吲哚美辛对结肠癌细胞HCT116的影响及机制探讨

目的:研究吲哚美辛对结肠癌细胞株HCT116增殖及体外侵袭的影响并对其机制进行探讨。方法:应用WST-8法和体外侵袭小室测定吲哚美辛对结肠癌细胞株HCT116增殖和侵袭能力的影响;Westen-blotting方法检测吲哚美辛作用后HCT116细胞β-连环素(β-Catenin)、细胞周期素D1(Cyclin D1)、基质金属蛋白酶7(matrix metalloproteinase-7,MMP-7)蛋白的表达。结果:吲哚美辛能够明显抑制结肠癌细胞株HCT116的增殖,呈时间-剂量依赖性,作用24、48、72h的IC50值分别为440.36、323.90、254.37μmol/L;吲哚美辛能够明显抑制结肠癌细胞株HCT116的体外侵袭,呈剂量依赖性;吲哚美辛作用24、48、72h后,β-Catenin、CyclinD1、MMP-7蛋白表达均有下降。结论:吲哚美辛能抑制结肠癌细胞株HCT116的增殖与迁移,其作用机制之一可能是通过Wnt/β-catenin信号通路。     

鸢尾黄酮通过促进自噬抑制结肠癌细胞增殖并诱导其凋亡研究

目的：探究鸢尾黄酮对结肠癌细胞自噬及其对细胞增殖能力和凋亡的影响。方法：鸢尾黄酮对结肠癌细胞的半抑制浓度（IC50）采用CCK-8法检测;结肠癌细胞的长期增殖能力采用克隆平板实验检测;采用CCK-8法检测不同抑制剂预处理后鸢尾黄酮对结肠癌细胞增殖活性的影响;采用蛋白免疫印迹法检测自噬相关蛋白的变化情况;透射电镜观察结肠癌细胞中自噬体的数量;采用CCK-8法检测小干扰RNA（siRNA）沉默自噬关键蛋白ATG5转染后鸢尾黄酮对结肠癌细胞增殖活性的影响。结果：通过不同浓度鸢尾黄酮作用下结肠癌细胞系SW480的生长抑制情况绘制IC50曲线,确定其IC50为（221.90±35.31） μM;克隆平板实验表明鸢尾黄酮对结肠癌细胞的长期增殖能力具有抑制作用;凋亡抑制剂Z-VAD显著逆转了鸢尾黄酮对结肠癌细胞的增殖抑制作用;Western blot实验结果表明,随着鸢尾黄酮作用浓度的升高,SW480细胞内LC3-Ⅱ含量逐渐上升,p62含量下降;电镜结果表明,经鸢尾黄酮作用后SW480细胞内自噬体含量明显增加;沉默ATG5可部分逆转鸢尾黄酮对SW480细胞的增殖抑制作用。结论：鸢尾黄酮通过促进自噬抑制了结肠癌细胞的增殖能力,并诱导结肠癌细胞的凋亡。     

鸢尾黄酮通过促进自噬抑制结肠癌细胞增殖并诱导其凋亡[基金项目：福建省自然科学基金项目（2016J01617）]

背景与目的：探究鸢尾黄酮对结肠癌细胞自噬的影响及其对细胞增殖能力和凋亡的影响。方法：鸢尾黄酮对结肠癌细胞的半抑制浓度（IC50）采用CCK-8法检测;结肠癌细胞的长期增殖能力采用克隆平板实验检测;CCK-8法检测不同抑制剂预处理后鸢尾黄酮对结肠癌细胞增殖活性的影响;蛋白免疫印迹法检测自噬相关蛋白的变化情况;透射电镜观察结肠癌细胞中自噬体的数量;小干扰RNA（siRNA）沉默自噬关键蛋白ATG5,CCK-8法检测联合凋亡抑制剂作用下鸢尾黄酮对结肠癌细胞增殖活性的影响。结果：通过CCK-8法分析不同浓度鸢尾黄酮作用下结肠癌细胞系SW480的生长抑制情况后绘制半抑制浓度（IC50）曲线,确定其半抑制浓度（IC50）为（221.9±35.31）μM;克隆平板实验表明鸢尾黄酮对结肠癌细胞的长期增殖能力具有抑制作用;凋亡抑制剂Z-VAD显著逆转了鸢尾黄酮对结肠癌细胞的增殖抑制作用;Western blot实验结果表明随着鸢尾黄酮作用浓度的升高,SW480细胞内LC3-II含量逐渐增高,p62含量下降;电镜结果表明鸢尾黄酮作用后SW480细胞内自噬体含量明显增加;沉默ATG5部分逆转鸢尾黄酮对SW480细胞的增殖抑制作用。结论：鸢尾黄酮通过促进自噬抑制了结肠癌细胞的增殖能力并诱导结肠癌细胞的凋亡。     

