菊苣酸诱导人白血病细胞HL-60凋亡作用及机制研究

目的观察菊苣酸诱导人急性髓系白血病细胞株HL-60凋亡的作用并初步探讨其机制。方法培养HL-60细胞,分别给予终浓度为10¹00μmol·L-1的菊苣酸48 h,检测细胞活性和凋亡、Caspase-3活性以及Bcl-2蛋白表达水平。结果终浓度为10100μmol·L-1的菊苣酸48 h,检测细胞活性和凋亡、Caspase-3活性以及Bcl-2蛋白表达水平。结果终浓度为10¹00μmol·L-1的菊苣酸能呈浓度依赖性降低HL-60细胞增殖活性和增加凋亡,增强Caspase-3活性和下调Bcl-2蛋白表达。结论菊苣酸具有抑制白血病细胞株HL-60增殖活性和诱导其凋亡作用,其机制与降低抗凋亡蛋白Bcl-2表达及增强Caspase-3活性有关。     

DuP-697对K562白血病细胞凋亡诱导作用观察及机制研究

目的：观察选择性COX-2抑制剂DuP697对慢粒白血病K562细胞的凋亡诱导效应,并探讨其作用机制。方法：细胞培养加入DuP-697作用后,透射电镜观察细胞凋亡的形态,流式细胞仪检测细胞周期和凋亡率,Western印迹检测K562细胞Caspase-8蛋白表达;用Z—IETD—FMK阻断Caspase8活性,以证实Caspase-8蛋白表达和细胞凋亡的关系。结果：DuP-697能诱导K562细胞凋亡,其作用呈浓度依赖性,这-效应与Caspase-8蛋白表达上调和裂解激活有关;用Z-IETD—FMK阻断Caspase-8的活性,细胞凋亡明显受抑。结论：DuP-697能诱导K562细胞凋亡,其机制涉及Caspase-8活化的信号转导途径。     

马钱子碱对乳腺癌细胞MDA-MB-231作用的实验研究

目的本研究旨在观察马钱子碱（Brucine）对人乳腺癌细胞MDA-MB-231的增殖抑制和诱导凋亡作用,并分析Brucine在诱导细胞凋亡过程中对Bcl-2、Bax和Caspase-3蛋白表达的调控作用。方法人乳腺癌细胞株MDA-MB-231（雌激素受体阴性）细胞以L-15培养基体外培养,用MTT法测定Brucine对细胞的增殖抑制作用;倒置显微镜观察细胞形态;以碘化丙啶（PI）单染流式细胞仪检测细胞凋亡;AnnexinV-FITC/PI双染流式细胞术检测Brucine对MDA-MB-231的诱导凋亡作用;Western蛋白印迹法检测凋亡相关蛋白Bcl-2、Bax和Caspase3的表达。结果Brucine对MDA-MB-231细胞有明显的增殖抑制作用;观察到典型的细胞凋亡形态学特征性改变;流式细胞术PI染色结果显示随着Brucine浓度的增加细胞凋亡率逐渐增高并呈明显的浓度依赖,与对照组相比差异有显著性（P〈0.05）;早期凋亡率和晚期凋亡率先增加后降低,但死亡细胞逐渐增加;且随着Brucine浓度的增加抗凋亡基因Bcl-2表达水平明显降低,而促凋亡基因Bax和Caspase-3表达明显增高。结论Brucine能够诱导乳腺癌MDA-MB-231细胞凋亡,其分子机制可能与激活Bax、Caspase-3和抑制Bcl-2等凋亡调控基因有关。     

诺美孕酮促进大鼠子宫内膜异位症细胞凋亡及其作用机制

目的探讨诺美孕酮促进实验性大鼠子宫内膜异位症模型细胞凋亡及其作用机制。方法外科手术法建立大鼠子宫内膜异位症模型;HE染色观察异位内膜病理组织学改变;ELISA测定血清中抗子宫内膜抗体(EMAb)水平;West-ern blot检测异位内膜组织中Bcl-2、Bax、Caspase-9、Caspase-3蛋白的表达情况。结果诺美孕酮(0.5、1.5、15 mg.kg-1)异位内膜萎缩,间质疏松,腺体数目明显减少,腺腔萎缩;诺美孕酮呈剂量依赖性地降低异位内膜厚度和EMAb的浓度;诺美孕酮(0.5、1.5、15 mg.kg-1)异位内膜组织中Bax、Caspase-9和Caspase-3蛋白表达升高、Bcl-2蛋白表达降低。结论诺美孕酮(0.5、1.5、15 mg.kg-1)可促进大鼠子宫异位内膜细胞凋亡,其作用机制可能与降低EMAb水平、上调Bax和下调Bcl-2蛋白表达、激活细胞凋亡的内源性途径启动因子Caspase-9蛋白、激活执行因子Caspase-3蛋白表达有关。     

