Survivin与XIAP mRNA在非小细胞肺癌组织中的表达及相关性

[目的]研究survivin基因表达与非小细胞肺癌（NSCLC）生物学行为及与XIAP表达的关系。[方法]采用RT—PCR技术检测49例NSCLC患者癌组织及相应的癌旁正常肺组织中survivin和XIAPmRNA的表达水平。[结果]49例NSCLC组织中smwivin与XIAP mRNA的阳性表达率分别为79．6％（39／49）和57．1％（28／49）,在癌旁正常肺组织中的阳性表达率分别为12．2％（6／49）和14.3％（7／49）．差异均有统计学意义（P〈0．01）。NSCLC组织中survivin和XIAP mRNA表达与肿瘤的病理组织类型、细胞分化程度、临床分期及淋巴结转移均无相关性（P〉0．05）。NSCLC组织中survivin与XIAP mRNA表达呈正相关（P=0．021）。[结论]Survivin与XIAP在抑制NSCLC细胞凋亡过程中可能起协同作用,以促进肿瘤发生发展。     

XIAP mRNA和Survivin mRNA在非小细胞肺癌的表达及其临床意义

 目的　检测非小细胞肺癌（NSCLC）中X连锁凋亡抑制蛋白（XIAP）mRNA和Survivin mRNA的表达,探讨其与患者临床病理因素的相关性。方法　收集59例NSCLC患者肿瘤和正常组织标本。采用RT-PCR检测XIAP mRNA和Survivin mRNA在肿瘤和正常组织中的表达。结果　XIAP mRNA在肿瘤组织的表达率高于正常组织,分别为61.0 %（36／59）和30.5 %（18／59）（P＜0.05）,其表达与临床病理因素无相关性;Survivin mRNA在肿瘤的表达率高于正常组织,分别为81.4 %（48／59）和23.7 %（14／59）（P＜0.05）,其表达与临床病理因素无相关性。结论　XIAP和Survivin可能在NSCLC发生、发展过程中有一定作用,有可能成为NSCLC诊断的标志物和治疗靶点。     

非小细胞肺癌中survivin 基因表达及其与p53 、bcl-2 基因表达的相互关系

 目的 探讨survivin基因在非小细胞肺癌（NSCLC）中的表达，及其与p53、bcl-2蛋白表达的相互关系。方法 应用免疫组织化学链霉茵抗生物素蛋白-过氧化酶连接法（SP法），检测survivin、p53、bcl-2基因在76例NSCLC肿瘤组织及survivin基因在30例病灶旁正常肺组织中的表达。结果 survivin基因在正常肺组织中不表达，76例肺癌组织中46例表达阳性，占60．5％。survivin基因表达与肺癌患者的年龄、性别、吸烟、病理类型、分化程度、肿瘤大小、淋巴结转移及TNM分期无明显相关关系。肺癌组织中p53蛋白表达阳性、阴性者中，survivin基因表达阳性率分别为71．7％（33／46）、43．3％（13／30），两者比较，差异有显著性（P〈0．05）；bcl-2蛋白表达阳性、阴性者中，survivin基因表达阳性率分别为94．7％（36／38）、26．3％（10／38），两者比较，差异有极显著性（P〈0．01）。结论 survivin基因在肺癌组织中的异常表达，对NSCLC的发生发展起重要作用。survivin基因表达与肺癌组织中p53、bcl-2蛋白的异常表达密切相关。survivin基因可能成为NSCLC新的诊断标志及基因治疗的新靶点。     

