罗格列酮对肝癌SMMC-7721细胞VEGF蛋白表达的影响

目的探讨过氧化物酶体增殖激活物受体γ( PPARγ) 配体罗格列酮对肝癌SMMC-7721细胞中VEGF表达的影响及其可能机制。方法经不同浓度罗格列酮（0、0.1、1、10、100μmol/L）分别作用SMMC-7721细胞24h、48h、72h后,采用Western印迹法检测细胞VEGF和PTEN、Akt1/2及P-Akt1蛋白表达的变化。结果罗格列酮可以显著抑制SMMC-7721细胞中VEGF蛋白表达水平（P<0.05）,呈时间和剂量依赖性;能上调细胞PTEN的表达,并呈时间和剂量依赖性（P<0.05）,但Akt_1/2及P-Akt₁的表达无明显改变（P>0.05）。结论罗格列酮可抑制SMMC-7721细胞中VEGF蛋白表达,该作用可能是与上调PTEN表达有关,但不是通过直接抑制PI3K/Akt信号转导途径来实现的。     

Thiazolidinediones/PPARγ agonists and fatty acid synthase inhibitors as an experimental combination therapy for prostate cancer

The prostate cancer (PCa) cell lines LNCaP, PC-3, and DU-145 express peroxisome proliferator-activated receptor γ (PPARγ) but its role in PCa is unclear. Thiazolidinediones (TZDs), a family of PPARγ activators and type 2 anti-diabetic drugs, exhibit anti-tumor apoptotic effects in human PCa cell lines. Likewise, pharmacological inhibitors of fatty acid synthase (FASN), a metabolic enzyme highly expressed in PCa, induce apoptosis in prostate and other cancer cells. Here, we show positive correlation between PPARγ and FASN protein in PCa cell lines and synergism between TZDs and FASN blockers in PCa cell viability reduction and apoptosis induction. Combined TZDs/FASN has enhanced anti-tumor properties in both androgen-dependent LNCaP and androgen-independent PC-3 and DU-145 cells when compared with single drug exposure. Low concentrations (5-10 μM) of the TZD drug rosiglitazone failed to alter cell viability but, paradoxically, upregulated lipogenic genes [PPARγ, FASN, sterol regulatory element binding protein-1c (SREBP-1c) and acetyl-Co A carboxylase-1 (ACC1)], which diminish the apoptotic effects of rosiglitazone. The mean IC50 in all cell lines was 45 ± 2 μM for rosiglitazone compared with significantly lower 5 ± 1 μM for rosiglitazone plus the FASN blocker cerulenin, and 10.2 ± 2 μM for rosiglitazone plus the cerulenin synthetic analog C75. The IC50 for the combined rosiglitazone and FASN blockers contrasts with the relatively higher IC50 for rosiglitazone (45 ± 2 μM), the TZD drug troglitazone (13 ± 2 μM), cerulenin (32 ± 1 μM), or C75 (26 ± 3 μM) when these drugs were used alone. In summary, this study shows proof-of-principle for combining FASN blockers and TZDs for PCa treatment.     

异土木香内酯通过bcr-abl-STAT5信号通路抑制慢性粒细胞白血病耐药细胞K562/A02增殖

目的 探讨异土木香内酯对慢性粒细胞白血病耐药细胞K562/A02增殖的抑制作用及其机制.方法6.25、12.5、25、50、100μmol/L的异土木香内酯作用于K562/A02细胞24、48 h,四甲基偶氮唑盐(MTT)法检测其对K562/A02细胞的增殖抑制效果;10、15、20μmol/L异土木香内酯作用于K562/A02细胞24 h,流式细胞术检测细胞周期及凋亡;Western blot法检测增殖相关蛋白表达水平.多组间比较采用单因素方差分析.结果异土木香内酯能够显著抑制K562/A02细胞增殖,并呈浓度依赖性(P<0.05),作用24 h的半数抑制浓度(IC50)值为(15.00±1.03)μmol/L;阴性对照组及10、15、20μmol/L异土木香内酯作用后K562/A02细胞凋亡率分别为(2.71±0.52)%、(19.10±1.55)%、(27.61±2.32)%和(32.01±3.01)%,呈浓度依赖性(F=33.901,P<0.05);S期细胞比例分别为(57.80±2.11)%、(68.62±2.89)%、(78.44±3.51)%和(80.61±2.90)%,呈浓度依赖性(F=51.328,P<0.05).异土木香内酯明显降低bcl-2、p-bcr-abl、p-STAT5、细胞周期蛋白依赖性激酶2(CDK2)和细胞周期蛋白A(cyclin A)的表达(P<0.05),上调细胞色素C、Bax和p21的表达(P<0.05).结论异土木香内酯能够通过bcr-abl-STAT5信号通路抑制K562/A02细胞增殖.     

