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Pro-opiomelanocortin抑制黑色素癌之細胞凋亡機轉 = ...

吳健慶

Pro-opiomelanocortin抑制黑色素癌之細胞凋亡機轉 = The Apoptotic Mechanism in Pro-opiomelanocortin-induced Melanoma Suppression

紀錄類型:	書目-語言資料,印刷品 : 單行本
並列題名:	The Apoptotic Mechanism in Pro-opiomelanocortin-induced Melanoma Suppression
作者:	吳健慶,
其他團體作者:	國立高雄大學
出版地:	[高雄市]
出版者:	撰者;
出版年:	民100
面頁冊數:	52葉部份彩圖，表格 : 30公分;
標題:	腦啡-黑色素激素-腎上腺皮質素激素
標題:	Pro-opiomelanocortin (POMC)
電子資源:	http://handle.ncl.edu.tw/11296/ndltd/36146870480314276833
附註:	參考書目：葉38-41
附註:	內容為英文
摘要註:	在我們先前研究顯示Pro-opiomelanocortin (POMC)基因傳送抑制黑色素瘤的腫瘤形成過程是經由NFκB/COX-2 訊息傳遞路徑，並且降低腫瘤血管新生的能力。在本篇研究中，我們發現在系統性Ad-POMC 轉染的腫瘤中，在遠離血管的組織部位有顯著的細胞凋亡表現，經存活試驗和細胞週期分析指出，在缺氧的情況下Ad-POMC 感染的細胞會降低細胞增生的能力以及增加細胞週期pre-G0 時期的數目。因此，我們的目標是在於研究探討在缺氧情況下POMC 基因傳送所誘發黑色素癌細胞走向計畫性細胞凋亡的機制。經由細胞過氧化物和粒線體膜電位測定分析，我們證明在缺氧的情況下Ad-POMC 感染的細胞被刺激增加1.2 倍的過氧化物產量並且降低粒線體的膜電位。經由免疫螢光染色和細胞質與粒腺體分離的實驗分析發現，Ad-POMC 感染的細胞中，轉位到粒線體的Bax 引起一連串的反應包括Cytochrome C 和AIF 從粒線體釋放到細胞質以及活化caspasescascade。此外Ad-POMC 感染的細胞也增加1 倍的caspse-3 活性而在有ROS 抑制劑NAC存在下則是可以挽救POMC 所誘導的細胞凋亡以及反轉部分地caspse-3 活性。接著，我們評估POMC 基因衍生的胜肽鏈α-MSH, β-MSH, ACTH, γ-MSH和β-endorphin 在缺氧情況下POMC 基因傳送所誘發細胞凋亡中扮演的角色，經存活試驗和細胞週期分析指出，在缺氧狀態下α-MSH, β-MSH, ACTH 能減低B16-F10 黑色素癌細胞增生的能力並且增加細胞趨向凋零的數量，而γ-MSH 和β-endorphin 則不參與在其中。以上總結，我們證明4POMC 基因傳送使黑色素癌細胞對於缺氧的環境更為敏感並且誘導細胞計畫性凋亡經由增加的過氧化物引發粒線體相關的細胞凋亡路徑，其中POMC 基因衍生的胜肽鏈α-MSH,β-MSH, ACTH 參與在POMC 基因傳送所誘導的細胞凋亡。 In our previous reports, Pro-opiomelanocortin (POMC) gene delivery could inhibit tumorprogression through NFκB/COX-2 pathway suppression and attenuate angiogenic processingin melanoma tumors. In this study, in systemic Ad-POMC infected melanoma tumors, aremarkable enhancement of apoptosis was found in the ischemic region away from vessels.Viability assay and cell cycle analysis indicated that Ad-POMC infected of B16-F10 cellsreduced proliferation capability and increased the population of pre-G0 phase in hypoxia,respectively. Therefore, our aim was to examine the mechanism of POMC induced apoptosis ofmelanoma cells in hypoxia. By ROS generation and mitochondrial membrane potential (ΔΨm)assay analysis, we determined that Ad-POMC infected of melanoma cells could stimulate1.2-fold of ROS production and decrease mitochondrial membrane potential (ΔΨm) inhypoxia. Immunofluorescence and cell fractionation identified the translocation of Bax causedsequentially events including release of cytochrome c and AIF from mitochondria to cytoplasmin Ad-POMC infected of melanoma cells. Besides, POMC induced of melanoma cells couldincrease 1-fold caspase-3 activity in hypoxia and present of ROS inhibitor NAS could rescuePOMC induced of apoptotic cells population and reverse partially caspas-3 activation. Next,2we evaluated the role of POMC-derived peptides α-MSH, β-MSH, ACTH, γ-MSH andβ-endorphin participated in apoptotic capacity of POMC-induced in melanoma cells in hypoxia.Viability assay and cell cycle assay elucidated that α-MSH, β-MSH and ACTH could reducecell proliferation and enhance the population of apoptotic cells not γ-MSH and β-endorphin inhypoxia. In summary, we demonstrated that POMC gene delivery rendered susceptibility ofB16-F10 melanoma cells to hypoxia and induced apoptosis via increase of ROS productiontrigged mitochondrial associated pathway, including POMC processing of peptides α-MSH,β-MSH, ACTH participated in POMC induced apoptosis of melanoma cells.