BTG1在非小细胞肺癌中的表达及其对肺癌细胞增殖、凋亡和侵袭转移的作用

目的 探讨B细胞易位基因1（BTG1） 在非小细胞肺癌（NSCLC）组织中的表达及其对NSCLC细胞生物学行为的影响。方法 采用免疫组织化学染色和Western blotting分别检测82例NSCLC及38例癌旁正常组织中BTG1蛋白的表达。采用慢病毒转染建立BTG1过表达的NSCLC H1299细胞株。采用实时荧光定量PCR和Western blotting检测BTG1转染后H1299细胞株中BTG1表达含量的变化。采用MTT法、流式细胞术及Transwell法检测BTG1过表达对NSCLC细胞增殖、凋亡及侵袭转移的影响。结果 BTG1蛋白在NSCLC及癌旁正常组织中的阳性表达率分别为37.8％（31/82）、84.2％（32/38）,差异有统计学意义（P＜0.05）。NSCLC组织中BTG1蛋白的相对表达量为0.331±0.035,明显低于癌旁正常组织的0.673±0.072,差异有统计学意义（P＜0.05）。NSCLC组织中BTG1的表达与淋巴结转移、临床分期和组织学分级有关（P＜0.05）。BTG1过表达的NSCLC细胞增殖能力明显减弱、细胞凋亡增加及侵袭转移能力降低,且Bcl-2、MMP-9表达量明显下调。结论NSCLC组织中BTG1蛋白的表达明显降低;BTG1 可能通过调控Bcl-2及MMP-9蛋白的表达影响NSCLC细胞的增殖、凋亡与转移。     

非小细胞肺癌组织中ABCG4表达与耐药的相关性研究

目的 检测ABCG4 mRNA和蛋白在非小细胞肺癌（NSCLC）组织中的表达,分析其表达与病理类型及NSCLC细胞耐药的相关性,为研究其耐药机制提供理论基础。方法 采用免疫组化染色、RT-PCR及Western blotting检测ABCG4在NSCLC组织中的表达;MTT法检测NSCLC对化疗药物的敏感性,分析药物敏感性与ABCG4 mRNA和蛋白表达的相关性。结果 ABCG4蛋白阳性主要定位于细胞膜和胞质,其在NSCLC组织中的阳性表达率为73.9%（68/92）,而在30例癌旁正常肺组织中几乎不表达。ABCG4蛋白在肺鳞癌和肺腺癌中的阳性表达率分别为67.3%和81.4％,差异无统计学意义（P＞0.05）。环磷酰胺、吉西他滨、多柔比星、紫杉醇和顺铂在NSCLC组织中的药物敏感程度与其相应组织中ABCG4蛋白阳性表达有关（rs均＞0.3,P均＜0.05）;除紫杉醇外,环磷酰胺、吉西他滨、多柔比星和顺铂在NSCLC组织中的药物敏感程度与其相应组织中ABCG4 mRNA表达量有关（P均＜0.05）。结论 ABCG4在肺鳞癌、肺腺癌中高表达,其表达程度与NSCLC部分化疗药物耐药有关,为进一步研究ABCG4在NSCLC中的表达及可能耐药机制提供实验依据。     

利用组织微阵列研究RASSF1A和survivin基因在非小细胞肺癌中的表达及其临床意义

目的利用高通量组织微阵列技术并结合免疫组化检测RASSFlA和survivin基因在非小细胞肺癌（NSCLC）组织中的蛋白表达,探讨RASSF1A和survivin基因的表达与NSCLC临床病理特征的关系及其临床意义。方法构建包含NSCLC组织和正常肺组织的组织微阵列,免疫组织化学S—P法检测RASSF1A和stlrvivin基因在NSCLC与正常肺组织中的蛋白表达。结果RASSF1A蛋白在NSCLC组织中的阳性表达率（46．8％,37／79）显著低于正常肺组织（92．9％,13／14）（P〈0．001）。临床I期和临床Ⅱ期NSCLC组织的RASSF1A蛋白阳性表达率显著高于临床Ⅲ期（P〈0．0001,P〈0．0001）。淋巴结转移NSCLC组织中RASSF1A蛋白阳性表达率显著低于无淋巴结转移NSCLC（P〈0．05）。NSCLC组织中survivin蛋白阳性表达率（75．8％,62／79）显著高于正常肺组织（0％,0／14）（P〈0．0001）。临床I期和临床Ⅱ期NSCLC组织的survivin蛋白阳性表达率显著低于临床Ⅲ期（P=0．003,P=0．001）。进一步研究发现NSCLC组织中RASSF1A与survivin蛋白的表达存在显著性负相关（r=-0．780;P〈0．0001）。结论RASSF1A蛋白在NSCLC组织中的表达缺失可能促进NSCLC的发生、发展,其有望成为评估肺癌患者预后的重要参考指标。survivin蛋白参与NSCLC的发生、发展,过表达survivin蛋白的NSCLC肺癌患者可能预后不良。RASSF1A和survivin基因表达的失平衡可能在NSCLC的发生、发展中具有重要作用。     