Combinational effect of PPARγ agonist and RXR agonist on the growth of SGC7901 gastric carcinoma cells in vitro

In order to investigate the inhibitory effects and mechanisms of troglitazone (TGZ), a peroxisome proliferator-activated receptor γ (PPARγ) agonist, and retinoid X receptor (RXR) agonist (9-cis-retinoic acid (RA)) on gastric carcinoma cells SGC7901, SGC7901 cells were treated with TGZ and 9-cis-RA, respectively, or in combination. Then, the cell growth, apoptosis, morphological changes, and the expression of PPARγ, RXRγ, Bcl-2, and Bax were detected by MTT assay, flow cytometry, HE staining, immunocytochemistry staining, and Western blot assay, respectively. Our results showed that the growth of SGC7901 cells was inhibited and the cells got sparser at the concentrations of 50 μmol/L TGZ, 20 μmol/L 9-cis-RA, or combination of TGZ (25 μmol/L) and 9-cis-RA (10 μmol/L). Immunocytochemistry and Western blot showed that after 72 h, the expression of PPARγ, RXRγ, and Bax were upregulated; Bcl-2 was downregulated compared with the negative control group. These data indicated that PPARγ agonist and RXR agonist could inhibit the proliferation of SGC7901 cells via inducing the apoptosis, which involved the increase in the level of Bax/Bcl-2. The combination of RXR agonist and PPARγ agonist could induce the maximal inhibitory effects on tumor growth and apoptosis via promoting the formation of RXR/PPARγ heterodimer.     

125I粒子联合AZD1152对三阴性乳腺癌细胞增殖和凋亡的影响

目的：研究¹²⁵I粒子联合Aurora激酶抑制剂AZD1152对三阴性乳腺癌(TNBC)细胞MDA-MB-231增殖和凋亡的影响。方法：试验设对照组(常规培养)、¹²⁵I粒子照射组(照射组)、1 μmol/L AZD1152作用MDA-MB-231细胞48 h组(抑制组)、¹²⁵I粒子照射与1 μmol/L AZD1152联合作用MDA-MB-231细胞48 h组(联合组)。采用免疫荧光检测细胞多核形成;四甲基噻唑蓝(MTT)法检测细胞增殖抑制率;CCK-8检测细胞活力;流式细胞术PI单染检测细胞周期;流式细胞术Annexin V/PI双染观察各组细胞凋亡情况;Western blot检测各组细胞中Cyclin B1、组蛋白H3的表达及其磷酸化水平的改变,以及凋亡相关蛋白Bcl-2、Bax、PARP表达的变化。结果：免疫荧光检测发现1 μmol/L AZD1152作用MDA-MB-231细胞48 h时可见到多核细胞形成;MTT试验结果显示对照组、照射组、抑制组和联合组的细胞增殖抑制率分别为(0.61±0.32)%、(17.62±1.41)%、(29.67±0.41)%、(53.17±1.26)%;CCK-8检测显示细胞存活率分别为(94.88±0.22)%、(59.21±0.14)%、(42.05±0.17)%、(32.12±0.36)%;细胞周期检测发现G2/M期占比分别为(18.99±0.15)%、(38.05±0.23)%、(49.80±0.32)%、(75.52±0.45)%,与对照组比较差异均具有统计学意义(P<0.05)。照射组、抑制组和联合组的细胞凋亡率分别为(17.48±0.24)%、(29.23±0.02)%、(63.11±0.27)%,均较对照组(0.31±0.03)%升高(P<0.05)。流式细胞术发现抑制组细胞出现多核及多倍体细胞,易形成非整倍体。Western blot检测结果显示联合组较其他3组,抗凋亡蛋白Bcl-2、组蛋白H3的磷酸化和Cyclin B1蛋白表达减少(P<0.05),而促凋亡蛋白Bax和PARP蛋白剪切明显增加(P<0.05)。结论：¹²⁵I粒子对AZD1152有增敏作用,¹²⁵I联合AZD1152可显著抑制MDA-MB-231细胞组蛋白H3磷酸化及Cyclin B1水平,从而抑制细胞增殖,诱导细胞凋亡。     

