Sonic hedgehog elevates N-myc gene expression in neural stem cells

Proliferation of neural stem cells is regulated by the secreted signaling molecule sonic hedgehog. In this study, neural stem cells were infected with recombinant adeno-associated virus expressing sonic hedgehog-N-enhanced green fluorescent protein. The results showed that overexpression of sonic hedgehog in neural stem cells induced the increased expression of Gill and N-myc, a target gene of sonic hedgehog. These findings suggest that N-myc is a direct downstream target of the sonic hedgehog signal pathway in neural stem cells. Sonic hedgehog and N-myc are important mediators of sonic hedgehog-induced proliferation of neural stem cells.

Expressions of myc and ras gene in human hepatocellular carcinoma by applying the double hybridization in situ

Objective: To establish a method of non-isotope double in situ hybridization in order to detect the expression of two kinds of oncogenes at single cell level simultaneously, and confirm the hypothesis of 'model of stepwise carcinogenesis'. Methods: The method of non-isotope double in situ hybridization was established with the digoxigenin (Dig) and biotin(Bio) labelled probes. The expression of two members of oncogenes of the myc and/or ras gene families (myc and N-ras, myc and K-ras, myc and H-ras, N-ras and K-ras , N-ras and H-ras, K-ras and H-ras) was further studied with the method in 10 cases of Chinese Hepatocellular Carcinomas (HCC). Results : Co-expression of two kinds of oncogenes was detected only in a few cases, reflected by coshowing two different hybridization signals ,i. e. , co-showing of Dig-myc and Bio-H-ras, Dig-myc and Bio-N-ras, Dig-myc and Bio-K-ras was observed in 2 cases, 2 cases and one case, respectively. The common characteristics were that positive cells of myc distributed diffusely, while positive cells of ras diatributed sporadically or locally among the positive cells of myc, and only a few cells exhibited co-showing of two oncogenes at single cell level. There were only 2 cases representing co-showing of two oncogenes in ras gene family (Dig-N-ras and bio-H-ras, Dig-N-ras and Bio-K-ras , respectively). The two kinds of positive cells of different ras gene represented mixed local and sporadical distribution, and co-showing of two signals was found in a few cells at single cell level. Conclusion: There are multiple oncogenes involving in tumorigenesis by their ordered activation. The activation of the ras gene family plays a role in promotion, while the activation of myc is an important event in late stage of tumorigenesis

Gene expression profiling of MYC-driven tumor signatures in porcine liver stem cells by transcriptome sequencing

AIM:To identify the genes induced and regulated by the MYC protein in generating tumors from liver stem cells.METHODS:In this study,we have used an immortal porcine liver stem cell line,PICM-19,to study the role of c-MYC in hepatocarcinogenesis.PICM-19 cells were converted into cancer cells(PICM-19-CSCs)by overexpressing human MYC.To identify MYC-driven differential gene expression,transcriptome sequencing was carried out by RNA sequencing,and genes identified by this method were validated using real-time PCR.In vivo tumorigenicity studies were then conducted by injecting PICM-19-CSCs into the flanks of immunodeficient mice.RESULTS:Our results showed that MYC-overexpressing PICM-19 stem cells formed tumors in immunodeficient mice demonstrating that a single oncogene was sufficient to convert them into cancer cells(PICM-19-CSCs).By using comparative bioinformatics analyses,we have determined that>1000 genes were differentially expressed between PICM-19 and PICM-19-CSCs.Gene ontology analysis further showed that the MYCinduced,altered gene expression was primarily associated with various cellular processes,such as metabolism,cell adhesion,growth and proliferation,cell cycle,inflammation and tumorigenesis.Interestingly,six genes expressed by PICM-19 cells(CDO1,C22orf39,DKK2,ENPEP,GPX6,SRPX2)were completely silenced after MYC-induction in PICM-19-CSCs,suggesting that the absence of these genes may be critical for inducingtumorigenesis.CONCLUSION:MYC-driven genes may serve as promising candidates for the development of hepatocellular carcinoma therapeutics that would not have deleterious effects on other cell types in the liver.

