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研究生:陳琦媛
研究生(外文):Chi-Yuan Chen
論文名稱:Tid1腫瘤抑制基因及腫瘤異質化在頭頸癌之探討
論文名稱(外文):CHARACTERIZATION OF TID1 TUMOR SUPPRESSOR AND TUMORIGENIC HETEROGENEITY IN HEAD AND NECK SQUAMOUS CELL CARCINOMA
指導教授:羅正汎
指導教授(外文):Jeng-Fan Lo
學位類別:博士
校院名稱:國立陽明大學
系所名稱:口腔生物研究所
學門:醫藥衛生學門
學類:牙醫學類
論文種類:學術論文
論文出版年:2009
畢業學年度:97
語文別:中文
論文頁數:134
中文關鍵詞:頭頸癌腫瘤抑制基因 Tid1腫瘤幹細胞上皮生長因子接受器腫瘤幹細胞標記 Bmi1
外文關鍵詞:HNSCCTid1Cancer stem cellEGFRBmi1
相關次數:
  • 被引用被引用:0
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  • 下載下載:16
  • 收藏至我的研究室書目清單書目收藏:0
尋找頭頸癌致癌因子研究之急切性,可說是刻不容緩。這此研究中,將藉由探討癌化之分子機轉以便更釐清頭頸癌之癌化過程。我們將分別探討腫瘤抑制基因 Tid1 及少數之腫瘤異質化族群在頭頸癌各扮演的角色。目前相關實驗發現 Tid1 可在不同癌症中扮演著腫瘤抑制者功能,然而其抗癌化過程的機制仍有許多未知。因此根據現有的研究結果,我們推測 Tid1 在頭頸癌之癌化過程中也可能扮演腫瘤抑制者的角色。首先,藉由免疫組織染色法偵測頭頸癌各時期 Tid1 的表現變化,實驗結果發現:在腫瘤發展後期、腫瘤再度復發及預後存活率低的病人組織中,Tid1 的表現有顯著減少。此外以西方墨點法分析頭頸癌細胞株 Tid1 表現量,發現具有高致癌力的 SAS、SCC9、SCC15 等細胞中,Tid1 的蛋白質表現量顯著減少。將 Tid1 大量表現在 SAS,明顯抑制 SAS 在體外 (in vitro) 或活體內 (in vivo) 之腫瘤生成能力。更進一步探討 Tid1 參與的分子作用機制發現:Tid1 會藉由與EGFR直接地作用,降低此接受器的活化,進而抑制 AKT 活化,促使細胞走向凋亡。綜合以上的研究結果,推測 Tid1 在頭頸癌之癌化過程中可能扮演腫瘤抑制者的角色。此外,在腫瘤細胞族群中,只有少數的腫瘤異質化族群具有腫瘤起始能力稱為腫瘤幹細胞。實驗證據顯示腫瘤幹細胞與人類癌化過程、復發及轉移有關。本實驗目的是建立具有高度表現腫瘤異質化族群之細胞株,並將此細胞株應用於頭頸癌之癌化過程的分子模式研究探討。將原本已具有致癌力的 SAS 頭頸癌細胞株經由連續三次異體移植的方式,建立更高度惡性程度的頭頸癌新細胞株,將之命名為 SASVO3。經實驗證明,SASVO3 在體外 (in vitro) 或活體內 (in vivo) 之腫瘤生成能力比 SAS 更惡性。實驗結果也顯示 SASVO3 具有腫瘤幹細胞特性,且腫瘤幹細胞標記 Bmi1 的表現量增加。最後將 SAS 及 SASVO3 分別注射入裸鼠的尾巴靜脈,只有 SASVO3 產生肺臟轉移現象。綜合以上的研究結果發現 SASVO3 細胞株是一株具有增強腫瘤幹細胞特性的頭頸癌細胞株,並且此細胞株將可應用於頭頸癌致癌機制的探討。期許更多對癌化分子機轉學理依據線索之累積,可更增加對此疾病之治療。
Appropriate treatment of head and neck squamous cell carcinoma (HNSCC) remains one of the most difficult changes in head and neck oncology. Here, we investigated the emerging information on genomic alterations; including a novel tumor suppressor gene ‘Tid1’ and tumorigenic heterogeneity, can help elucidate the molecular mechanisms underlying HNSCC progression. Tid1 is involved in multiple intracellular signaling pathways such as apoptosis, cell proliferation and cell survival. Here, we investigated the anti-tumorigenic activity of Tid1 in head and neck squamous cell carcinoma in vitro and in vivo. Initially, it was found that expression of Tid1 was negatively associated with tumor status, recurrence and survival prognosis using immunohistochemical analysis of primary HNSCC patient tumor tissue. Secondly, ectopic expression of Tid1 in HNSCC cells was shown to significantly inhibit tumorigenic ability in vitro and in vivo. Thirdly, we showed that overexpression of Tid1 attenuated EGFR activity and blocked the activation of AKT in HNSCC cells. On the other hand, ectopic expression of constitutively active AKT greatly reduced apoptosis induced by Tid1 overexpression. These findings suggest that Tid1 functions as a tumor suppressor in HNSCC tumorigenesis. Furthermore, the progression and metastasis of HNSCC have been related to the behavior of a small subpopulation of cancer stem cells. Here, we have established a highly malignant HNSCC cell line, SASVO3, from primary tumors using three sequential rounds of xenotransplantation. SASVO3 possesses enhanced tumorigenic ability both in vitro and in vivo. Moreover, SASVO3 exhibits properties of cancer stem cells, including that increased the abilities of stemness and elevated expression of the stem cell marker Bmi1. Injection of SASVO3 into the tail vein of nude mice resulted in lung metastases. These results are consistent with the postulate that the malignant and/or metastasis potential of HNSCC cells may reside in a stem-like subpopulation. Further study of molecular mechanisms will increase our knowledge of this devastating disease.
SIGNATURE PAGE iii
THESIS APPROVAL FORM iv
ACKNOWLEDGMENTS v
CHINESE ABSTRACT vi
ENGLISH ABSTRACT vii
TABLE OF CONTENTS viii
LIST OF FIGURES ix
LIST OF TABLES xi
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