| 王媛 刘莉 陆远 李发凯 吴健雄 李昂 赵晶 任新玲.紫草素逆转埃克替尼对肺癌EGFR-TKI 耐药及其机制的研究[J].现代生物医学进展英文版,2016,16(16):3044-3047. |
| 紫草素逆转埃克替尼对肺癌EGFR-TKI 耐药及其机制的研究 |
| Shikonin Sensitizes EGFR-TKI Resistant Lung Adenocarcinoma Cells toIcotinib |
| |
| DOI： |
| 中文关键词: 紫草素 埃克替尼 非小细胞肺癌 表皮生长因子受体酪氨酸激酶抑制剂 耐药机制 |
| 英文关键词: Shikonin Icotinib Non-small Cell Lung Cancer Epidermal Growth Factor Receptor Tyrosine Kinase Inhibitor Resistance Mechanisms |
| 基金项目:国家自然科学基金项目（81172222） |
|
| Hits: 949 |
| Download times: 0 |
| 中文摘要: |
| 目的：观察紫草素联合埃克替尼对肺腺癌耐药细胞H1975 增殖的影响，探讨克服耐药可能的作用机制。方法：应用MTT 法
检测紫草素(1.25~20 umo/L)、埃克替尼(5~100 umol/L)及两药联合干预对H1975 细胞生长的抑制作用；流式细胞术观察紫草素
(1.25 umol/L)、埃克替尼(10 umol/L)及联合使用对H1975 凋亡作用；Western blot 检测不同干预对H1975 细胞EGFR、p-EGFR、
AKT、p-AKT、ERK、p-ERK 和凋亡相关蛋白PARP 表达水平的影响。结果：MTT 检测结果显示，与单药组相比，联合用药组细胞
H1975 增殖能力明显减弱，差异有统计学意义(P<0.05)；流式细胞术结果显示，联合用药组细胞的凋亡率达到(52.45± 3.04) %，较
紫草素组细胞凋亡率(22± 1.17) %和埃克替尼处理组细胞凋亡率(15.35± 5.85) %明显提高，差异有统计学意义(P<0.05)。Western
blot 结果显示，单药组下调了p-EGFR、p-Akt 蛋白水平的表达，而联合用药组显著抑制了p-ERK、PARP 蛋白水平的表达，差异有
统计学意义(P<0.05)，EGFR、AKT、ERK蛋白表达无差异(P>0.05)。结论：紫草素联合埃克替尼能明显抑制H1975细胞增殖，促进
肿瘤细胞凋亡；抗肿瘤机制可能与调节EGFR 信号通路相关蛋白表达有关。 |
| 英文摘要: |
| Objective:To assess the anti-proliferation effect of Shikonin combined with Icotinib on Non-small cell lung cancer
(NSCLC) H1975 cells, and explore the potential mechanism to overcome Tyrosine kinase inhibitor (TKI) resistance.Methods:The
cytostatic effects of shikonin (1.25-20 umol/L), icotinib (5-100 umol/L), and shikonin plus icotinib on H1975 cells were evaluated by
MTT assay. Their effects on apoptosis of H1975 cells were determined by flow cytometry (FCM). Their effects on expressions of
epidermal growth factor receptor (EGFR) signal pathway related proteins in H1975 cells were detected by Western blot.Results:MTT
assay showed that compared with single drug group, shikonin plus icotinib could potently inhibit the growth of H1975 cells, showing
statistical difference (P＜0.05). FCM showed the apoptotic rate was (52.45± 3.04) %in the shikonin plus icotinib group, significantly
higher than that of the group shikonin (22± 1.17)%and the icotinib group (15.35± 5.85) %, showing statistical difference (P＜0.05).
The protein expression of p-EGFR, p-Akt in H1975 cells could be down-regulated by shikonin or icotinib, and protein expressions of
p-ERK, PARP could be markedly down-regulated by shikonin plus icotinib as shown byWestern blot, and the difference was statistically
significant (P＜0.05). The protein expression of EGFR, AKT, ERK showed no statistical difference(P>0.05).Conclusion:Combination
of Shikonin and icotininb can significantly inhibit H1975 cell proliferation, promote tumor cell apoptosis; and its mechanism may be
related to regulating the related protein expression in EGFR signaling pathway. |
|
View Full Text
View/Add Comment Download reader |
| Close |