神经酰胺促胃癌SGC7901细胞凋亡的实验

目的探讨神经酰胺(Ceramide,Cer)对胃癌SGC7901细胞的促凋亡作用及可能作用机制。方法体外培养人胃癌SGC7901细胞,分别给予Cer、顺铂（DDP）;DDP联合Cer作用后,MTT检测单独使用Cer及联合DDP应用对SGC7901细胞增殖的影响,流式细胞仪检测细胞凋亡率,免疫组织化学染色、Western blot 检测SGC7901细胞NF-κB、Bcl-2、Bax蛋白表达。结果Cer 2.5 μmol/L及以上时可以抑制细胞增殖,与对照组相比差异有统计学意义(P<0.05)。Cer联合DDP后,联合用药作用强于单独DDP及Cer组(P<0.05),q值在24、48、72 h分别为1.05、1.01、0.99。Cer、DDP作用48h可诱导SGC7901细胞凋亡,Cer 5 μmol/L、DDP 2.5 mg/L单独用药组及Cer 5 μmol/L 联合DDP 2.5 mg/L组凋亡率分别为：（39.23±1.62）%、（4727±113）%、（50.13±2.76）%,与对照组［（1846±1.64）%］相比差异有统计学意义（P<0.05）,联合用药作用强于单独DDP及Cer组(P<0.05)。NF-κB、Bcl-2在SGC7901细胞中较高表达［（74.10±2.69）%、（69.37±4.54）%］,Bax在SGC7901细胞中表达较低［（2460±373）%］,Cer 5 μmol/L、DDP 25 mg/L单独用药组及Cer 5 μmol/L 联合DDP 2.5 mg/L组NF-κB、Bcl-2阳性表达率降低(65.13±1.71、 62.17±2.12, 44.8±3.65;57.70±2.22、55.13±5.77、37.67±2.14),Bax表达率上调(33.80±1.10、35.50±2.27、51.73±3.76),Bcl-2/Bax 比值降低(1.71±0.10、1.56±0.26、0.73±0.09),与对照组相比差别有统计学意义（P<0.05）,联合用药作用强于单独DDP及Cer组(P<0.05)。相关性分析显示NF-κB与Bcl-2呈正相关（Spearman^,s rho =0.9510,Prob>|t|=0.0000）。结论Cer通过下调NF-κB进而调节Bcl-2/Bax比值诱导SGC7901细胞凋亡。     

过氧化酶增殖因子活化受体对胃癌组织中血管内皮生长因子C的调节作用

目的:探讨过氧化酶增殖因子活化受体(peroxisome proliferator-activated receptor gamma,PPARγ)和血管内皮生长因子C(vascular endothelial growth factor-C,VEGF-C)在胃癌组织中的表达及其相关性。研究PPARγ受体激动剂罗格列酮(rosiglitazone,ROS)对VEGF-C的调节作用。方法:选取经病理证实为胃癌的手术切除石蜡标本60例,同时选取相同病例的癌旁组织,癌旁正常组织作为对照,采用免疫组化法检测PPARγ和VEGF-C表达,分析其与临床病理特征的关系。采用免疫印迹法观察不同浓度的罗格列酮作用于MKN-45胃癌细胞48 h时VEGF-C蛋白表达的变化。结果:免疫组化提示PPARγ阳性率在胃癌中是68.33%,癌旁组织中是51.67%,癌旁正常组织中是20%,三者表达差异有统计学意义(P=0.00);VEGF-C阳性率在胃癌中是63.33%,癌旁组织中是45%,癌旁正常组织中是23.33%,三者表达差异有统计学意义(P=0.00);PPARγ的蛋白表达与VEGF-C表达为负相关(r=-0.897,P=0.000);2者的表达均与胃癌淋巴结转移及TNM分期有关(均P<0.05)。West-blot结果提示选择12.5μmol/L,25μmol/L,50μmol/L,100μmol/L四个浓度的ROS,VEGF-C/β-actin灰度比分别为:0.42,0.35,0.33,0.32,抑制率分别为:57.8%,64.6%,66.6%,68%,对VEGF-C蛋白表达差别具有统计学意义,(P=0.000)。随着PPARγ配体浓度的增加,对VEGF-C的抑制作用增强。β-actin表达在各组中无明显差异。结论:胃癌组织中PPARγ和VEGF-C呈高表达,联合检测这2个指标对评估胃癌浸润转移及判断病情、监测预后有重要意义。PPARγ可能通过抑制VEGF-C的表达而阻止胃癌的淋巴转移。     