Pro-opiomelanocortin抑制黑色素癌之細胞凋亡機轉 = The Apoptotic Mechanism in Pro-opiomelanocortin-induced Melanoma Suppression
吳, 健慶

Pro-opiomelanocortin抑制黑色素癌之細胞凋亡機轉 = The Apoptotic Mechanism in Pro-opiomelanocortin-induced Melanoma Suppression / 吳健慶撰 - [高雄市] : 撰者, 民100. - 52葉 ; 部份彩圖，表格 ; 30公分.
參考書目：葉38-41內容為英文.
腦啡-黑色素激素-腎上腺皮質素激素Pro-opiomelanocortin (POMC)

Pro-opiomelanocortin抑制黑色素癌之細胞凋亡機轉 = The Apoptotic Mechanism in Pro-opiomelanocortin-induced Melanoma Suppression
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330 $a 在我們先前研究顯示Pro-opiomelanocortin (POMC)基因傳送抑制黑色素瘤的腫瘤形成過程是經由NFκB/COX-2 訊息傳遞路徑，並且降低腫瘤血管新生的能力。在本篇研究中，我們發現在系統性Ad-POMC 轉染的腫瘤中，在遠離血管的組織部位有顯著的細胞凋亡表現，經存活試驗和細胞週期分析指出，在缺氧的情況下Ad-POMC 感染的細胞會降低細胞增生的能力以及增加細胞週期pre-G0 時期的數目。因此，我們的目標是在於研究探討在缺氧情況下POMC 基因傳送所誘發黑色素癌細胞走向計畫性細胞凋亡的機制。經由細胞過氧化物和粒線體膜電位測定分析，我們證明在缺氧的情況下Ad-POMC 感染的細胞被刺激增加1.2 倍的過氧化物產量並且降低粒線體的膜電位。經由免疫螢光染色和細胞質與粒腺體分離的實驗分析發現，Ad-POMC 感染的細胞中，轉位到粒線體的Bax 引起一連串的反應包括Cytochrome C 和AIF 從粒線體釋放到細胞質以及活化caspasescascade。此外Ad-POMC 感染的細胞也增加1 倍的caspse-3 活性而在有ROS 抑制劑NAC存在下則是可以挽救POMC 所誘導的細胞凋亡以及反轉部分地caspse-3 活性。接著，我們評估POMC 基因衍生的胜肽鏈α-MSH, β-MSH, ACTH, γ-MSH和β-endorphin 在缺氧情況下POMC 基因傳送所誘發細胞凋亡中扮演的角色，經存活試驗和細胞週期分析指出，在缺氧狀態下α-MSH, β-MSH, ACTH 能減低B16-F10 黑色素癌細胞增生的能力並且增加細胞趨向凋零的數量，而γ-MSH 和β-endorphin 則不參與在其中。以上總結，我們證明4POMC 基因傳送使黑色素癌細胞對於缺氧的環境更為敏感並且誘導細胞計畫性凋亡經由增加的過氧化物引發粒線體相關的細胞凋亡路徑，其中POMC 基因衍生的胜肽鏈α-MSH,β-MSH, ACTH 參與在POMC 基因傳送所誘導的細胞凋亡。 In our previous reports, Pro-opiomelanocortin (POMC) gene delivery could inhibit tumorprogression through NFκB/COX-2 pathway suppression and attenuate angiogenic processingin melanoma tumors. In this study, in systemic Ad-POMC infected melanoma tumors, aremarkable enhancement of apoptosis was found in the ischemic region away from vessels.Viability assay and cell cycle analysis indicated that Ad-POMC infected of B16-F10 cellsreduced proliferation capability and increased the population of pre-G0 phase in hypoxia,respectively. Therefore, our aim was to examine the mechanism of POMC induced apoptosis ofmelanoma cells in hypoxia. By ROS generation and mitochondrial membrane potential (ΔΨm)assay analysis, we determined that Ad-POMC infected of melanoma cells could stimulate1.2-fold of ROS production and decrease mitochondrial membrane potential (ΔΨm) inhypoxia. Immunofluorescence and cell fractionation identified the translocation of Bax causedsequentially events including release of cytochrome c and AIF from mitochondria to cytoplasmin Ad-POMC infected of melanoma cells. Besides, POMC induced of melanoma cells couldincrease 1-fold caspase-3 activity in hypoxia and present of ROS inhibitor NAS could rescuePOMC induced of apoptotic cells population and reverse partially caspas-3 activation. Next,2we evaluated the role of POMC-derived peptides α-MSH, β-MSH, ACTH, γ-MSH andβ-endorphin participated in apoptotic capacity of POMC-induced in melanoma cells in hypoxia.Viability assay and cell cycle assay elucidated that α-MSH, β-MSH and ACTH could reducecell proliferation and enhance the population of apoptotic cells not γ-MSH and β-endorphin inhypoxia. In summary, we demonstrated that POMC gene delivery rendered susceptibility ofB16-F10 melanoma cells to hypoxia and induced apoptosis via increase of ROS productiontrigged mitochondrial associated pathway, including POMC processing of peptides α-MSH,β-MSH, ACTH participated in POMC induced apoptosis of melanoma cells.
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