the expression of specific microRNAs. In many cases, the involved factors are also used as biomarkers to demonstrate the passage of a cell through an EMT. The role of chronic inflammation in cancer development was first described in 1863, and has since been linked to tissue invasion and metastasis. Inflammatory cytokines produced by local cells, tumor-associated macrophages in particular, have long been known to positively correlate to metastatic occurrences. In addition, accumulating evidence has suggested that certain types of cancer cells directly respond to bacterial virulence factors by synthesizing molecules that further promote invasion and/or metastasis. Oral squamous cell carcinoma (OSCC) is the most common malignancy affecting the oral and maxillofacial complex. Common risk factors, such as cigarette smoking, alcohol consumption, and oral microbiota, have been linked to the development of OSCC. It is well known that the gut microbiota release substances that affect EMT. Therefore, the oral microbiota potentially promote EMT in OSCC in a similar manner. In this study, we present current knowledge on EMT, including its regulatory genes and their target proteins, and the role of chronic inflammation associated with OSCC in initiating EMT. We will also discuss the preliminary data and suggest potential future experiments.
Format
Event
The Role of Inflammation in Epithelial-Mesenchymal Transition in Oral Squamous Cell Carcinoma: Literature Review, Preliminary Data, and Proposal of Experiments
The epithelial-mesenchymal transition (EMT) is a trans-differentiation process of epithelial cells into motile mesenchymal cells. It plays an integral role in embryonic development, wound healing and cancer progression. During EMT, epithelial cells lose their cellular polarity due to the loss of intercellular adhesion and acquire migratory and invasive characteristics associated with mesenchymal cells. EMT is tightly regulated by a number of distinct molecular processes which allow its initiation and progression to completion. These processes include activation of transcription factors, expression of specific cell-surface proteins, reorganization and expression of cytoskeletal proteins, production of extracellular matrix-degrading enzymes and changes in the expression of specific microRNAs. In many cases, the involved factors are also used as biomarkers to demonstrate the passage of a cell through an EMT. The role of chronic inflammation in cancer development was first described in 1863, and has since been linked to tissue invasion and metastasis. Inflammatory cytokines produced by local cells, tumor-associated macrophages in particular, have long been known to positively correlate to metastatic occurrences. In addition, accumulating evidence has suggested that certain types of cancer cells directly respond to bacterial virulence factors by synthesizing molecules that further promote invasion and/or metastasis. Oral squamous cell carcinoma (OSCC) is the most common malignancy affecting the oral and maxillofacial complex. Common risk factors, such as cigarette smoking, alcohol consumption, and oral microbiota, have been linked to the development of OSCC. It is well known that the gut microbiota release substances that affect EMT. Therefore, the oral microbiota potentially promote EMT in OSCC in a similar manner. In this study, we present current knowledge on EMT, including its regulatory genes and their target proteins, and the role of chronic inflammation associated with OSCC in initiating EMT. We will also discuss the preliminary data and suggest potential future experiments.