大蒜素联合5-FU对结肠癌HT-29细胞凋亡的影响及机制

目的 探讨大蒜素与5-FU联合应用治疗结肠癌的作用机制。方法 利用HT-29细胞模拟结肠癌,设置空白对照组、大蒜素组(15 μg/mL)、5-FU组(15 μg/mL)和大蒜素+5-FU组(各15 μg/mL)共4组,采用CCK-8法测定细胞增殖抑制率,流式细胞术观察细胞凋亡情况,Real-time PCR检测mTOR、PTEN、Bcl-2与Bax mRNA表达情况。结果 CCK-8检测结果显示,与空白对照组比较,各用药组均可以抑制HT-29细胞的增殖(P＜0.05)。其中大蒜素+5-FU组的抑制作用最为显著;流式细胞术检测结果显示,各用药组凋亡细胞显著多于空白对照组,大蒜素+5-FU组凋亡细胞最为显著;Real-time PCR结果显示,与空白对照组比较,各用药组Bcl-2、mTOR的mRNA表达量显著降低而Bax、PTEN的mRNA表达量显著升高,大蒜素+5-FU组变化最为显著。结论 大蒜素与5-FU联合应用可以抑制HT29细胞的增殖,促进凋亡,并且大蒜素具有增强5-FU诱导结肠癌细胞凋亡的能力。     

过氧化酶增殖因子活化受体对胃癌组织中血管内皮生长因子C的调节作用

目的：探讨过氧化酶增殖因子活化受体（peroxisome proliferator-activated receptor gamma,PPARγ）和血管内皮生长因子C（vascular endothelial growth factor-C,VEGF-C）在胃癌组织中的表达及其相关性。研究PPARγ受体激动剂罗格列酮（rosiglitazone,ROS）对VEGF-C的调节作用。方法：选取经病理证实为胃癌的手术切除石蜡标本60例,同时选取相同病例的癌旁组织,癌旁正常组织作为对照,采用免疫组化法检测PPARγ和VEGF-C表达,分析其与临床病理特征的关系。采用免疫印迹法观察不同浓度的罗格列酮作用于MKN-45胃癌细胞48 h时VEGF-C蛋白表达的变化。结果：免疫组化提示PPARγ阳性率在胃癌中是68.33%,癌旁组织中是51.67%,癌旁正常组织中是20%,三者表达差异有统计学意义（P=0.00）;VEGF-C阳性率在胃癌中是63.33%,癌旁组织中是45%,癌旁正常组织中是23.33%,三者表达差异有统计学意义（P=0.00）;PPARγ的蛋白表达与VEGF-C表达为负相关（r=-0.897,P=0.000）;2者的表达均与胃癌淋巴结转移及TNM分期有关（均P〈0.05）。West-blot结果提示选择12.5μmol/L,25μmol/L,50μmol/L,100μmol/L四个浓度的ROS,VEGF-C/β-actin灰度比分别为：0.42,0.35,0.33,0.32,抑制率分别为：57.8%,64.6%,66.6%,68%,对VEGF-C蛋白表达差别具有统计学意义,（P=0.000）。随着PPARγ配体浓度的增加,对VEGF-C的抑制作用增强。β-actin表达在各组中无明显差异。结论：胃癌组织中PPARγ和VEGF-C呈高表达,联合检测这2个指标对评估胃癌浸润转移及判断病情、监测预后有重要意义。PPARγ可能通过抑制VEGF-C的表达而阻止胃癌的淋巴转移。     

Growth Inhibiton of H uman Breast Cancer Cell Line MDA-MB-231 by Rosiglitazone through Activation of PPARy