青蒿琥酯对结肠癌HCT116细胞间黏附分子蛋白表达的影响

目的：研究青蒿琥酯对结肠癌细胞锚着不依赖性增殖及其细胞间黏附分子-1（intercellular adhesion molecule-1，ICAM-1）基因蛋白表达的影响。方法：以人结肠癌细胞株HCT116为模型，以软琼脂集落培养试验检测青蒿琥酯对肿瘤细胞的增殖抑制效应；Western blot方法检测青蒿琥酯作用前后细胞ICAM-1蛋白表达的变化。结果：青蒿琥酯能有效地抑制结肠癌细胞HCT116的恶性增殖，且呈剂量依赖性。青蒿琥酯能有效地抑制ICAM-1基因蛋白表达，作用呈时间和浓度依赖性。结论：青蒿琥酯可明显抑制结肠癌HCT116细胞增殖，可能与下调ICAM-1表达有关。     

双氢青蒿素抗人结肠癌HCT116细胞作用的研究

目的:研究双氢青蒿素(dihydroartemisinin,DHA)对人结肠癌HCT116细胞增殖及凋亡的影响,观察人结肠癌HCT116细胞中肿瘤转移相关因子尿激酶型纤溶酶原激活剂(urokinase-type plasminogen activator,uPA)表达的变化。方法:MTT法观察不同浓度和时间DHA对HCT116细胞增殖抑制作用;AO/EB双染法及流式细胞仪AnnexinⅤ-FITC法检测HCT116细胞凋亡率;免疫组化及图像分析法观察uPA蛋白的表达的动态变化。结果:MTT显示与对照组相比,各实验组DHA可以显著抑制HCT116细胞增殖(P<0.05);AO/EB双染法可观察到各实验组典型的凋亡细胞,流式细胞仪AnnexinⅤ-FITC法显示DHA可以诱导HCT116细胞凋亡具有浓度依赖性;免疫组化及图像分析显示uPA蛋白阳性单位明显下降。结论:DHA能够有效抑制HCT116细胞增殖并诱导其凋亡,DHA能够下调HCT116细胞中uPA蛋白的表达。     

以KDR为启动子的双自杀基因系统诱导结肠癌细胞凋亡的实验研究

目的研究以KDR为启动子的双自杀基因系统CDglyTK诱导结肠癌细胞凋亡的实验研究。方法用联合基因AdKDR-CDglyTK腺病毒转染表达KDR不同的人结肠癌细胞HCT116和LS174T,检测转染效率;RT-PCR检测双自杀基因CDglyTK的表达;用梯度浓度的前药5-FC及GCV处理,MTT法检测双自杀基因系统对HCT116和LS174T的细胞毒性作用;流式细胞术观察细胞凋亡变化;免疫组织化学法检测caspase-3蛋白的表达。结果携带双自杀基因的重组腺病毒载体成功转染结肠癌细胞。RT-PCR结果显示：表达KDR的HCT116细胞能表达目的基因,而不表达KDR的LS174T细胞不表达目的基因。5-FC和GCV对转染腺病毒的HCT116有明显的细胞毒作用而对LS174T细胞不敏感。流式细胞仪结果显示：给予5-FC和GCV后HCT116细胞出现凋亡峰,G0/G1升高、S期下降。Caspase-3表达增强（P〈0.01）。结论 KDR启动子驱动的双自杀基因系统CDglyTK能特异性杀伤结肠癌HCT116细胞,KDR可作为结肠癌基因治疗的靶点,并通过增强caspase-3途径诱导细胞凋亡。     