Gene therapy with antisense c-myc adenovirus for human gastric carcino-ma cell line in vitro and for implanted carcinoma in nude mice

Objective:To study the effects of recombinant antisense c-myc adenovirus (rAS-c-myc-Ad) on SGG 7901 human gastric carcinoma cell line in for and in nude mice. Methods:The effects of rAS-c-myc-Ad and LacZ-Ad on SGG 7901 gastric carcinoma cells were observed with X-galstaining, MTT, DNA gradient degradation test, TUNEL, flow cytometry, PCR and western blot. The therapeutic effects of rAS-c-myc-Ad on the implanted ax 7901 cells in nude mice were also ob served.Results: rAS-c-myc-Ad significantly inhibited the growth of SGG 7901 cells and induced their apoptosis. After the treatment of rAS-c-myc-Ad, the prolifetion rate of the cells was decreased by 44’ l% in de and SGC 7901 cells failed to form caxcinoma ther they were implanted into nude mice. Injection of rAS-c-myc-Ad into the carcinoma subcutaneously implanted to the nude mice significantly inhibited the growth of the implanted carcinoma with an inhibition rate of 68. 9%. Conclusion: rAS-c- myc- Ad significantly inhibits the growth of SGG 7901 human gastric carcinoma cells in vitro and in nude

Expression and Biological Function of N-myc Down-regulated Gene 1 in Human Cervical Cancer

The expression of N-myc down-regulated gene 1 (NDRG1) has previously been reported to be involved in the proliferation,differentiation,invasion and metastasis of cancer cells,but its role in cervical cancer is still unclear.This study aimed to investigate the expression of NDRG1gene in human cervical cancer and its effect on aggressive tumor behaviors.The NDRG1 expression in cervical tissues and cells was detected by RT-PCR.Specific expression plasmid pEGFP-N1-NDRG1-GFP was used to enhance the expression of NDRG1 in human cervical cancer cell lines.The mRNA and protein level of NDRG1 was assessed by RT-PCR and Western blotting,respectively.Its effects on cell proliferation,migration,invasion,cell cycle and apoptosis were detected by MTT,transwell migration assay and flow cytometry (FCM),respectively.The results showed that the expression of NDRG1 in cervical cancer tissues and cells was significantly lower than in normal cervical tissues (P【0.001).After transfection with pEGFP-N1-NDRG1-GFP,the mRNA and protein expression of NDRG1 was up-regulated in Siha cells,which suppressed cell proliferation (P【0.001),induced cell cycle arrest (P【0.05),reduced invasion and migration of Siha cells (P【0.05),but caused no cell apoptosis.Moreover,vascular endothelial growth factor (VEGF),a tumor-induced angiogenesis factor,was markedly reduced and E-cadherin,a cell adhesion molecule,was increased in the cells transfected with pEGFP-N1-NDRG1-GFP.It was concluded that up-regulated NDRG1 may play a role in the suppression of malignant cell growth,invasion and metastasis of human cervical cancer.

c-Myc Knockout as a Model for Gene Editing for Training Healthcare Professional Students

Correction of genetic errors, commonly known as gene editing, holds promise to treat diseases with unmet medical needs. However, gene therapy trials do encounter unwanted outcomes, because of an incomplete understanding of the disease states, and gene therapy processes, among others. This situation encourages a concept that healthcare professionals receiving laboratory research training will not only identify inadequacies in basic biomedical knowledge of gene therapies but also provide tangible refinements. To this end, we have undertaken the PharmD student training in gene editing in a basic research laboratory setting. As a model, MYC gene was chosen for knockout using CRISPR-Cas9 method in HT29 and OVCAR8 cells. Students were involved in the design of MYC-specific gRNAs, subcloning into Cas9-carrying plasmid, and selection of knockout clones from the transfected cells. Subsequently, genomic DNA isolation and sequencing, analysis of clonal DNA sequences using online bioinformatics tools, western blotting, cell proliferation and cell division cycle experiments, were performed to characterize the MYC knockout clones. Results presented in this communication suggest that healthcare professionals who received laboratory training gain a better understanding of the disease states and mechanisms, gene therapy protocols, limitations of gene therapies, ability to critically evaluate the literature and confidence in the oversight of gene therapies in the clinic.