胃肠道间质瘤PI3K-Akt信号转导通路介导的细胞凋亡相关因子的检测及其意义

目的:研究P13K/Akt信号转导通路介导的细胞凋亡相关因子在胃肠道间质瘤(GIST)中的表达及意义.方法:RT-PCR检测P13K、NF-κB、XIAP、bcl-2与survivin在:124例GIST及癌旁正常组织中mRNA水平.结果:在GIST中,PI3K、NF-κB mRNA表达与NIH分级、肿瘤侵袭转移、黏膜受侵密切相关,而与年龄、性别、组织学类型无关.XIAP mRNA随NIH分级表达上调;XIAP表达与GIST组织分化程度呈负相关,即分化程度越低,XIAP阳性表达率愈高,伴有肿瘤侵袭转移的GIST病例XIAP表达水平较高,同时XIAP的表达与黏膜受侵密切相关,而与年龄、性别、组织学类型无关.bcl-2 mRNA水平表达上调,与NIH分级、黏膜受侵有关,而与年龄、性别、组织学类型、转移复发及周围组织浸润无关.survivin mRNA在GIST中的表达与NIH分级、肿瘤侵袭转移、黏膜受侵等因素有关,而与年龄、性别以及组织学类型无关.由于NF-κB的调控作用,各指标之间mRNA的水平变化旱正相关.结论:GIST中PI3K/Akt信号转导通路的活化可以进一步激活NF-κB mRNA,从而进入细胞核内调控凋亡相天因子XIAP、bcl-2以及survivin mRNA水平的表达.     

非小细胞肺癌中survivin、bcl-2和bax蛋白与多药耐药基因的表达及其相关性

目的检测非小细胞肺癌(NSCLC)中凋亡蛋白survivin、bcl2、bax与多药耐药有关基因MDR1mRNA和MRPmRNA的表达,探讨其相互关系及意义。方法选取113例NSCLC病例,采用原位分子杂交检测MDR1和MRP基因mRNA的表达,SP免疫组化法检测survivin、bcl2、bax蛋白的表达。结果113例NSCLC中,MDR1mRNA、MRPmRNA及survivin、bcl2、bax蛋白的检出率分别为51.3%、80.5%、79.6%、59.3%、54.9%。survivin和bax的表达与肿瘤分化程度有关(P<0.05),bcl2的表达与肿瘤组织学类型有关(P<0.01)。MDR1mRNA与MRPmRNA(P<0.01)、survivin与MDR1mRNA(P<0.05)、bcl2与MRPmRNA(P<0.05)表达之间存在明显相关性。结论凋亡抑制蛋白survivin的高表达和bcl2的过表达可能是导致NSCLC原发耐药的重要因素,检测survivin和bcl2对临床逆转NSCLC多药耐药性具有指导意义     

ERCC1在非小细胞肺癌组织中的表达及临床意义

目的 探讨ERCC1在非小细胞肺癌(NSCLC)组织中的表达及临床意义.方法 采用免疫组化法检测36例NSCLC组织中ERCCI蛋白的表达,并长期随访患者.结果 ERCC1蛋白在NSCLC组织中的表达与患者的年龄、性别、组织学类型、TNM分期、肿瘤大小无关,而与淋巴结转移有关(P<0.01);36例NSCLC组织中ERCC1蛋白阳性表达组生存率低于阴性表达组(P<0.01).结论 ERCC1蛋白阳性的NSCLC淋巴结转移率高;ERCC1蛋白检测对患者的预后判断及术后化疗具有指导意义.     

Ezrin和survivin在非小细胞肺癌的表达及其相关性

 目的 探讨Ezrin和survivin在非小细胞肺癌（NSCLC）组织中的表达情况及其相关性。方法 利用免疫组织化（Envision法）对86例非小细胞肺癌组织石蜡标本进行Ezrin和survivin蛋白表达的检测和分析。结果 非小细胞肺癌中Ezrin蛋白高表达率为60.5%（52/86）,其与患者有无淋巴结转移密切相关（P<0.05）,与性别、肿瘤组织学类型、分化程度、临床TNM分期、吸烟无明显相关性（P>0.05）,survivin的阳性表达率为65.1%(56/86),并且与患者临床TNM分期、有无淋巴结转移密切相关（P<0.05）,与性别、肿瘤组织学类型、分化程度、吸烟无关（P>0.05）,同时,Ezrin和survivin表达呈显著正相关（r=0.384）。结论 Ezrin和survivin在NSCLC的发生发展中具有协同作用,其表达与非小细胞肺癌转移密切相关,两者联合有助于判断肿瘤转移和为临床治疗提供参考依据。     

