中华肿瘤杂志
中華腫瘤雜誌
중화종류잡지
CHINESE JOURNAL OF ONCOLOGY
2014年
10期
733-738
,共6页
癌,小细胞%细胞凋亡%WIG-1%多药耐药%RNA,小分子干扰
癌,小細胞%細胞凋亡%WIG-1%多藥耐藥%RNA,小分子榦擾
암,소세포%세포조망%WIG-1%다약내약%RNA,소분자간우
Carcinoma,small cell%Apoptosis%WIG-1%Multidrug resistance%RNA,small interfering
目的 探讨WIG-1在调节小细胞肺癌多药耐药中的作用.方法 运用实时荧光定量PCR(real-time PCR)和Western blot检测小细胞肺癌敏感细胞株H69和耐药细胞株H69AR中WIG-1的表达,real-time PCR法检测化疗敏感和耐药患者血液标本中WIG-1的表达,小干扰RNA (siRNA)抑制耐药细胞株H69AR中的WIG-1的表达,CCK-8法检测细胞对化疗药物的敏感性,流式细胞仪检测细胞凋亡,分析WIG-1的表达与患者临床特征和预后的关系.结果 H69AR和H69细胞株中WIG-1mRNA的表达水平分别为5.965±0.890和1.023 ±0.127,差异有统计学意义(P =0.007).化疗耐药患者和化疗敏感患者的血液标本中WIG-1 mRNA的表达水平分别为4.169 ±0.970和1.673-±0.127,差异有统计学意义(P＜0.001).siRNA抑制耐药细胞株H69AR中WIG-1的表达能增加细胞对化疗药物的敏感性,差异有统计学意义(P＜0.01).H69AR细胞组和H69细胞组的凋亡率分别为(1.037±0.049)％和(7.963±0.097)％,差异有统计学意义(P＜0.01).下调H69AR细胞中WIG-1的表达后,H69AR-Si-WIG-1组细胞的凋亡率为(20.915±0.890)％,高于空白对照组细胞[(1.037±0.049)％]和阴性对照组细胞[(2.025±0.097)％],差异均有统计学意义(均P＜0.01).WIG-1的表达与患者的性别、年龄无关(均P ＞0.05);与患者的疾病分期、化疗药物敏感性和生存状况有关(均P ＜0.05).结论 WIG-1参与调节小细胞肺癌的多药耐药机制,下调WIG-1基因的表达可能通过增加细胞的凋亡逆转小细胞肺癌的多药耐药性.
目的 探討WIG-1在調節小細胞肺癌多藥耐藥中的作用.方法 運用實時熒光定量PCR(real-time PCR)和Western blot檢測小細胞肺癌敏感細胞株H69和耐藥細胞株H69AR中WIG-1的錶達,real-time PCR法檢測化療敏感和耐藥患者血液標本中WIG-1的錶達,小榦擾RNA (siRNA)抑製耐藥細胞株H69AR中的WIG-1的錶達,CCK-8法檢測細胞對化療藥物的敏感性,流式細胞儀檢測細胞凋亡,分析WIG-1的錶達與患者臨床特徵和預後的關繫.結果 H69AR和H69細胞株中WIG-1mRNA的錶達水平分彆為5.965±0.890和1.023 ±0.127,差異有統計學意義(P =0.007).化療耐藥患者和化療敏感患者的血液標本中WIG-1 mRNA的錶達水平分彆為4.169 ±0.970和1.673-±0.127,差異有統計學意義(P＜0.001).siRNA抑製耐藥細胞株H69AR中WIG-1的錶達能增加細胞對化療藥物的敏感性,差異有統計學意義(P＜0.01).H69AR細胞組和H69細胞組的凋亡率分彆為(1.037±0.049)％和(7.963±0.097)％,差異有統計學意義(P＜0.01).下調H69AR細胞中WIG-1的錶達後,H69AR-Si-WIG-1組細胞的凋亡率為(20.915±0.890)％,高于空白對照組細胞[(1.037±0.049)％]和陰性對照組細胞[(2.025±0.097)％],差異均有統計學意義(均P＜0.01).WIG-1的錶達與患者的性彆、年齡無關(均P ＞0.05);與患者的疾病分期、化療藥物敏感性和生存狀況有關(均P ＜0.05).結論 WIG-1參與調節小細胞肺癌的多藥耐藥機製,下調WIG-1基因的錶達可能通過增加細胞的凋亡逆轉小細胞肺癌的多藥耐藥性.