芹黄素对体外人大肠癌Lovo细胞生物学活性的影响及机制研究

目的探讨芹黄素对体外人大肠癌Lovo细胞生物学活性的影响及其可能的作用机制。方法不同浓度的芹黄素作用于体外培养的人大肠癌Lovo细胞24、48或72 h,采用光学显微镜和透射电镜分别观察芹黄素对Lovo细胞形态和超微结构的影响;采用四甲基偶氮唑盐比色法(MTT法)和平板克隆形成实验分别检测芹黄素对Lovo细胞增殖和克隆形成能力的影响;采用PI染色法、Annexin V FITC/PI双染法,流式细胞术分别检测芹黄素对Lovo细胞周期分布和凋亡的影响;采用Western blot法检测芹黄素对Bcl-2、pro-caspase-3、cleaved caspase-3表达的影响。结果芹黄素可浓度-时间依赖性的抑制人大肠癌Lovo细胞的增殖及克隆形成,作用48、72 h时的半数抑制浓度IC50分别为98.05μmol·L-1及33.91μmol·L-1;细胞周期分布发生改变,主要表现在G0/G1期细胞比例减少、G2/M期细胞比例增加,细胞周期阻滞于G2/M期;细胞凋亡率增加;Bcl-2、pro-caspase-3表达下调;cleaved caspase-3表达上调;差异具有统计学意义(P<0.05)。结论芹黄素可通过阻滞细胞周期于G2/M期抑制Lovo细胞增殖,通过下调Bcl-2、pro-caspase-3表达,上调cleaved caspase-3表达,诱导Lovo细胞凋亡,是一种有开发前景的大肠癌化疗药物。     

地塞米松对顺铂诱导的HepG2细胞凋亡及Bcl-2和Caspase-3蛋白表达的影响

目的:探讨地塞米松对顺铂诱导HepG2细胞凋亡的影响,并观察Bcl-2和Caspase-3蛋白的表达。方法:HepG2细胞与顺铂及不同浓度的地塞米松共培养,RT-PCR检测Bcl-2、Caspase-3的mRNA表达,Western blot检测Bcl-2、Caspase-3蛋白表达,流式细胞术(FACS)检测各组HepG2细胞的凋亡情况。结果:随着地塞米松浓度的增加,HepG2细胞中Bcl-2蛋白表达量升高,Caspase-3蛋白表达量下降。同时细胞凋亡率降低。结论:地塞米松部分通过Bcl-2途径抑制肝癌细胞的凋亡,而Caspase-3又在调控细胞凋亡中起重要作用。     

伪士的宁对人结肠癌HT-29细胞凋亡的影响及其机制研究

目的:探讨伪士的宁对人结肠癌HT-29细胞凋亡的影响及其机制。方法:取人结肠癌HT-29细胞,随机分为空白组和低、中、高剂量伪士的宁组(125、250、500μmol/L),加入不含药培养基或含相应浓度伪士的宁的培养基培养48 h。采用流式细胞仪检测细胞凋亡情况和线粒体跨膜电位;采用Western blotting法检测细胞中P53、Caspase-3、Caspase-9、兔源DNA修复酶(c-PARP)、Bcl-2的蛋白表达水平。结果:与空白组比较,低、中、高剂量伪士的宁组细胞凋亡率显著升高,线粒体跨膜电位均显著降低(P<0.01),且均呈现浓度依赖趋势。中、高剂量伪士的宁组细胞中P53、Caspase-3、Caspase-9、c-PARP蛋白表达水平较空白组均显著升高,低、中、高剂量伪士的宁组细胞中Bcl-2蛋白表达水平则显著降低(P<0.05或P<0.01)。结论:伪士的宁可能通过上调P53蛋白、下调Bcl-2蛋白的表达,改变线粒体膜电位,然后激活Caspase-3、c-PARP、Caspase-9的表达,进而激活内源性线粒体通路,发挥促进HT-29细胞凋亡的作用。     