Expression of the inhibitors of apoptosis proteins in cisplatin-resistant prostate cancer cells

Acquired multi-drug resistance remains a major obstacle in the management of prostate cancer. The objective of this study was to examine whether chemoresistance could be due in part to the expression of the inhibitors of apoptosis proteins (IAPs). We established cisplatin-resistant LNCaP sublines. We examined the effects of cisplatin on cell growth and apoptosis in LNCaP cells and LNCaP sublines by 2-(4-lodophenyl)-3-(4-nitrophenyl)-5-(2,4-disulfophenyl)-2H-tetrazolium, monosodium salt (WST-1) assay and Hoechst 33258 staining, and analyzed cross-resistance to adriamycin, 5-fluorouracil, taxol, taxotere, and etoposide. In addition, the expression of IAP-1, IAP-2, X-linked IAP (XIAP), neuronal apoptosis inhibitory protein, and survivin was investigated by immunoblot analysis in LNCaP sublines. Although the growth rates were reduced in a dose-dependent manner by cisplatin in LNCaP sublines, the anti-proliferative effects of cisplatin were significantly decreased in LNCaP sublines compared to LNCaP cells. Cisplatin-resistant sublines, LNCaP/C1, LNCaP/ C2, and LNCaP/C3 cells, were 6.3-, 9.1-, and 22.3-fold more resistant to cisplatin than LNCaP cells, respectively, and this resistance was paralleled with reduced induction of apoptosis. LNCaP/C3 cells showed cross-resistance to adriamycin, 5-fluorouracil, and etoposide whereas those cells exhibited no or only weak cross-resistance against taxol and taxotere. With the exception of survivin, all the IAPs were identified in LNCaP cells by immunoblot analysis. Interestingly, the expression of IAP-2, XIAP, and survivin gradually increased with the extent of cisplatin-resistance. Altered expression of IAP-2, XIAP, and survivin was involved in these phenotypes of cisplatin-resistant LNCaP sublines. IAPs may make an important contribution to the resistance to the apoptotic effect of cisplatin in prostate cancer.     

Elevated expression level of survivin protein in soft-tissue sarcomas is a strong independent predictor of survival.

PURPOSE: Survivin is a member of the inhibitor-of-apoptosis gene family and is known to be overexpressed in a number of tumor types. The aim of this study was to evaluate the prognostic value of survivin protein expression in tumor tissue extracts in a group of well-characterized soft-tissue sarcoma (STS) patients. EXPERIMENTAL DESIGN: In this investigation, malignant tissue samples from 63 STS patients as well as from a panel of tumor cell lines were investigated, with nonmalignant tissues serving as controls. The survivin protein level was quantified by a novel ELISA and by Western blot analysis. Results obtained by both methods were compared with clinicopathological parameters regarding tumor grade and tumor entity, and they were then correlated to survival in a multivariate Cox regression model. RESULTS: High survivin levels were detected by ELISA and Western blot analysis in tumor tissue extracts and in lysates of tumor cell lines. None or only weak expression of survivin protein was found in nonmalignant cells and tissues. When comparing survivin values obtained by ELISA or Western blot, we found a significant correlation between both methods (P = 0.013, Pearson test). Our findings revealed that, in multivariate Cox regression analyses, survivin levels measured by ELISA and Western blot were significantly associated with tumor-related death in STS patients (P = 0.001, RR = 19.8, and P = 0.004, RR = 5.1, respectively). However, in a direct comparison of both survivin protein detection assays, we found a higher sensitivity and a stronger correlation to prognosis in survivin ELISA as compared with the Western blot assays. Furthermore, a higher tumor grade and more aggressive STS entity showed an elevated survivin protein expression level. CONCLUSION: Altogether, an elevated survivin content in tumor tissue extracts has a significant and independent negative predictive value on the survival-rate of STS patients. This finding corresponds well to data obtained for the mRNA level of survivin, as shown previously (M. Kappler et al., Int. J. Cancer, 95: 360-363, 2001).     