EXPRESSION OF c－myc GENE AND BIOSYNTHESIS OF BIOLOGICAL MACROMOLECULES IN ANTISENSE TRANSFECTANT HL_（60）~R－9

The recombinant plasmid PGC was constructed for transcription unit of c-myc gene with diorientation in vitro, to make RNA probes for detection of c-myc mRNA and antisence RNA expression of tranfectant HL-9,which was obtained from HL60 cells transfected with inducible c-myc antisense RNA expression plasmid. The results from HL-9 cells induced by Cd2+ indicated that expression of c-myc antisense RNA increased with Cd2+ concentration and exposure time, while c-myc mRNA expression progressively reduced. Using immunohistochemical technique no c-myc P62 protein expression was detected. The incorporation of 3H-TdR, 3H-UR and 3H-Leu revealed significant suppression of DNA, RNA and protein biosynthesis. It is suggested that the reversion changes previously reported in malignant Phenotypes of HL-9 cells and the inhibition of macromolecular biosynthesis mentioned above were associated with the blockade of c-myc gene expression by its antisense RNA.

Inhibition of N-Myc down regulated gene 1 in in vitro cultured human glioblastoma cells

AIM: To study short ds RNA oligonucleotides(si RNA)as a potent tool for artificially modulating gene expression of N-Myc down regulated gene 1(NDRG1) gene induced under different physiological conditions(Normoxia and hypoxia) modulating NDRG1 transcription, m RNA stability and translation. METHODS: A cell line established from a patient with glioblastoma multiforme. Plasmid DNA for transfections was prepared with the Endofree Plasmid Maxi kit. From plates containing 5 × 107 cells, nuclear extracts were prepared according to previous protocols. The p SUPERNDRG1 vectors were designed, two sequences were selected from the human NDRG1 c DNA(5'-GCATTATTGGCATGGGAAC-3' and 5'-ATGCAGAGTAACGTGGAAG-3'. reverse transcription polymerase chain reaction was performed using primers designed using published information on β-actin and hypoxia-inducible factor(HIF)-1α m RNA sequences in Gen Bank. NDRG1 m RNA and protein level expression results under different conditions of hypoxia or reoxygenation were compared to aerobic control conditions using the Mann-Whitney U test. Reoxygenation values were also compared to the NDRG1 levels after 24 h of hypoxia(P < 0.05 was considered significant).RESULTS: si RNA- and iodoacetate(IAA)-mediated downregulation of NDRG1 m RNA and protein expression in vitro in human glioblastoma cell lines showed a nearly complete inhibition of NDRG1 expression when compared to the results obtained due to the inhibitory role of glycolysis inhibitor IAA. Hypoxia responsive elements bound by nuclear HIF-1 in human glioblastoma cells in vitro under different oxygenation conditions and the clearly enhanced binding of nuclear extracts from glioblastoma cell samples exposed to extreme hypoxic conditions confirmed the HIF-1 Western blotting results. CONCLUSION: NDRG1 represents an additional diagnostic marker for brain tumor detection, due to the role of hypoxia in regulating this gene, and it canrepresent a potential target for tumor treatment in human glioblastoma. The si RNA method can represent an elegant alternative to modulate the expression of the hypoxia induced NDRG1 gene and can help to monitor the development of the cancer disease treatment outcome through monitoring the expression of this gene in the patients undergoing the different therapeutic treatment alternatives available nowadays.

Regulation of HIF-1 α to Expression of N-myc Downstream Regulated Gene 1 in Colorectal Carcinoma

Plasmid expressing small interfering RNA （siRNA） against HIF-1α （pSilence-2.1-U6-siRNA） was constructed and transfected into LS174T cells in hypoxia condition.After expression of siRNA against HIF-1 α in LS174T cells, expressions of HIF-1 α and N-myc downstream regulated gene 1 （NDRG1） gene were inhibited significantly. HIF-1 cta transcripts were positive in 67.7% （42/62） and 44.4% （8/18） of colorectal adenocarcinoma and adenoma, re- spectively. The mean percentage of cells with positive hybridization of HIF-1 α mRNA increases with the development from Duke stage A to stage C＋D （p〈 0.05）. The positive staining rate of NDRG1 protein was significant higher in than that in colorectal adenoma colorectal adenocarcinoma group group （p〈 0.05）. The level of HIF-1 a transcripts was positively correlated with the level of NDRG1 protein （p 〈 0.05） during colorectal tumor progression. HIF-1α and its down stream gene NDRG1 may play roles in tumor progression of human colorectal carcinoma.

