医学临床研究
醫學臨床研究
의학림상연구
JOURNAL OF CLINICAL RESEARCH
2012年
11期
2065-2067
,共3页
张东%刘长庭%于晓妉%刘岩
張東%劉長庭%于曉妉%劉巖
장동%류장정%우효담%류암
肺肿瘤/病理学%细胞系%腺癌%组蛋白类
肺腫瘤/病理學%細胞繫%腺癌%組蛋白類
폐종류/병이학%세포계%선암%조단백류
lung neoplasms/PA%cell line%adenocarcinoma%histones
[目的]评价组蛋白去乙酰化酶( HDAC)抑制剂 Depsipeptide 对肺腺癌细胞株 H1299的生长抑制作用及机制.[方法]分别以体外药物敏感试验观察 Depsipeptide 处理肺癌细胞株 H1299后其生长抑制情况,Western blot 检测 survivin 及细胞外信号调节激酶(ERK)蛋白表达水平的变化.[结果]Depsipeptide 作用48 h 及96 h 后对 H1299细胞具有明显的生长抑制作用,其细胞毒性呈时间依赖性和浓度依赖性;同时Depsipeptide 作用后 survivin 蛋白表达明显下降,磷酸化 ERK (pERK)蛋白表达明显下降.[结果]Depsipep‐tide 对肺腺癌细胞株 H1299具有生长抑制作用,其机制可能是下调具有抗细胞凋亡作用的 survivin 蛋白的表达,并阻断 ERK 信号通路的活化,从而抑制肺腺癌细胞株 H1299的生长.
[目的]評價組蛋白去乙酰化酶( HDAC)抑製劑 Depsipeptide 對肺腺癌細胞株 H1299的生長抑製作用及機製.[方法]分彆以體外藥物敏感試驗觀察 Depsipeptide 處理肺癌細胞株 H1299後其生長抑製情況,Western blot 檢測 survivin 及細胞外信號調節激酶(ERK)蛋白錶達水平的變化.[結果]Depsipeptide 作用48 h 及96 h 後對 H1299細胞具有明顯的生長抑製作用,其細胞毒性呈時間依賴性和濃度依賴性;同時Depsipeptide 作用後 survivin 蛋白錶達明顯下降,燐痠化 ERK (pERK)蛋白錶達明顯下降.[結果]Depsipep‐tide 對肺腺癌細胞株 H1299具有生長抑製作用,其機製可能是下調具有抗細胞凋亡作用的 survivin 蛋白的錶達,併阻斷 ERK 信號通路的活化,從而抑製肺腺癌細胞株 H1299的生長.
[목적]평개조단백거을선화매( HDAC)억제제 Depsipeptide 대폐선암세포주 H1299적생장억제작용급궤제.[방법]분별이체외약물민감시험관찰 Depsipeptide 처리폐암세포주 H1299후기생장억제정황,Western blot 검측 survivin 급세포외신호조절격매(ERK)단백표체수평적변화.[결과]Depsipeptide 작용48 h 급96 h 후대 H1299세포구유명현적생장억제작용,기세포독성정시간의뢰성화농도의뢰성;동시Depsipeptide 작용후 survivin 단백표체명현하강,린산화 ERK (pERK)단백표체명현하강.[결과]Depsipep‐tide 대폐선암세포주 H1299구유생장억제작용,기궤제가능시하조구유항세포조망작용적 survivin 단백적표체,병조단 ERK 신호통로적활화,종이억제폐선암세포주 H1299적생장.
Objective]To assess the histone deacetylase (HDAC) inhibitor depsipeptide for inhibiting the growth of human lung cancer cells H1299 and its mechanism .[Methods]In vitro drug sensitivity test was used to observe the growth inhibition of H1299 cells after the treatment with depsipeptide .Western blot was used to detect the change of the expression of survivin and extracellular signal‐regulated kinase(ERK) .[Results]Depsipeptide on H1299 cells after 48h and 96h had obvious inhibitory effect on the growth of H1299 cells .Its cytotoxicity was time and concentration dependent .Meanwhile ,the expression of survivin obviously decreased after H1299 cells treated with depsipeptide .The expression of phosphorylation ERK (pERK ) obviously de‐creased after H1299 cells treated with depsipeptide .[Conclusion] Depsipeptide can inhibit the growth of hu‐man lung cancer cells H1299 .The mechanism may be related to the down‐regulation of antiapoptotic protein survivin and the blockage of ERK signal pathway so as to inhibit the growth H1299 cells .