半枝莲提取物对人大肠癌细胞系凋亡的影响

目的 探讨半枝莲提取物(SBE)诱导人大肠癌细胞系(SW480、LoVo、HT-29)的凋亡作用及其可能机制.方法 体外培养SW480、LoVo、HT-29细胞,以药物康复新、露蜂房作对照,应用MTT法和流式细胞术检测不同浓度SBE处理三种细胞48 h后的抑制率、细胞凋亡率及周期变化;RT-PCR检测SBE处理后凋亡相关基因Bcl-2和Caspase-3 mRNA表达.结果 与康复新、露蜂房比较,SBE对三种细胞的抑制率和细胞凋亡率均呈剂量依赖性显著升高(P＜0.01);S期细胞含量增多,出现S期阻滞;Caspase-3 mRNA表达亦显著上升,Bcl-2表达明显下降(P＜0.01).结论 SBE具有诱导大肠癌细胞系凋亡和抑制增殖作用,作用强于康复新和露蜂房提取物.其机制可能与Caspase-3基因表达的上调及Bcl-2基因表达下降有关.     

地塞米松衍生物对K562细胞增殖的抑制作用及机制

目的：研究地塞米松衍生物对K562细胞的增殖抑制作用，并对其作用机制进行初步的探讨。方法：以地塞米松为原料合成并纯化得到新的衍生物。用不同浓度的地塞米松衍生物对K562细胞进行处理，通过MTT比色法检测细胞增殖抑制率，电镜法观察细胞凋亡的形态学变化，免疫细胞化学法测定细胞Bcl-2，Fas表达，比色法检测Caspase-3的活性变化。结果：地基米松衍生物能抑制K562细胞的增殖，使Bcl-2表达降低，Fas表达上调，Caspase-3活性增强，诱导K562细胞凋亡。结论：地塞米松衍生物可能通过诱导K562细胞凋亡而抑制细胞增殖。其诱导细胞凋亡的机制可能与抑制Bcl-2蛋白的表达，上调Fas受体，进而激活细胞内的Caspase-3有关。     

SOD类似物阻断百草枯诱导的N27细胞凋亡的作用

目的探讨在离体培养的细胞中,SOD类似物[manganese(Ⅲ)meso-tetrakis(N,N′-diethylimidazolium-2-yl)porphyrin,MnTDM]阻断百草枯诱导的N27细胞凋亡的作用。方法以N27细胞为多巴胺能神经元的细胞模型,检测不同浓度的MnTDM对百草枯诱导的N27细胞凋亡的保护作用,四甲基偶氮唑盐(MTT)法检测细胞活性及代谢状态;电镜观察凋亡形态;免疫细胞化学染色法观察凋亡相关蛋白Bax、Bcl-2蛋白的表达。结果经百草枯作用后N27细胞活性下降,且其下降程度与百草枯浓度的升高呈线性关系,MnTDM明显阻断百草枯诱导的细胞活性下降(P<0.05),且该阻断作用与MnTDM的浓度成正相关;MnTDM预处理后,电镜观察到细胞凋亡形态好转,凋亡相关蛋白Bcl-2表达升高,Bax表达降低,Bcl-2/Bax值升高。结论MnTDM对百草枯介导的凋亡有一定的保护作用,提示其可能对帕金森病患者的临床防治有一定作用。     

氟尿嘧啶对结直肠癌RKO细胞SHP2基因表达的影响

目的 探究氟尿嘧啶（5-FU）对结直肠癌RKO细胞SHP2基因表达的影响。方法 培养对数生长期的人结直肠癌细胞RKO,5-FU处理48 h后,采用免疫荧光和Western免疫印迹观察SHP2的蛋白表达水平;将能够特异性抑制SHP2表达的siRNA（siSHP2）转染RKO细胞,5-FU处理48 h,CCK8测定细胞吸光度（A）值,流式检测细胞凋亡,观察RKO对5-FU的敏感性变化及5-FU诱导细胞凋亡的影响。结果 结直肠癌细胞RKO在5-FU处理48 h后,其细胞核中SHP2的蛋白表达水平明显增高;siSHP2转染后,RKO细胞对5-FU的敏感性降低,且降低了5-FU诱导的细胞凋亡率。结论 5-FU可能通过影响SHP2的表达,促进RKO细胞的凋亡,发挥抑癌作用。     