靶向MYC基因抗肿瘤研究进展

MYC是研究最为广泛的原癌基因之一,属于碱性螺旋-环-螺旋亮氨酸拉链(bHLH-Zip)DNA结合蛋白超家族,通过与MAX形成MYC-MAX异二聚体发挥功能。MYC影响蛋白质合成、细胞黏附、增殖、分化、细胞周期、代谢、细胞凋亡和血管形成等多种生物学过程。因其结构与位置的特殊性,难以直接靶向,针对MYC的治疗策略是研究的热点,本文将系统回顾MYC基因的结构、功能和其抑制剂的研究进展,为靶向MYC治疗肿瘤提供新思路。

NFE2L2和MYC基因相对拷贝数在肺癌诊断中的临床价值分析

目的探究肺癌患者NFE2L2和MYC基因相对拷贝数的变化,并初步探讨其对肺癌的诊断价值。方法研究纳入2021年9月~2023年6月在我院住院的36例肺癌患者,采用实时荧光定量PCR方法检测肿瘤组织和邻近非肿瘤组织样本中的NFE2L2和MYC基因相对拷贝数,使用受试者工作特征(ROC)曲线评估诊断性能。结果肿瘤组织样本NFE2L2和MYC基因相对拷贝数高于非肿瘤组织样本,差异有统计学意义(P<0.05)。ROC曲线分析显示,NFE2L2和MYC基因相对拷贝数是较好的肺癌诊断指标(AUC=0.765、0.761)。结论NFE2L2和MYC基因相对拷贝数可能与肺癌的发生有关,对肺癌的诊断具有一定参考价值。

N-MYC及NDRG1在胃癌组织中的表达及对胃癌细胞生物学特性的影响

目的分析N-MYC及N-MYC下游调节基因1(NDRG1)在胃癌组织中的表达及对胃癌细胞生物学特性的影响。方法收集2021年1月至2023年5月于该院行手术切除且经病理确诊为胃癌的82例患者的胃癌组织及癌旁正常组织,采用实时荧光定量PCR(qPCR)检测N-MYC、NDRG1 mRNA相对表达量,收集患者临床资料,分析N-MYC、NDRG1 mRNA表达与患者临床病理特征关系。选择对数生长期NCI-N87细胞,将N-MYC干扰质粒(si-N-MYC)与其阴性对照(si-NC)分别转染到NCI-N87细胞中,记为si-NC组、si-N-MYC组;将si-N-MYC分别与anti-NC、anti-NDRG1共转染至NCI-N87细胞中,记为si-N-MYC+anti-NC组、si-N-MYC+anti-NDRG1组。采用CCK-8实验检测细胞增殖活性,Transwell侵袭实验检测细胞侵袭能力,Western blotting法检测细胞中N-MYC、NDRG1蛋白表达。结果胃癌组织N-MYC mRNA相对表达量高于癌旁组织(P<0.05),NDRG1 mRNA相对表达量低于癌旁组织(P<0.05)。不同胃癌TNM分期、淋巴结转移、远处转移患者N-MYC、NDRG1 mRNA表达差异有统计学意义(P<0.05)。与si-NC组比较,si-N-MYC组细胞增殖和侵袭能力下降(P<0.05),NDRG1蛋白表达下调(P<0.05)。与si-N-MYC+anti-NC组比较,si-N-MYC+anti-NDRG1组细胞增殖、侵袭能力增加(P<0.05)。N-MYC可靶向调控NDRG1,敲低NDRG1可逆转N-MYC对细胞产生的生物学作用。结论胃癌组织N-MYC mRNA表达上调、NDRG1 mRNA表达下调,二者参与胃癌的发生发展过程,并对胃癌细胞增殖、侵袭等恶性生物学行为有重要调控作用。

