凝溶膠蛋白是一個位在第九條染色體上具有多功能的蛋白，可以和肌動蛋白結合，進而影響細胞的結構、移動性，並調控細胞凋亡。透過不同的轉錄起始點，此蛋白具有血漿和細胞質的兩種亞型。血漿凝溶膠蛋白在氨基端比細胞質凝溶膠蛋白多出一段胜肽。我們先前的研究指出凝溶膠蛋白在頭頸癌對化療的抗性扮演重要的角色。另一方面，血漿凝溶膠蛋白長期來都被認為是一具有潛力的免疫系調節者，並能做為診斷感染病、發炎、外傷的預後指標。至今，卻僅有少數研究報導血漿凝溶膠蛋白在癌症預後的角色及其分子機制。因此，本研究即旨在探討在頭頸癌中，血漿凝溶膠蛋白是否影響癌症進展，並探討其分子機制。
我使用來自人體組織銀行資料庫的頭頸癌患者血液檢體進行分析，結果顯示血漿凝溶膠蛋白表現量較高的頭頸癌患者其腫瘤進展較為活躍，並且具有較短的存活率。其中又以後期病人更為明顯。這些結果支持先前實驗室以c-GSN在癌細胞表現作為生物標誌物的發表。而我們先前的研究也證明高表現c-GSN的癌細胞或病人癌組織具有較強化療抗藥性。而我的研究結果顯示，化療抗藥性細胞株中，p-GSN之mRNA以及培養液中的p-GSN蛋白質表現量都明顯高於頭頸癌化療敏感性細胞株。進一步地發現外加的血漿凝溶膠蛋白基因質體進入頭頸癌細胞株，會同時影響c-GSN與p-GSN的mRNA和蛋白質表現。有趣的是，當在頭頸癌細胞（化療敏感性細胞株HONE1和成對化療抗藥細胞株HONE1-cis6）的無血清培養液中加入p-GSN蛋白質時，可以觀察到c-GSN蛋白質的表現隨著p-GSN濃度增加而上升，但並不會影響mRNA的表現。透過共軛焦顯微鏡觀察，我證實培養液中的p-GSN能進入癌細胞並保留24小時以上。此外，外加p-GSN蛋白的誘導下，癌細胞的遷移能力和抗藥性都顯著增加，但卻不影響癌細胞增殖速度。這些結果支持p-GSN具有作為頭頸癌預後的新循環生物標誌物以及治療靶點之潛力。

Gelsolin is a multifunctional actin-binding protein that acts as a regulator of cell structure, motility and apoptosis. Both plasma and cytosolic forms of gelsolin (c-GSN) were encoded by the same gene on chromosome 9 in human derived from alternative initiation sites. Plasma gelsolin (p-GSN) differs from cytosolic form by an extended amino-terminal peptide which remains in mature protein after secret outside. p-GSN has long been recognized as a potential immune system modulator and an indicator of the prognosis in infectious disease, inflammation and trauma. Despite the role of inflammation in carcinogenesis attracted increasing attention, only few researches have reported the potential roles of p-GSN in cancer progression and prognosis as well as their regulatory mechanisms. This study aimed to investigate the roles of p-GSN in head and neck cancer from clinical sample to cell based investigation of the underlying molecular mechanisms.
. My study using tissue bank resources of paired head and neck cancer patient biopsy tissues and blood demonstrated that higher expression of plasma gelsolin in the blood had more advanced tumor progression and poorer long-term survival. The significance is higher at late disease stage subgroup. These results are highly consistent with previous reports using tissue expression of c-GSN in cancer cells as the biomarker. High c-GSN expression confer chemoresistance was demonstrated in our previous study. My study showed that p-GSN in both mRNA levels and medium concentrations are significantly higher in chemoresistant head and neck cancer cell line than in chemosensitive lines. I further showed that modulation of plasma gelsolin gene expression could influence the c-GSN expression in both mRNA and proteins levels. Interestingly, when head and neck cancer lines (chemosensitive line HONE1 and paired chemoresistant line HONE1-cis6) were incubated in serum free culture medium containing p-GSN proteins, elevated c-GSN protein expression in the total cell extract but not its mRNA levels were observed in both lines in a dose dependent manner. Both laser confocal imaging confirmed that p-GSN enter the cells and retained for more than 24hrs. Furthermore, treatment of p-GSN protein although enhanced cancer cell migration and chemoresistance phenotypes, but failed to significantly affect cell proliferation. These results indicate that p-GSN may serve as a novel circulating biomarker for head and neck cancer prognosis and a potential therapeutic target.

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