LncRNA-MALAT1通过miR-142-3p/TEAD1分子轴调控结直肠癌细胞增殖与凋亡#br#

目的　探讨长链非编码RNA-肺腺癌转移相关转录子1（LncRNA-MALAT1）对结直肠癌细胞增殖与凋亡的影响及相关作用机制。方法　通过Real-time PCR与Western blot实验检测结直肠癌细胞株与人正常结肠上皮细胞中LncRNA-MALAT1、miR-142-3p基因以及TEA结构域转录因子1（TEAD1）蛋白的表达;使用si-MALAT1转染HCT116细胞,在此基础上共转染miR-142-3p inhibitor,利用Real-time PCR与Western blot检测细胞中LncRNA-MALAT1与miR-142-3p基因以及TEAD1、Bax、Bcl-2与Cyclin D1蛋白的表达,通过CCK-8实验检测细胞的增殖水平,通过流式细胞术检测细胞的凋亡水平,通过双荧光素酶实验检测LncRNA-MALAT1与miR-142-3p以及miR-142-3p与TEAD1的结合。结果　与人正常结肠上皮细胞相比,结直肠癌细胞株中LncRNA-MALAT1基因与TEAD1蛋白呈高表达,miR-142-3p基因呈低表达（P＜0.05）;沉默LncRNA-MALAT1能够促进miR-142-3p基因与Bax蛋白表达,抑制LncRNA-MALAT1基因以及Bcl-2、Cyclin D1与TEAD1蛋白表达,抑制细胞增殖,并促进细胞凋亡;在此基础上沉默miR-142-3p能够对上述调控作用实现部分逆转;双荧光素酶实验结果显示,LncRNA-MALAT1与miR-142-3p以及miR-142-3p与TEAD1能够结合。结论　LncRNA-MALAT1能够结合miR-142-3p,促进miR-142-3p靶基因TEAD1表达,进而促进结直肠癌细胞增殖,抑制其细胞凋亡,促进结直肠癌的病理进程。     

Regulation of gamma-H2AX and securin contribute to apoptosis by oxaliplatin via a p38 mitogen-activated protein kinase-dependent pathway in human colorectal cancer cells

Oxaliplatin, a chemotherapeutic drug, induces DNA strand breaks leading to apoptosis in colorectal cancer cells. gamma-H2AX is a phosphorylated histone H2AX that can act as a marker of DNA double-strand breaks (DSBs). It has been shown that securin proteins were over-expressed in a variety of cancer cells. However, the roles of gamma-H2AX and securin on the oxaliplatin-induced apoptosis in human colorectal cancer cells remain unclear. Treatment of oxaliplatin (1-10muM for 6-24h) persistently induced gamma-H2AX formation and inhibited securin protein expression via a time- and concentration-dependent manner in HCT116 securin-wild type colorectal cancer cells. Compared with HCT116 securin-wild type cells, the induction of apoptosis and persistent gamma-H2AX formation by oxaliplatin was reduced in the HCT116 securin-null colorectal cancer cells. Furthermore, the blockage of caspases by specific caspase inhibitors reduced the levels of gamma-H2AX proteins and cytotoxicity but increased securin protein expression in the oxaliplatin-exposed cells. The gene knockdown of H2AX by transfection with a short interfering RNA of H2AX enhanced the oxaliplatin-induced cell death. Interestingly, the phosphorylation of p38 mitogen-activated protein kinase (MAPK) was markedly increased by oxaliplatin. Pre-treatment of a specific p38 MAPK inhibitor SB202190 reduced gamma-H2AX proteins and increased securin protein expression in the oxaliplatin-treated cells. Our findings suggest that p38 MAPK may oppositely regulate securin protein expression and gamma-H2AX formation in the oxaliplatin-induced apoptosis of human colorectal cancer cells.     

PDCD4对DAP5表达及大肠癌细胞凋亡的影响

【摘要】目的 探讨程序性死亡基因4(PDCD4)对死亡相关蛋白5（DAP5) 的表达及对人大肠癌细胞系LOVO凋亡的影响。方法 构建重组真核表达载体pFLAG/PDCD4,转染人大肠癌细胞LOVO,G418（500 mg/L）筛选获得稳定表达PDCD4的细胞系。RT-PCR及Western blotting检测LOVO细胞中PDCD4的mRNA及蛋白表达,流式细胞仪检测LOVO细胞凋亡情况,Western blotting检测LOVO细胞DAP5表达的变化。结果 成功建立稳定表达PDCD4的大肠癌 细胞LOVO-pFLAG/PDCD4。转染PDCD4 的LOVO-pFLAG/PDCD4 组与空白对照LOVO 组、转染空载质粒的LOVO-pFLAG组相比,PDCD4蛋白表达和mRNA水平明显升高（P < 0.01）;细胞凋亡率明显增加（P < 0.01）;同时伴有DAP5蛋白表达明显升高（P < 0.01）。结论PDCD4能够诱导大肠癌细胞LOVO的凋亡,其机制可能与上调DAP5的表达有关。     