猫CDH1基因在过表达c-MYC成纤维细胞中的表达变化及生物信息学分析

[目的]试验旨在研究骨髓细胞瘤病毒癌基因同源物(myelocytomatosis viral oncogene homolog, c-MYC)对猫成纤维细胞的影响及其与E-钙黏蛋白(cadherin 1,CDH1)基因表达和分子特性的关系,为将其应用于猫肿瘤疾病防治和组织损伤修复提供依据。[方法]通过组织贴壁法对猫胎儿成纤维细胞进行分离培养,利用电转仪将PB-TRE-c-MYC质粒转染至细胞并观察细胞形态,利用实时荧光定量PCR检测CDH1基因的表达情况,并通过生物信息学软件分析CDH1蛋白的理化性质和结构特征。[结果]过表达c-MYC导致细胞形态发生变化,从间质细胞的长梭型向上皮细胞的鹅卵石状发生转变,且使上皮细胞标志基因CDH1的表达极显著上调(P<0.01)。生物信息学分析显示,猫CDH1蛋白有881个氨基酸,其中含量最多的是亮氨酸,定位于细胞膜,存在4个CA结构域,介导细胞与细胞的接触,属于亲水性的酸性蛋白,主要由无规则卷曲组成,可能存在由Sec易位子转运并被信号肽酶Ⅰ(Sec/SPⅠ)切割的信号肽位点。[结论]猫CDH1基因的表达可被外源性重编程因子c-MYC激活,其编码的钙黏蛋白可促进猫胎儿成纤维细胞的间质-上皮转化,以抑制细胞癌化。

反义c-myc寡核苷酸抑制大鼠气道平滑肌细胞增殖

目的 观察反义 c- myc寡核苷酸对大鼠气道平滑肌增殖的抑制作用 .方法 大鼠气道平滑肌细胞原代培养 ,4～12代用于实验 .利用 L ipofectin将正义、反义及错配 c- myc寡核苷酸导入大鼠气道平滑肌细胞 ,MTT法检测不同寡核苷酸对大鼠气道平滑肌细胞增殖的抑制作用 ,RT- PCR检测 c- mycm RNA的表达 ,免疫组织化学染色检测 c- Myc蛋白的表达 .结果 反义 c- myc寡核苷酸可抑制大鼠气道平滑肌细胞增殖 ,且这种抑制作用呈浓度依赖性 ;反义 c- myc寡核苷酸可降低 c- myc m RNA的表达 ,同时降低了 c- myc m RNA的翻译 .结论 反义 c-

转化生长因子β1对胃癌和多药耐药胃癌细胞增殖及c-myc表达的影响

目的探讨TGF-β1对SNU-601/WT胃癌细胞及SNU-601/cis2多药耐药胃癌细胞增殖及c-myc基因和蛋白表达的影响。方法利用MTT、RT-PCR及Westernblot方法检测细胞生长抑制率、c-mycmRNA及蛋白的表达水平。结果TGF-β1对细胞生长的抑制率在实验组细胞中随着浓度的增加和时间的延长而逐渐增高,与对照组相比,抑制率均显著增高(P<0.01),同时,SNU-601/cis2细胞的生长抑制率与SNU-601/WT细胞相比在48和72h时明显增高(P<0.05或P<0.01),c-mycmRNA和蛋白的表达水平在实验组中随着时间的延长逐渐地下调,与对照组相比显著降低(P<0.01)。结论TGF-β1可呈浓度和时间依赖性抑制SNU-601/WT细胞及SNU-601/cis2细胞增殖,其抑制作用在多药耐药胃癌细胞中更明显,其机制可能与TGF-β1抑制c-myc基因和蛋白的表达有关。

β-连环蛋白在肝门部胆管癌中的表达及其与c-myc表达的关系

目的 探讨 β 连环蛋白异常表达和c myc阳性表达在肝门部胆管癌发生、发展过程中的作用及其机理。方法 应用免疫组织化学SP法对 4 2例肝门部胆管癌及 10例胆管良性病变组织中的 β 连环蛋白和c myc蛋白进行检测 ,并结合临床资料进行分析。结果 β 连环蛋白在 10例胆管良性病变组织中均呈正常表达 ,且c myc均呈阴性表达 ;而在 4 2例胆管癌患者中 30例癌组织细胞胞浆内的 β 连环蛋白的异常表达率明显高于胆管良性病变组织 ,且异常表达率与肝门部胆管癌的淋巴结转移显著相关 (P<0 .0 5 ) ,而与肝门胆管癌大小、分化程度和侵袭状况无关 (P>0 .0 5 )。胆管癌中c myc表达阳性率与肝门胆管癌的大小、侵袭状况及淋巴结转移无关 (P>0 .0 5 ) ,而与肝门部胆管癌的分化程度密切相关 (P<0 .0 5 )。β 连环蛋白异常表达与c myc阳性表达在肝门部胆管癌中呈显著的正相关性 (r =0 .32 4 ,P<0 .0 1)。结论 肝门部胆管癌细胞中存在 β 连环蛋白异常表达和c myc蛋白阳性表达的现象 ,与胆管癌的一些生物学行为密切相关。β 连环蛋白的异常表达可能是肝门部胆管癌转移的分子机理之一。