목적 탐토WIG-1재조절소세포폐암다약내약중적작용.방법 운용실시형광정량PCR(real-time PCR)화Western blot검측소세포폐암민감세포주H69화내약세포주H69AR중WIG-1적표체,real-time PCR법검측화료민감화내약환자혈액표본중WIG-1적표체,소간우RNA (siRNA)억제내약세포주H69AR중적WIG-1적표체,CCK-8법검측세포대화료약물적민감성,류식세포의검측세포조망,분석WIG-1적표체여환자림상특정화예후적관계.결과 H69AR화H69세포주중WIG-1mRNA적표체수평분별위5.965±0.890화1.023 ±0.127,차이유통계학의의(P =0.007).화료내약환자화화료민감환자적혈액표본중WIG-1 mRNA적표체수평분별위4.169 ±0.970화1.673-±0.127,차이유통계학의의(P＜0.001).siRNA억제내약세포주H69AR중WIG-1적표체능증가세포대화료약물적민감성,차이유통계학의의(P＜0.01).H69AR세포조화H69세포조적조망솔분별위(1.037±0.049)％화(7.963±0.097)％,차이유통계학의의(P＜0.01).하조H69AR세포중WIG-1적표체후,H69AR-Si-WIG-1조세포적조망솔위(20.915±0.890)％,고우공백대조조세포[(1.037±0.049)％]화음성대조조세포[(2.025±0.097)％],차이균유통계학의의(균P＜0.01).WIG-1적표체여환자적성별、년령무관(균P ＞0.05);여환자적질병분기、화료약물민감성화생존상황유관(균P ＜0.05).결론 WIG-1삼여조절소세포폐암적다약내약궤제,하조WIG-1기인적표체가능통과증가세포적조망역전소세포폐암적다약내약성.
Objective To investigate the role of wild-type p53-induced gene 1 (WIG-1) on the regulation of multi-drug resistance in small cell lung cancer.Methods The expressions of WIG-1 protein and gene were detected by Western blot and real-time PCR (RT-PCR) in both the drug-sensitive H69 and drug-resistant H69AR cell lines,respectively.Meanwhile,the differential expression of WIG-1 was also detected in peripheral blood samples of responders and non-responder patients.Furthermore,the WIG-1 expression was inhibited by siRNA in H69AR cells,then the drug-sensitivities of H69AR cells to chemotherapy agents such as ADM,DDP,VP-16 were detected by CCK8 assay,and apoptosis rate was detected by flow cytometry.The possible association of WIG-1 with clinical parameters was evaluated.Results The expression of WIG-1 was significantly increased in H69AR cells (5.965 ± 0.890) than that in the H69 cells(1.023 ± 0.127) (P =0.007).The expression of WIG-1 was significantly increased in the non-responder patients (4.169 ±0.970) than in the H69 cells and responders (1.673 ±0.127) (P ＜ 0.001).The drug-sensitivities of H69AR cells to chemotherapeutic drugs were increased when the expression of the WIG-1 was down-regulated.The apoptosis rate was significantly decreased in the H69AR cells (1.037 ±0.049)％ compared with that in the H69 cells [(7.963 ±0.097)％,(P ＜0.01)].The apoptosis rate was increased in the H69AR-Si-WIG-1 cells (20.915 ± 0.890) ％ than that of (1.037 ± 0.049) ％ in the H69AR and H69AR-NC group (2.025 ± 0.097)％ (P ＜ 0.01).The expression of WIG-1 was not significantly associated with gender,and age (P ＞ 0.05),but significantly correlated with chemosensitivity,overall survival and clinical stage (P ＜ 0.001 for all).Conclusions Our results suggest that WIG-1 is involved in the regulation of the multidrug resistance mechanism in small cell lung cancer.Selective silencing of the WIG-1 gene may reverse the multidrug resistance of SCLC via increasing cell apoptosis.