肝X受体激动剂GW3965对人结肠癌细胞增殖的抑制作用

目的:探讨激活肝X受体(liver X receptors,LXRs)对人结肠癌细胞增殖的影响。方法:采用实时定量聚合酶链反应检测人结肠癌细胞HCT116和Lovo中LXRα和LXRβ的mRNA表达;LXRs激动剂GW3965分别处理2种细胞后,以CCK-8法检测细胞生长曲线的变化,流式细胞仪检测细胞增殖周期的变化,蛋白印迹法检测AMPK、mTOR和p70S6K蛋白及相应磷酸化蛋白的表达变化。结果 :设定LXRαmRNA在HCT116细胞的表达水平为1,LXRβmRNA在HCT116和Lovo细胞中的相对表达量分别是LXRαmRNA在HCT116细胞表达水平的3.1倍和4.6倍。经10μmol/L和20μmol/L的GW3965处理48 h及72 h后,2种结肠癌细胞的生长都受到明显抑制(P<0.05);相应G1~G0期细胞百分比显著增多,而S期细胞百分比明显减少(P<0.01);磷酸化AMPK蛋白(p-AMPK)的表达水平在HCT116和Lovo细胞中分别上升了2.97倍和3.48倍(P<0.05);p-mTOR和p-p70S6K在HCT116细胞中的表达分别下降了33.14%和38.44%,在Lovo细胞中的表达分别下降了51.68%和31.52%(P<0.05)。结论:激活LXRs可通过干预细胞周期和AMPK-mTOR-S6K信号通路抑制结肠癌细胞增殖。     

姜黄素联合沙利度胺抑制KG-1细胞增殖及相关作用机制研究

目的：探讨姜黄素联合沙利度胺对急性髓系白血病KG-1细胞增殖、凋亡的影响及与抗凋亡蛋白（Bcl-x L）、信号转导和转录激活因子3(STAT3)的关系。方法：MTT法检测KG-1细胞增殖,筛选姜黄素、沙利度胺的最佳联合浓度;分别采用MTT法、流式细胞术分析姜黄素、沙利度胺单药及两药联用对KG-1细胞增殖、凋亡的影响;实时定量PCR检测单药组、两药联用组、对照组（未处理细胞）的STAT3、Bcl-x L m RNA表达水平。结果：姜黄素和沙利度胺在20-100μmol/L范围内对KG-1细胞增殖的抑制作用均呈浓度依赖性（r=0.657,r=0.681）。姜黄素在作用48 h的IC50值为（42.07±0.50）μmol/L,沙利度胺为（57.01±2.39）μmol/L。姜黄素（40μmol/L）+沙利度胺（60μmol/L）两药联用的细胞增殖抑制率为（86.67±1.53）%,明显高于单用姜黄素的（51.67±1.15）%和单用沙利度胺的（55.33±1.53）%（均P<0.05）。姜黄素、沙利度胺单药及两药联用作用48 h,KG-1细胞凋亡率分别为（18.67±2.08）%、（...     

miR-320a靶向FOXQ1抑制结肠癌细胞增殖和侵袭的分子机制

目的探讨miR-320a在人结肠癌细胞中的生物学行为,并初步阐明miR-320a对癌基因FOXQ1的靶向调控机制。方法采用qRT-PCR检测结肠癌细胞中miR-320a和FOXQ1的表达;用miR-320a mimics转染结肠癌细胞株HTC-116;采用CCK-8法、克隆形成试验检测miR-320a对结肠癌细胞增殖的影响,采用Transwell小室分析miR-320a对结肠癌细胞侵袭能力的影响;双荧光素酶报告基因和Western Bloting验证miR-320a对FOXQ1的靶向调控作用。结果 QRT-PCR结果显示miR-320a mimics明显上调miR-320a在HCT-116细胞中的表达;CCK-8法和克隆形成试验显示上调miR-320a表达显著抑制结肠癌细胞增殖;Transwell试验表明上调miR-320a可抑制HCT-116结肠癌细胞侵袭;蛋白印迹实验显示上调miR-320a降低FOXQ1蛋白在结肠癌细胞中的表达,双荧光素酶报告基因试验进一步确认miR-320a可以调控FOXQ1的表达。结论过表达miR-320a可以抑制结肠癌细胞增殖、侵袭,这种抑制作用是通过靶向调控FOXQ1来实现的。     