重楼活性单体PP-22对人结肠癌SW620细胞增殖和凋亡的影响

目的 探讨重楼活性单体PP-22对人结肠癌SW620细胞增殖和凋亡的影响及其联合5-氟尿嘧啶(5-FU)和洛铂的抗肿瘤效果。方法 采用噻唑蓝(MTT)法和克隆形成抑制实验观察不同浓度PP-22对人结肠癌SW620细胞增殖的抑制作用;分别观察PP-22联合5-FU和洛铂对人结肠癌SW620细胞增殖的抑制作用;碘化丙锭单染流式细胞术检测细胞周期变化及细胞凋亡水平;Western blot法检测PP-22作用后细胞凋亡相关蛋白的表达。结果 重楼单体PP-22能显著抑制SW620细胞的生长,作用呈剂量-效应关系;随着PP-22浓度的增加,细胞克隆形成逐渐减少,与细胞对照组和DMSO组相比有显著差异;PP-22联合不同浓度的5-FU和洛铂作用于SW620细胞48 h,可提高SW620细胞对5-FU和洛铂的敏感性;不同浓度PP-22作用于SW620细胞后,细胞周期阻滞于S期;PP-22作用后存在Caspase-3和Caspase-9蛋白的活化和降解,抗凋亡蛋白Bcl-2、Bcl-xL减少,促凋亡蛋白Bax的表达增加。结论 PP-22能显著抑制人结肠癌SW620细胞增殖,诱导细胞凋亡,提高SW620细胞对5-FU和洛铂的敏感性。     

Structure–activity relationship of butyrate analogues on apoptosis,proliferation and histone deacetylase activity in HCT‐116 human colorectal cancer cells

1. Butyrate, a bacteria fermentative product in the colonic lumen, has been shown to produce a wide variety of biological effects in human cancer cells in vitro. However, there are pharmacological drawbacks associated with the use of butyrate therapy and there are limited published data on the structure–activity relationship of butyrate analogues in colorectal cancer cells. Previously, we determined structure–activity relationship using HT‐29 human colorectal cancer cells. However, it was viewed as important to explore similar relationships in another colorectal cancer cell line. 2. Therefore, in the present study, the in vitro structure–activity relationship of butyrate analogues was examined by investigating their effects on apoptosis, cell proliferation, histone deacetylase (HDAC) activity and lactate dehydrogenase (LDH) leakage as a measure of cell toxicity in HCT‐116 human colorectal cancer cells. 3. Of the 32 analogues tested, only 4‐benzoylbutyrate, 3‐benzo‐ylpropionate, 4‐(4‐nitrophenyl)butyrate and 3‐(4‐fluorobenzoyl)propionate exhibited comparable biological effects to butyrate. The common structural properties of the compounds of interest were to lack amino or hydroxyl substitutions at the 2‐, 3‐ and/or 4‐position of the aliphatic moiety of butyrate. 4. The present study reveals a dissociation between the induction of apoptosis, inhibition of cell proliferation, HDAC activity and LDH leakage. The results indicate differential responses of butyrate analogues in HT‐29 and HCT‐116 colorectal cancer cells.     

Approach for mechanism of BH3 domain counterpart BH3I-2' inducing colorectal cancer cell apoptosis

Objective To discuss mechanism of BH3 domain counterpart BH3I-2' inducing colorectal cancer cell apoptosis.Methods Detected inhibition ratio and apoptosis of colorectal cancer cells HCT-116,which were treated by BH3I-2',with microplate reader and flow cytometry.Results Inhibition ratio of colorectal cancer cells,which were treated by BH3I-2',could reach about 50%.Ratio of viable apoptotic cell decreased and that of non-viable apoptotic cell increased as time went.Conclusions BH3I-2' can induce colorectal cancer cell apoptosis.     

Gene silencing of Rac1 with RNA interference mediated by ultrasound and microbubbles in human LoVo cells: evaluation of cell invasion inhibition and metastatic

Objective: The objective of this study was to assess the change of cytoskeleton and cell cycle in LoVo (human colorectal cancer) cell via gene silencing of Rac1 with RNA interference mediated by microbubble (SonoVue) and ultrasound (US).

