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題 名 | 葉酸營養調節人類結腸癌細胞發炎相關Nuclear Factor-κB與侵犯相關Hedgehog訊息傳遞路徑=Folate Status Modulates Inflammatory-associated Nuclear Factor-κB and Invasion-related Hedgehog Signaling Pathway in Human Colorectal Carcinoma Cells |
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作 者 | 許舒涵; 許瑞芬; | 書刊名 | 臺灣營養學會雜誌 |
卷 期 | 38:2 2013.06[民102.06] |
頁 次 | 頁29-39 |
分類號 | 411.38 |
關鍵詞 | 結腸癌; 葉酸缺乏; 葉酸補充; NF-κB訊息傳遞; Hedgehog訊息傳遞; Colorectal cancer; Folate deficiency; Folate supplement; NF-κB signaling; Hedgehog signaling; |
語 文 | 中文(Chinese) |
中文摘要 | 低葉酸營養狀態為結腸癌之風險因子,我們過去研究發現葉酸缺乏增加結腸癌細胞之發炎因子Nuclear factor-κB(NF-κB)及腫瘤轉移相關Hedgehog(Hh)訊息路徑分子表現,並促進癌細胞之侵犯性。但其活化NF-κB與Hh機制尚不明確。本研究以人類結腸癌HCT116細胞為實驗模式,進一步釐清葉酸營養狀態調控結腸癌細胞NF-κB與Hh訊息傳遞路徑。我們發現葉酸缺乏合併lipopolysaccharide(LPS)刺激其顯著促進NF-κB抑制者IκBα降解50%(p < 0.05)。之後利用促發炎細胞激素Interleukin-1β(IL-1β)模式探討葉酸補充是否可改善癌細胞之發炎反應,結果顯示葉酸補充顯著降低IL-1β誘導之phospho-Akt表現33%和Gli表現14%,IκBα蛋白顯著提升1.3倍(p < 0.05),並減少Tumor necrosis factor-α(TNF-α)分泌(p < 0.05)。綜合結果,葉酸缺乏促進HCT116細胞發炎現象,反之葉酸補充則降低發炎情形,其可能經由PI3K/Akt/Hh傳訊路徑調節NF-κB活化與否,進而調控結腸癌細胞HCT116其促發炎細胞激素TNF-α的分泌,影響癌細胞發炎反應。 |
英文摘要 | The chronic inflammatory response and folate malnutrition may increase the risk of developing colorectal cancer. Our previous study showed that folate deprivation modulated the proinflammatory factor of nuclear factor (NF)-κB and Hedgehog (Hh) signaling molecules that were related with colorectal cancer cell invasion. The regulatory mechanism is not clear. The aims of this study were to investigate how the nutritional folate status might modulate NF-κB and the Hh signaling pathway in a human colorectal carcinoma cell line (HCT116). The data revealed that lipopolysaccharide (LPS) treatment significantly promoted IκBα protein degradation of folate-deficient HCT116 cells (p < 0.05). When HCT116 cells were treated with interleukin (IL)-1β for 30 min, IL-1β expression of phospho-Akt, phospho-IκBα, and Gli respectively increased by 1.5-, 4.3-, and 1.3-fold, and total IκBα decreased by 70% (p < 0.0001). Folate supplementation reduced IL-1β-induced protein levels of phospho-Akt by 33% and Gli by 14%, and increased total IκBα by 1.3-fold and tumor necrosis factor (TNF)-α secretion (p < 0.05). Taken together, a folate deficiency or folate supplementation may modulate NF-κB signaling activation to regulate TNF-α secretion through PI3K/Akt and Hh signaling. |
本系統中英文摘要資訊取自各篇刊載內容。