细胞色素酶CYP2C19介导的沙利度胺体外抗血管生成作用研究

本研究探讨人肝细胞微粒体代谢系统对治疗多发性骨髓瘤的沙利度胺体外抗血管生成的影响及细胞色素酶CYP2C19在其中的作用。采用沙利度胺原药或与人肝细胞微粒体在体外共孵育后用MTY法检测人脐带静脉内皮细胞（human umbilical cord vein endothelial cells，hUCVEC）增殖活力，用流式细胞术测定hUVCEC细胞周期和细胞凋亡，以改良的Boyden小室法检测hUCVEC细胞迁移力，以体外小管形成实验检测hUCVEC分化。结果表明：沙利度胺原药对hUCVEC活力无明显抑制作用，细胞凋亡比例也无明显增加，轻度影响细胞迁移，无抗小管形成作用；当与人肝细胞微粒体共孵育后hUCVEC增殖活力明显受抑。100μg／ml沙利度胺与肝细胞微粒体共孵育后hUCVEC增殖活力的抑制率达（11．7±3．9）％，凋亡细胞增加达27．2％，明显下调细胞迁移力并抑制体外小管形成。在共孵育体系中加入CYP2C19特异性抑制剂奥美拉唑，可减弱沙利度胺抑制hUCVEC增殖活力和诱导凋亡的作用，减低细胞迁移力和部分逆转抗小管形成的作用。结论：沙利度胺的体外抗血管生成作用依赖于人细胞微粒体的作用，细胞色素酶系中的CYP2C19可能参与了这一过程。     

结直肠癌TP53相关外泌体的差异蛋白分析

目的 比较分析T P53突变、敲除及野生的结直肠癌细胞分泌外泌体的蛋白质组差异.方法 从TP53野生型[HCT116-p53(WT)]、敲除型[HCT116-p53(-/-)]和构建的273位点突变型的结直肠癌HCT116细胞[HCT116-p53(R273H)]培养上清中分别提取外泌体,通过透射电镜观察其形态和免疫印...     

The role of spermidine/spermine N1-acetyltransferase in determining response to chemotherapeutic agents in colorectal cancer cells

Polyamines have been shown to play a role in the growth and survival of several solid tumors, including colorectal cancer. We identified the polyamine catabolic enzyme spermidine/spermine N(1)-acetyltransferase (SSAT) as being one of the most highly inducible genes in two DNA microarray screens to identify novel determinants of response to chemotherapeutic agents in colorectal cancer. SSAT was shown to be inducible in response to 5-fluorouracil (5-FU) or oxaliplatin in parental and drug-resistant HCT116 cell lines. It was also shown that SSAT mRNA was up-regulated in response to 5-FU or oxaliplatin in a panel of six colorectal cancer cell lines. The polyamine analogue N(1),N(11)-diethylnorspermine (DENSpm) depletes polyamine pools and potently induces SSAT. We evaluated the effect of combining DENSpm with chemotherapeutic agents in HCT116 p53(+/+) cells and in HCT116 drug-resistant daughter cell lines. Western blot analyses showed that SSAT protein expression was dramatically enhanced when DENSpm was combined with oxaliplatin or 5-FU in HCT116 p53(+/+) cells. Using cell viability assays and flow cytometry, synergistic induction of cell death was observed following cotreatment of HCT116 p53(+/+) cells with DENSpm and each chemotherapeutic agent. Of note, this combined therapy increased the chemosensitivity of cells rendered resistant to each of these chemotherapeutic agents. Small interfering RNA-mediated down-regulation of SSAT resulted in loss of synergy between DENSpm and these agents. These results show that SSAT plays an important role in regulating cell death following combined cytotoxic drug and DENSpm treatment. Furthermore, DENSpm sensitizes both sensitive and resistant cells to chemotherapeutic agents. Taken together, these results suggest that SSAT may be an important target for therapeutic intervention in colorectal cancer.     

Down-regulation of X-linked inhibitor of apoptosis synergistically enhanced peroxisome proliferator-activated receptor gamma ligand-induced growth inhibition in colon cancer

