查詢結果分析
相關文獻
- 抗藥性大腸癌細胞株及其小鼠腫瘤動物模式之建立
- 茲卡病毒感染症之病毒檢驗鑑定與動物模式研究
- 激活方式對小鼠及家兔卵母細胞激活率及原核形成時間分佈之影響
- 取卵時間與小鼠及家兔卵母細胞第一極體(PB1)形態之完整性和染色體之相對位置之關係
- 建立無特定病原大小鼠之血液化學參考值
- 以基因顯微注射法產製基因轉殖ICR小鼠之效率評估
- 顯微注射反轉錄病毒轉染早期小鼠胚以產生基因轉殖小鼠
- C57BL/6小鼠脾臟的黑色顆粒沉積現象
- Structural Changes in the Mouse Heart One Year after Brain Exposure to 佄Co Gamma Ray
- 應用業經反轉錄病毒載體法轉染PSN之小鼠胚幹細胞產生基因轉殖小鼠
頁籤選單縮合
題名 | 抗藥性大腸癌細胞株及其小鼠腫瘤動物模式之建立=Establishment of a Multidrug Resistant (MDR) Colon Carcinoma Cell Line and MDR Tumor Model in BALB/c Mice |
---|---|
作者 | 林慶齡; 郭馥華; 廖美秀; 許維倫; 沈立漢; 詹東榮; | 書刊名 | 臺灣獸醫學雜誌 |
卷期 | 33:3/4 2007.12[民96.12] |
頁次 | 頁194-202 |
分類號 | 437.23 |
關鍵詞 | CT-26大腸癌; 多重藥物抗藥性; 動物模式; 小鼠; CT-26; Multidrug resistance; Animal model; Mouse; |
語文 | 中文(Chinese) |
中文摘要 | 腫瘤細胞過度表現多重藥物抗藥性(multidrug resistance; mdr)基因為癌症化學治療失敗的主要原因之一,mdr1基因產物為細胞膜上之轉運蛋白P-glycoprotein (P-gp),此蛋白將藥物從細胞中排出而呈現抗藥性。本論文的研究目的篇建立具有多重藥物抗藥性的腫瘤細胞株及其小鼠腫瘤動物模式,以應用於腫瘤抗藥性之研究。小鼠大腸癌CT-26細胞(CT-26/WT)培養於加入doxorubicin (DOX)的培養基中,DOX濃度以漸進式由低至高濃度(1nM-1μM),所得的抗藥性細胞稱為CT-26/DOX1。結果顯示CT-26/DOX1細胞對於DOX的抵抗倍率(resistant Index; RI)相較於CT-26/DOX1。結果顯示CT-26/DOX1細胞對於DOX的抵抗倍率(resistant index; RI)相較於CT-26/WT爲90倍,P-gp基質化療藥物vincristine和etoposide的RI也高於CT-26/WT,而非P-gp基質之化療藥物5-FU和methotrexate,其RI則與CT-26/WT相似。在P-gp蛋白表現和功能方面,CT-26/DOX1細胞顯著高於CT-26/WT。將細胞皮下接種於小鼠,於CT-26/WT和CT-26/DOX1活體腫瘤大小約75-250 mm^3時,每週靜脈注射DO×1劑,劑量為10 mg/kg,共投與三劑,發現CT-26/DO×1腫瘤大小極顯著高於CT-26/WT。綜合上述結果顯示本研究已建立抗藥性CT-26/DO×1細胞模式以及CT-26/DOX1的實驗動物模式。 |
英文摘要 | Overexpression of the mdr1 gene in cancer cells is one of the major underlying mechanisms responsible for failure of cancer chemotherapy. P-glycoprotein (P-gp), the plasma membrane protein encoded by mdr1 gene, acts as an energy-dependent efflux transporter that reduces intracellular concentrations of various cytotoxic drugs to sublethal concentrations. The objective of the present study is to establish a MDR colon carcinoma cell line and a murine tumor model for study of tumor MDR in vitro and in vivo. The parental CT-26 cells (CT-26ANT) were cultured in RPMI medium with gradually increased concentrations of doxorubicin (DOX; from 1 nM to 1 μM) to establish a MDR sub-line (CT-26/DOX1). Cytotoxicity measured by the MU assay demonstrated that the 50% inhibition concentration (IC50) of DCX in CT-26/DOX1 was significantly higher than that in CT-26/WT. The resistant index (RI) of CT-26/DOX1 cells to DOX was 90 folds as compared to the CT-26/WT cells. In addition to DCX, CT-26/DOX1 exhibited resistance to vincristine and etoposide that are also P-gp substrates, but not to 5-fluoruracil and methotrexate that are not P-gp substrates. These data suggest a phenotype of MDR in the CT-26/DOX1 sub-line. The phenotype of MDR was further confirmed by the increased levels of P-gp protein expression, and P-gp function in CT26/DOX1. Finally, the effect of DOX on the growth rate of CT-26/WT and CT-26/DOX1 tumor implants in BALB/c mice was measured. DOX was intravenously administered (10 mg/kg; once per week for 3 doses) into tumor-bearing mice when the size of tumor implants reached 75-250 mm^3. The results showed that the tumor growth rate in CT-26/DOX1 was significantly greater than that in CT-26M/T after the 2 dose of DCX. In conclusion, the present studies have established a MDR CT-26/DOX cell sub-line, and a CT-26/DOX1 syngeneic murine model with MDR phenotype. |
本系統之摘要資訊系依該期刊論文摘要之資訊為主。