To investigate the anti-proliferative effect ofrosiglitazone and its relationship to peroxisome proliferator-activated receptor γ(PPARγ)in human breast cancer cell lineMDA-MB-231 and evaluate the potential application value ofrosiglitazone for breast cancer therapy.METHoDS The cytostatic effect of rosiglitazone on MDA-MB-231 cellS was measured by the MTT assay.Cell-cyclekinetics.was assessed by flow cytometry.Apoptotic cells weredetermined by the TUNEL assay.MDA.MB-231 cells weretreated with rosiglitazone or in combination with the PPARyantagonist GW9662 to investigate the effect of rosiglitazone on cellproliferation and its relationship to PPARγ.RESUITS The results showed that rosiglitazone could inhibitgrowth of MDA-MB-231 cells in a dose-and time-dependentmanner with an IC50 value of 5.2 pmol/L at 24 h after the drugwas added into the culture.Cell cycle analysis showed that thepercentage of G0/G1 phase cells increased,S phase cells decreased,and cells were arrested in G1 phase with increasing concentrationsof rosiglitazone.Detectable signs of apoptotic cell death caused byrosiglitazone occurred at a concentration of 100 pmol/L and theapoptotic rate was(18±3)%.PPARγ selective antagonist GW9662could partially reverse the inhibitory effect of rosiglitazone onproliferation of MDA.MB-231 cells.CoNCLUSION It was concluded that rosiglitazone Can inhibitgrowth of MDA-MB-231 cells via PPARγ activation and a highconcentration of rosiglitazone can also induce MDA-MB-231 cellapoptosis.These results suggest that PPARv represents a putativemolecular target for chemopreventive therapy and rosiglitazonemay be effective in the treatment of breast cancer.     

白藜芦醇对人胃癌耐药细胞SGC-7901/5-FU生物学效应的影响及其作用机制

目的 探讨白藜芦醇(resveratrol,RES)对5-氟尿嘧啶(5-fluorouracil,5-FU)耐药胃癌细胞(SGC-7901/5-FU)生物学效应的影响及其作用机制.方法 用不同浓度(0μmol/L、10μmol/L、50μmol/L、200μmol/L、400μmol/L)的RES分别处理SGC-790...     

重楼皂苷D对人慢性粒细胞白血病K562细胞增殖的抑制作用及其机制

目的 探讨重楼皂苷D对人慢性粒细胞白血病细胞株K562增殖的抑制作用及其机制.方法 选用浓度为0、0.1、0.2、0.4、0.8、1.2、2.4μmol/L重楼皂苷D作用于K562细胞24 h,用CCK-8法检测重楼皂苷D对K562细胞增殖的抑制作用;流式细胞术检测重楼皂苷D对K562细胞凋亡以及细胞周期分布的影响;Western blot方法检测相关蛋白的表达.结果 重楼皂苷D可显著抑制K562细胞增殖,24 h的半数有效抑制浓度(IC50)为(0.9±0.1)μmol/L.流式细胞术检测结果显示,浓度为0.9μmol/L重楼皂苷D作用于K562细胞12、24 h后,细胞早期凋亡率较对照组的(2.05±0.45)%分别提高到(11.46±1.51)%、(28.87±2.35)%,差异有统计学意义(F=38.637,P<0.05).重楼皂苷D能够显著下调bcl-2、CDK1、cyclin B1、bcr-abl融合蛋白的表达,上调Bax、细胞色素C、活化的caspase-3以及p21的表达(均P<0.05).此外,重楼皂苷D能够将细胞周期阻滞在G2/M期(F=42.355,P<0.05).结论 重楼皂苷D能够明显抑制慢性粒细胞白血病K562细胞增殖,其作用机制可能是诱导细胞凋亡及促进细胞周期阻滞.     

The Effect of miR-200c Inhibition on Chemosensitivity (5- FluoroUracil) in Colorectal Cancer

5-Fluorouracil (5-FU) as a chemotherapeutic drug is used to treat colorectal cancer (CRC). However, 5-FU is associated with acquired CRC resistance, which decreases the therapeutic potential of 5-FU. Several studies indicated that miR-200c is also involved in chemotherapeutic drug resistance, but the exact mechanism of miR-200c mediated chemoresistance has not yet been fully understood. In this study, we examined the effect of inhibition of miR-200c on the sensitivity of HCT-116 cells to 5-FU. HCT-116 cells were transfected with LNA-anti- miR-200c for 48 h. mRNA expression of miR-200c was investigated by qRT-PCR. The protein expression of phosphatase and tensin homolog (PTEN) and E-cadherin were evaluated by western blotting. Annexin V/ PI staining and caspase 3 activity were used to detect apoptosis. LNA-anti-miR-200c inhibited the miR-200c expression in the transfected cells compared with that in the control group. LNA-anti-miR-200c suppressed the expression of PTEN and E-cadherin independent of the presence of the chemotherapeutic drug 5-FU. LNA-anti-miR-200c reduced the 5-FU-induced apoptosis and caspase 3 activity. miR-200c, as a novel prognostic marker in CRC, can be a potential therapeutic approach to overcome chemoresistance during 5-FU chemotherapy.     