We found previously that X-linked inhibitor of apoptosis protein (XIAP), a potent endogenous inhibitor of apoptosis, is overexpressed in colon cancer. Ligand-induced activation of peroxisome proliferator-activated receptor gamma (PPARgamma) has been shown to exert proapoptotic and antiproliferative effects in many cancer cell types. However, neither XIAP down-regulation alone nor monotherapy using PPARgamma ligands is potent enough to control colon cancer. We explored whether XIAP inhibition and PPARgamma activation offer a synergistic anticancer effect in colon cancer. HCT116-XIAP(+/+) and HCT116-XIAP(-/-) cells were treated with troglitazone or 15-deoxy-Delta(12,14)-prostaglandin J(2) (15-PGJ(2)). Cell growth and apoptosis were measured. Nude mice were s.c. inoculated with HCT116 cells with or without oral troglitazone. Tumor growth, angiogenesis, and apoptosis were measured. Troglitazone- and 15-PGJ(2)-induced growth inhibition and apoptosis were more prominent in HCT116-XIAP(-/-) cells. Troglitazone- and 15-PGJ(2)-induced apoptosis correlated with enhanced cleavage of caspases and poly(ADP-ribose) polymerase, which were more profound in HCT116-XIAP(-/-) cells. Pretreatment of cells with XIAP inhibitor 1396-12 also sensitized HCT116-XIAP(+/+) cells to PPARgamma ligand-induced apoptosis. Troglitazone significantly retarded the growth of xenograft tumors, more significantly so in HCT116-XIAP(-/-) cell-derived tumors. Reduction of tumor size was associated with reduced expression of Ki-67, vascular endothelial growth factor, and CD31 as well as increased apoptosis. Loss of XIAP significantly sensitized colorectal cancer cells to PPARgamma ligand-induced apoptosis and inhibition of cell proliferation. Thus, simultaneous inhibition of XIAP and activation of PPARgamma may have a synergistic antitumor effect against colon cancer.     

顺铂诱导直肠癌HCT116细胞凋亡及其作用机制的研究

目的 研究顺铂诱导直肠癌HCT116细胞凋亡及其作用机制.方法 采用酶联免疫吸附法M30-ApoptosisTM-ELISA-kits、流式细胞仪测定不同浓度顺铂作用不同时间HCT116细胞的凋亡情况;West-ern-Blotting测定p53、p21、Bcl-2蛋白水平的表达.结果 顺铂可抑制直肠癌HCT116细胞生长,并呈时效(F=1129.383,P=0.000)和量效(F=125.267,P=0.000)关系;2.5、5.0、10.0、15.0 μmol/L顺铂分别作用直肠癌HCT116细胞0、12、24、48、72 h,通过亚G1峰检测其凋亡率,顺铂作用24、48、72 h细胞凋亡率与对照组比较差异有统计学意义(χ2值分别为5.669、14.110、12.221,P值分别为0.010、0.003、0.000),不同时间顺铂抑制HCT116细胞生长率的差异有统计学意义(χ2=14.008,P=0.003);不同时间顺铂诱导HCT116细胞释放CK18-Asp237-Asp396含量的比较,不同药物浓度结果差异有统计学意义(F=48.667,P=0.000),同时间结果差异有统计学意义(F=1194.394,P=0.000),Western-Blotting结果提示顺铂作用直肠癌HCT116细胞后p53、p21蛋白水平表达随着12、24、48、72 h与0 h比较逐步升高,p53蛋白(t值分别为9.873、-2.906、7.229、2.776,P值分别为0.000、0.007、0.000、0.011);p21蛋白(t值分别为-10.692、-8.867、-15.063、-16.281,P值分别为0.000、0.001、0.000、0.000);Bcl-2蛋白的表达无变化(t值分别为1.429、2.011、2.247、2.001,P值分别为0.178、0.069、0.053、0.062).结论 顺铂通过恢复pS3的功能,诱导肿瘤细胞凋亡,起到抑制肿瘤生长的作用.     

Effect of CLN3 silencing by RNA interference on the proliferation and apoptosis of human colorectal cancer cells

Apoptosis constitutes a system for the removal of aged, or damaged cells, which is regulated by the interplay of pro-apoptotic and antiapoptotic proteins. Previous study has shown that Juvenile Batten disease protein, CLN3, is antiapoptotic gene in NT2 neuronal precursor cells and a few types of cancers. However, in colorectal cancer, whether CLN3 also play its antiapoptotic role and the effect of targeted controlling CLN3 on the biological behavior of human colorectal cancer cell is unknown. We employed the sequence-specific siRNA silencing the CLN3 gene and investigated its effects on growth and apoptosis of colorectal cancer HCT116 cells, which has highest elevation of CLN3 expression among four colorectal cancer cell lines. After CLN3 specific siRNA transfection, mRNA and protein expression levels of CLN3 in HCT116 cells were noticeably decreased. Moreover, CLN3-siRNA inhibited the proliferation of colorectal cancer cells, promoted their apoptosis and induced G0/G1 cell cycle arrest. Our current study demonstrated that CLN3 was expressed in colorectal cancer cells at a high frequency. Moreover, CLN3 down-regulation with RNA interference can inhibit proliferation, apoptosis, and cell cycle progression of colorectal cancer cells. Our study represented a potential new approach to understanding the role of CLN3 in cancer and provides a potential novel strategy colorectal cancer therapy.     