WT1在非小细胞肺癌中的表达及其与肺癌细胞增殖的关系

目的:探讨人非小细胞肺癌及其相应癌旁组织中WT1基因(Wilms' tumor gene 1,WT1)的表达,体外研究其与肺癌细胞增殖的关系.方法:应用实时荧光定量PCR法检测79例非小细胞肺癌组织及其相应癌旁组织中WT1 mRNA的表达情况.构建重组质粒pLV-GFP-WT1,并通过脂质体LipofectAMINE 2000将其瞬时转染至非小细胞肺癌H1299细胞中,应用蛋白质印迹法检测转染后H1299细胞中WT1蛋白的表达,CCK-8 (cell counting kit-8)法检测细胞的增殖情况.结果:非小细胞肺癌组织中WT1 mRNA的表达水平高于相应的癌旁组织,差异有统计学意义(P＜0.01).重组质粒pLV-GFP-WT1成功构建,并将其成功转染至H1299细胞中;转染后的H1299细胞中,WT1蛋白的表达水平上调;在pLV-GFP-WT1转染后24、36和48 h时,过表达WT1的H1299细胞增殖率高于对照组,差异有统计学意义(P＜0.05).结论:WT1 mRNA在非小细胞肺癌组织中的表达水平明显高于相应癌旁组织,高表达WT1基因能促进非小细胞肺癌H1299细胞的增殖,提示WT1在非小细胞肺癌中扮演癌基因的角色.     

High expression of FOXC1 is associated with poor clinical outcome in non-small cell lung cancer patients

The aim of this study was to detect FOXC1 expression in human non-small cell lung cancer (NSCLC) and to analyze its association with prognosis of NSCLC patients. Expressional levels of FOXC1 mRNA and protein in 30 cases of NSCLC and corresponding non-tumor tissue samples were examined by quantitative real-time PCR and Western blotting. Immunohistochemistry was performed to detect the expression of FOXC1 in 125 NSCLC tissues. We found that the expression levels of FOXC1 mRNA and protein in NSCLC tissues were significantly higher than those in corresponding non-tumor tissues. High-level FOXC1 expression was correlated with poor tumor differentiation, tumor–node–metastasis stage, and lymph node metastasis. Patients with high expression levels of FOXC1 showed lower overall survival rate than those with low expression levels. Multivariate analysis showed that high FOXC1 protein expression was an independent prognostic factor for NSCLC patients. Our study suggests that over-expression of FOXC1 may play an important role in the progression of NSCLC, and FOXC1 expression may offer a valuable marker for predicting the outcome of patients with NSCLC.     

Preclinical studies of the proteasome inhibitor bortezomib in malignant pleural mesothelioma

Malignant pleural mesothelioma (MPM) is a highly lethal neoplasm that is resistant to chemotherapy. Bortezomib is an FDA-approved proteasome inhibitor that is currently under clinical investigation in multiple neoplasms but has not been studied extensively in MPM. In this report, we determine the biological and molecular response of cultured MPM cells to bortezomib alone and in combination with cisplatin or pemetrexed. We used four MPM cell lines (MS589, H28, H2052, JMN), a normal mesothelial cell line (HM3), and a lung cancer cell line (H23) in survival studies utilizing bortezomib, cisplatin, and pemetrexed alone and in combination by administering concurrently or by varying the order of administration. We determined the effect of bortezomib on the cell cycle, apoptosis, and on the expression of cell cycle proteins p21/WAF1 and p27/KIP1 and on apoptosis-related proteins IAP-1, IAP-2, survivin, and XIAP. Bortezomib was highly cytotoxic to MPM cells and induced both G₂/M and G₁/S cell cycle arrest. Apoptosis increased in a concentration- and time-dependent manner in 3 of 4 MPM cell lines. Bortezomib stabilized or increased protein levels of p21/WAF1 and IAP-1 and to a lesser degree p27/KIP1, IAP-2, XIAP, and survivin. In combination studies with cisplatin, bortezomib was generally synergistic at high concentrations and antagonistic at low concentrations. Bortezomib increased the cytotoxicity of cisplatin and pemetrexed in a concentration-dependent manner when administered prior to either. Bortezomib may improve outcome in MPM patients alone or in combination with standard chemotherapy but the order of administration is likely to be important. This study justifies further evaluation of bortezomib in MPM.     

