投稿已於2022年5月23日(星期一)上午8點截止, 主辦單位已於2022年6月2日(星期四)通知複審錄取者。 臺北榮民總醫院教學部於2022年6月17~18日(星期五、六)舉辦國際醫學教育研討會,本次研討會的主題為「Interprofessional Education-Will the Metaverse reshape the Vein of Medical Education (醫教跨域新解方—科技賦能創新應用)」,我們邀請國內外專家學者們遠距或蒞臨現場演講與實務經驗分享,相信透過本活動,將對臨床教育提供嶄新思維,同時發展更加創新的內容,歡迎全國學術界及研究人員踴躍投稿。 本次研討會以視訊方式進行,論文展示以電子化的形式線上呈現,評選方式分為兩階段:
Tid1 in Head and Neck Cancer Tumorigenesis Tid1頭頸癌化過程之角色 Jeng-Fan Lo 羅正汎 Institute of Oral Biology, National Yang-Ming University School of Dentistry, and Department of Dentistry, Taipei Veterans General Hospital, Taipei, Taiwan, ROC 國立陽明大學牙醫學院口腔生物研究所及台北榮民總醫院口腔醫學部
Background: Tid1 is the human homologue of the Drosophila tumor suppressor Tid56, whose null mutation causes lethal tumorigenesis during the larval stage. The physiological function of Tid1 to mediate the tumorigenesis in various human cancer types has been reported. However, the molecular mechanism by which Tid1 involves in carcinogenesis in human head and neck squamous cell carcinoma (HNSCC) remains poorly understood. Herein, we investigated the clinical significance of Tid1 expression in HNSCC and its role in tumorigenesis.
Methods: To determine the expression patterns of Tid1 in HNSCC, the biopsies of 47 HNSCC cancerous tissues were examined by immunohistochemistry analysis. To evaluate the physiological function of Tid1 in human oral cancer cells, HNSCC cells overexpressing Tid1 were generated and the cell proliferation, cell motility, cell invasion, anchorage-independent growth of those cell, and in vivo tumorigenicity were examined. To verify the molecular mechanism of Tid1 involving in HNSCC, the EGFR molecular pathway of Tid1-expressing cells were examined.
Results: We showed that ectopically overexpression of Tid1 negatively regulated cell proliferation, anchorage-independent growth, cell motility, cell invasion, and tumorigenicity of oral cancer cells. Low Tid1 expression is associated with increased cancer recurrence and tumor status, but reduced patient survival in HNSCC patients. In addition, Tid1 attenuates EGFR activity and blocks the activation of AKT in HNSCC cells.
Conclusion: We demonstrate that Tid1 functions as a tumor suppressor in human HNSCC. Furthermore, molecular mechanism mediated by Tid1 might be a potential therapeutic target for HNSCC therapy.