反义c-myc诱导MCF-7细胞凋亡作用的研究

目的探讨脂质体LipfectAM INETM(LR)介导的c-myc反义寡核苷酸(ASODN)对MCF-7细胞凋亡作用的影响。方法MCF-7细胞经脂质体包裹c-myc反义寡核苷酸作用24、48、72、96小时后,应用Gimsa染色法及流式细胞仪检测MCF-7细胞凋亡情况;DNA琼脂糖凝胶电泳检测MCF-7细胞经反义核酸作用72小时时,MCF-7细胞DNA变化情况。结果经LR介导的ASODN可以诱导MCF-7细胞凋亡,且随着时间的延长,凋亡细胞逐渐增加,24、48、72、96小时及正义组72小时各时间点的凋亡率分别为4.3%、4.6%、13.5%、28.8%、29.1%、4.4%(P<0.01);DNA凝胶电泳显示脂质体反义核酸72小时组有凋亡特征的DNA改变,呈现典型的DNA降解"梯状"条带片断。结论c-myc反义寡核苷酸(ASODN)可以诱导MCF-7细胞凋亡。

P16、Rb、C-myc基因在肾癌中的表达及其与细胞凋亡的关系

目的 探讨P16、Rb、C-myc基因在肾癌中的表达以及肾癌组织中细胞凋亡的发生,了解两者之间的相互关系。方法 采用免疫化学法检测肾癌组织中的P16、Rb、C-myc基因的表达情况,同时用TUNEL法观察肾癌中细胞凋亡现象。结果 在肾癌中.P16总阳性率为61β3％,Rb总阳性率为64.5％,C-myc总阳性率为48.4％,它们的阳性表达与细胞凋亡有机关性。结论 肾癌中P16、Rb,C-myc基因促进肾癌细胞凋亡的发生,在机体抗肿瘤机制中起积极作用。

应用siRNA抑制K562细胞中c-Myc基因的表达

目的利用小分子干扰RNA(siRNA)技术抑制白血病细胞系K562细胞中c鄄Myc基因的表达,为研究c鄄Myc基因在K562细胞中的作用提供一个新的方法。方法设计c鄄Myc基因特异性小分子干扰RNA,用体外转录方法合成c鄄Myc基因的小分子干扰RNA并转染K562细胞,培养48h后,收集细胞,应用实时荧光定量RT鄄PCR和westernblot方法检测转染细胞中c鄄Myc基因mRNA水平和蛋白表达量的变化,四甲基偶氮唑蓝(MTT)法检测细胞增殖活性。结果转染siRNA后,与对照组相比,实验组c鄄MycmRNA水平和蛋白表达量明显降低,抑制率分别为82.16%和74.0%,MTT法表明实验组的增殖速率明显低于对照组的增殖速率。结论在K562细胞中存在RNA干扰的机制,特异性siRNA能够有效的抑制c鄄Myc基因的表达,为研究c鄄Myc基因在肿瘤细胞中的调节途径提供了一个新的方法。

重组反义c-myc腺病毒诱导HL-60细胞分化的作用

目的 研究重组反义c myc腺病毒 (Ad AS c myc)对人急性早幼粒HL 60细胞系的诱导分化作用及分子机制 ,探讨Ad AS c myc用于急性早幼粒白血病基因治疗的可能性。方法 采用重组腺病毒Lac Z(Ad LacZ)及Ad AS c myc联合多聚阳离子转染HL 60细胞 ,X gal染色判断转染效率。采用形态学、MTT试验、RT PCR、流式细胞仪及免疫细胞化学等方法进行研究。结果 多聚阳离子可提高腺病毒对HL 60细胞的转染 ,Ad LacZ +protaminesulfate转染率达 79 8%。Ad AS c myc能抑制HL 60细胞c myc基因在转录及蛋白水平的表达。Ad AS c myc抑制HL 60细胞生长及活力 (抑制率5 1%) ,降低其核浆比例 ,增加其过氧化酶活性 ,引起其G0 G1 阻滞及分化相关基因c fos基因表达增强。结论 Ad AS c myc对HL 60细胞具有抑制生长及诱导分化作用。其生物学作用与HL 60细胞过氧化酶活性及c fos的表达有关。Ad AS c