Growth Inhibiton of Human Breast Cancer Cell Line MDAMB-231 by Rosiglitazone through Activation of PPARγ

Objective  To investigate the anti-proliferative effect of rosiglitazone and its relationship to peroxisome proliferator-activated receptor γ (PPARγ) in human breast cancer cell line MDA-MB-231 and evaluate the potential application value of rosiglitazone for breast cancer therapy. Methods  The cytostatic effect of rosiglitazone on MDA-MB-231 cells was measured by the MTT assay. Cell-cycle kinetics was assessed by flow cytometry. Apoptotic cells were determined by the TUNEL assay. MDA-MB-231 cells were treated with rosiglitazone or in combination with the PPARγ antagonist GW9662 to investigate the effect of rosiglitazone on cell proliferation and its relationship to PPARγ. Results  The results showed that rosiglitazone could inhibit growth of MDA-MB-231 cells in a dose- and time-dependent manner with an IC₅₀ value of 5.2 μmol/L at 24 h after the drug was added into the culture. Cell cycle analysis showed that the percentage of G₀/G₁ phase cells increased, S phase cells decreased, and cells were arrested in G1 phase with increasing concentrations of rosiglitazone. Detectable signs of apoptotic cell death caused by rosiglitazone occurred at a concentration of 100 μmol/L and the apoptotic rate was (18 ± 3)%. PPARγ selective antagonist GW9662 could partially reverse the inhibitory effect of rosiglitazone on proliferation of MDA-MB-231 cells. Conclusion  It was concluded that rosiglitazone can inhibit growth of MDA-MB-231 cells via PPARγ activation and a high concentration of rosiglitazone can also induce MDA-MB-231 cell apoptosis. These results suggest that PPARγ represents a putative molecular target for chemopreventive therapy and rosiglitazone may be effective in the treatment of breast cancer.     

Loss of XIAP sensitizes rosiglitazone-induced growth inhibition of colon cancer in vivo

Ligands for peroxisome proliferator-activated receptor gamma (PPAR gamma) possess anticancer properties. However, the efficacy of PPAR gamma ligands varies in different cancers. In colon cancer, the role of PPAR gamma and its ligands is controversial. We recently showed that downregulation of X-linked inhibitor of apoptosis protein (XIAP) could sensitize colon cancer cells to troglitazone, and 15-deoxy-D12,14-prostaglandin J2 (15-PGJ2) induced cell killing. In our study, we aimed to examine whether rosiglitazone, another more clinically relevant PPAR gamma ligand, has any synergistic anticancer effect with XIAP downregulation in colon cancer. Human colon cancer cell lines HCT116-XIAP(+/+) cells and HCT116-XIAP(-/-) cells were treated with various concentrations of rosiglitazone. The effects of rosiglitazone on cell proliferation, apoptosis and growth of xenograft colon cancers were studied. Rosiglitazone barely suppressed the growth and only very weakly induced apoptosis in HCT116 cells in vitro. Loss of XIAP did not sensitize HCT116 cells to rosiglitazone-induced growth inhibition or apoptosis. In vivo studies revealed that rosiglitazone strongly suppressed the growth of xenograft colon cancer, especially tumors derived from HCT116-XIAP(-/-) cells. The rosiglitazone-treated tumor had reduced expression of ki-67 and lowered mitotic rate. Downregulation of XIAP was associated with an impaired activation of PPAR gamma by its ligand. Rosiglitazone induced marked upregulation of PTEN in HCT116-XIAP(-/-) cells, as well as in xenograft tumors derived from HCT116-XIAP(-/-) cells. We concluded that rosiglitazone significantly suppresses the growth of xenograft colon cancer, and downregulation of XIAP sensitizes the xenograft tumors to rosiglitazone-induced tumor suppression in vivo via upregulation of PTEN.