Methods: The compound of plasmid Rac1-shRNA, LoVo cells, and SonoVue was exposed to US (1?MHz, 2?W/cm², 5?min). The expression of Rac1 mRNA and Rac1 protein was detected by RT-PCR and Western blot. Cytoskeleton was taken by confocal microscope in a random fashion. Cell invasion was assayed using modified Boyden chambers, and cell cycle and apoptosis were analyzed by flow cytometry in LoVo cells.

Results: Rac1 gene is overexpressed in human colorectal cancer cells, gene silencing of Rac1 with RNA interference mediated by microbubble and US strongly inhibited lamellipodia formation, cell invasion, and delayed cell cycle, as well as enhanced cell apoptosis of LoVo cells in vitro.

Conclusion: Silencing Rac1 gene mediated by microbubble and US may become a new treatment option for the inhibition of the invasion and metastasis of colorectal cancer cells.     

Activation of p38 mitogen-activated protein kinase by celecoxib oppositely regulates survivin and gamma-H2AX in human colorectal cancer cells

Cancer cells express survivin that facilitates tumorigenesis. Celecoxib has been shown to reduce human colorectal cancers. However, the role and regulation of survivin by celecoxib in colorectal carcinoma cells remain unclear. Treatment with 40-80 muM celecoxib for 24 h induced cytotoxicity and proliferation inhibition via a concentration-dependent manner in RKO colorectal carcinoma cells. Celecoxib blocked the survivin protein expression and increased the phosphorylation of H2AX at serine-193 (gamma-H2AX). The survivin gene knockdown by transfection with a survivin siRNA revealed that the loss of survivin correlated with the expression of gamma-H2AX. Meanwhile, celecoxib increased caspase-3 activation and apoptosis. Celecoxib activated the phosphorylation of p38 mitogen-activated protein (MAP) kinase. The phosphorylated proteins of p38 MAP kinase and gamma-H2AX were observed in the apoptotic cells. SB203580, a specific p38 MAP kinase inhibitor, protected the survivin protein expression and decreased the levels of gamma-H2AX and apoptosis in the celecoxib-exposed cells. The blockade of survivin expression increased the celecoxib-induced cytotoxicity; conversely, overexpression of survivin by transfection with a survivin-expressing vector raised the cancer cell proliferation and resisted the celecoxib-induced cell death. Our results provide for the first time that p38 MAP kinase participates in the down-regulation of survivin and subsequently induces the activation of gamma-H2AX for mediating apoptosis following treatment with celecoxib in human colorectal cancer cells.     

Octahedral Pt(IV) complex K101 induces apoptosis via ERK1/2 activation and the p53 pathway in human colon cancer cells

Recently, the synthesized octahedral Pt(IV) compound trans,cis-Pt(acetato)2Cl2(1,4-butanediamine), K101, showed potent anti-tumor activity in vitro and in vivo. For the further investigation of K101-induced anti-cancer activity, we tested cytotoxicity against various cancer cell lines and performed the histoculture drug response assay (HDRA) against human colorectal tumor tissues in vitro. We investigated the signaling pathway of K101-induced apoptosis via expression of p53 and ERK1/2 in the human colon cell line HCT116. The cytotoxicity and the three-dimensional HDRA of K101 were evaluated using the MTT assay. To study the K101-induced apoptosis pathway, we performed FACS analysis and immunoblotting of p53, p21, Bax, Fas and ERK1/2 in HCT116 cells treated with or without K101. The cytotoxic IC50 values of K101 ranged from 1.15 to 2.38 micromol/l, compared to cisplatin ranging from 2.13 to 13.1 micromol/l. Among several cancer cell lines, K101 showed greater potency than cisplatin in colon cancer cell lines. In the HDRA, K101 showed 80.0-91.4% efficacy rates compared with 48.6% for cisplatin against colorectal cancer patient tissues. In the signaling pathway, the expression of p53 and phospho-ERK1/2 was increased in a time-dependent manner by treatment with K101 in the HCT116 cells. When K101 was treated with MEK inhibitor U0126, the cell death rate was increased. The octahedral Pt(IV) complex K101 could be an attractive candidate as a chemotherapeutic agent against colon cancer. ERK1/2 activation and the p53 pathway may play significant functions in mediating K101-induced apoptosis in human colon cancer cells.