P53上游凋亡调节蛋白在依托泊苷诱导直肠癌细胞凋亡中作用机制的研究

目的 研究P53上游凋亡调节蛋白(PUMA)在直肠癌细胞HCT116中的表达及其关联性作用机制.方法 应用依托泊苷诱导直肠癌细胞HCT116,采用酶联免疫吸附试验(ELISA)、流式细胞仪测定依托泊苷作用前后细胞HCT116的凋亡情况;蛋白印迹法(Western blot)测定PUMA、P53蛋白的表达水平.结果 依托...     

Role of p21waf1/cip1 in effects of oxaliplatin in colorectal cancer cells

Clinical studies have shown that oxaliplatin, a novel platinum derivative, is a potent chemotherapeutic agent for colorectal cancer when combined with 5-fluorouracil and leucovorin. Although the toxic activity is based on covalent adducts between platinum and DNA, its actual biological behavior is mostly unknown. In an effort to explore the mechanism of tumor susceptibility to oxaliplatin, we examined the cytotoxic effects of oxaliplatin in colorectal cancer cell lines in reference to p53 gene status. Although p53 gene status did not clearly predict sensitivity to oxaliplatin, p53 wild-type cells including HCT116 were sensitive but HCT116 p53-/- were found to be resistant to oxaliplatin. Oxaliplatin caused strong p21waf1/cip1 induction and G0-G1 arrest in p53 wild-type cells, whereas cisplatin did not induce G0-G1 arrest. Assays using p53 wild but p21waf1/cip1 null HCT116 cells revealed that oxaliplatin did not show G0-G1 arrest and reduced growth-inhibitory effects, suggesting that p21waf1/cip1 may be a key element in oxaliplatin-treated p53 wild-type cells. Although HCT116 is DNA mismatch repair-deficient, a mismatch repair-proficient HCT116+ch3 cell line displayed similar responses with regard to p21waf1/cip1-mediated growth inhibition and G0-G1 arrest. In p53 mutant cells, on the other hand, oxaliplatin caused an abrupt transition from G1 to S phase and eventually resulted in G2-M arrest. This abrupt entry into S phase was associated with loss of the p21waf1/cip1 protein via proteasome-mediated degradation. These findings suggest that p21waf1/cip1 plays a role in oxaliplatin-mediated cell cycle and growth control in p53-dependent and -independent pathways.     

18F-FMISO PET显像评价结直肠癌肝转移的实验研究

目的探究^18F-FMISO PET定量参数(肿瘤/肝脏SUVmax)在检测小鼠CRC肝转移潜能中的应用价值。方法采用伤口愈合实验检测CRC细胞迁移能力,采用细胞摄取实验检测体外^18F-FMISO摄取能力。建立肝转移及皮下移植瘤小鼠模型以进行Micro-PET显像和定量分析。采用皮尔森相关系数分析18F-FMISO参数、肝转移数量及生物学指标(HIF-1α、GLUT-1)之间的相关性。结果在HT29、HCT116及LoVo三种肝转移模型中,LoVo小鼠具有更高的肝转移率及较短的中位生存时间。与HT29和HCT116细胞相比,LoVo细胞具有更强的迁移能力和更高的18F-FMISO体外摄取能力。体内Micro-PET显像表明,LoVo肝转移模型及皮下荷瘤模型的T/L SUVmax值明显高于HT29和HCT116模型。相关性分析显示,肝转移瘤的18F-FMISO T/L SUVmax值与肝转移瘤(直径大于0.5 cm)数量存在显著相关性(r=0.6408,P=0.0013),与HIF-1α(r=0.8145,P=0.0075)和GLUT-1(r=0.8252,P=0.0062)表达也存在显着相关性。结论18F-FMISO定量参数T/L SUVmax在动物模型中为评价CRC肝转移提供了有价值的分子影像信息,其在预测CRC肝转移潜能方面具有一定的应用价值。