Clinical correlation of nuclear survivin in esophageal squamous cell carcinoma

To examine the correlation of survivin (both total and nuclear survivin) with clinicopathological parameters of esophageal squamous cell carcinoma (ESCC) patients. Tumors and non-tumor tissues near the proximal resection margins were resected from ESCC patients undergone esophagectomy. Quantitative polymerase chain reaction (qPCR) was performed to detect survivin mRNA expression level in the 10 paired tumor and adjacent non-tumor tissues. To confirm with the clinical situation, survivin mRNA and protein expression were measured by qPCR and immunoblot, respectively, in 5 ESCC cell lines and a non-neoplastic esophageal epithelial cell line. Immunohistochemistry was employed to reveal the cellular localization of survivin in tumor tissues isolated from the 64 ESCC patients undergone surgery alone. Up-regulation of survivin mRNA and protein was found in 5 ESCC lines (HKESC-1, HKESC-2, HKESC-3, HKESC-4, and SLMT-1) when compared to a non-neoplastic esophageal epithelial cell line NE-1. In particular, HKESC-3, HKESC-4, and SLMT-1 cells demonstrated ~50-fold increase in survivin mRNA. High level of survivin mRNA in tumor tissues when compared to non-tumor tissues was found in 70?% (7 of 10) of clinical cases. The increase in expression ranged from ~twofold to ~16-fold. Immunohistochemistry results showed that survivin was found at the cell nuclei in all specimens examined. Nuclear expression of survivin was inversely associated with the likelihood of developing nodal metastasis (p?=?0.021) and significantly associated with early-stage ESCC (p?=?0.039). Nuclear survivin could serve as a marker for indicating disease status in ESCC patients.     

PKM2 基因在非小细胞肺癌中表达及其与放疗敏感性的关系

目的:研究PKM 2 在非小细胞肺癌组织中的表达及其与放疗敏感性的关系。方法:选取2011年5 月至2013年10月四川省人民医院非小细胞肺癌120 例患者,术后进行2 个月的放射治疗,按照疗效将患者分为4 组。RT-PCR 检测患者放疗前手术切除的肿瘤组织和癌旁组织中PKM 2 mRNA 表达水平。Westernblot和免疫组织化学检测肿瘤组织和癌旁组织中PKM 2 蛋白表达。RT-PCR 和Westernblot方法检测不同疗效组PKM 2 表达水平。结果:非小细胞肺癌放疗2 个月后,治疗有效率为49.2% 。PKM 2 在非小细胞肺癌癌组织中表达显著高于相应的癌旁组织。PKM 2 表达水平与患者放疗疗效呈负相关。结论:PKM 2 在非小细胞肺癌中表达高于癌旁组织,PKM 2 低表达患者对放疗敏感性高。      

Effects of matrine in combination with cisplatin on liver cancer

Matrine, an alkaloid isolated from Sophora flavescens, promotes tumor cell apoptosis and strengthens the anticancer capacity of chemotherapeutic drugs. The present study aimed to investigate the inhibitory effect and underlying mechanism of matrine in combination with cisplatin on liver cancer progression. Tumor progression was studied in nude mice. The human liver cancer cell line HepG2 was injected into BALB/c nude mice subcutaneously to establish a tumor model. Mice were subsequently treated with matrine, cisplatin, matrine + cisplatin or normal saline. Nude mice and tumor growth were monitored. Tumors were excised and the expression of survivin, caspase-3, caspase-7 and caspase-9 was detected by immunohistochemistry. Western blotting was used to determine the expression of survivin, caspase-3, caspase-7, caspase-9 and X-linked inhibitor of apoptosis protein (XIAP) in tumor tissues. The results demonstrated that matrine exerted anticancer effects in liver cancer-transplanted tumors, as evidenced by decrease in tumor weight and volume. Furthermore, the tumor inhibition rate in mice treated with matrine + cisplatin was 83.3%, whereas it was of 37.5 and 75% in mice treated with matrine or cisplatin alone, respectively. In addition, the expression of survivin and XIAP was significantly downregulated, whereas the expression of caspase-3, caspase-7 and caspase-9 was significantly upregulated in tumor tissues from nude mice treated with matrine + cisplatin, compared with those treated with cisplatin, matrine or normal saline. These findings suggested that the combination of matrine and cisplatin may promote tumor cell apoptosis in liver cancer by activating the caspase apoptosis pathway and suppressing the survivin-associated inhibition of caspase-9.