Antitumor effect of betulinic acid on human acute leukemia K562 cells <Emphasis Type="Italic">in vitro</Emphasis>

The effects of betulinic acid (BA), a pentacyclic lupane-type triterpene, on the cell viability, cell cycle and apoptosis in human leukemia K562 cells were investigated. The effects of BA on the growth of K562 cells were studied by MTT assay. Apoptosis was assayed through Annexin V/propidium iodide (PI) double-labeled cytometry. The effects of BA on the cell cycle of K562 cells were studied by a PI method. The expression of Bax and capase-3 was detected by using Western blot. The results showed that BA was ...     

PTEN基因对慢性粒细胞白血病Survivin、Xiap、Smac调控的研究

目的 探讨肿瘤抑制基因PTEN对人慢性粒细胞白血病(CML)中生存素(Survivin)、X连锁凋亡抑制蛋白(Xiap)、线粒体促凋亡蛋白(Smac)调控的作用.方法(1)将携带有野生型PTEN和绿色荧光蛋白的腺病毒(Ad-PTEN-GFP)及对照载体腺病毒(Ad-GFP)转染人慢性粒细胞白血病细胞系K562,四甲基偶氮唑盐(MTT)检测细胞增殖抑制率;流式细胞仪检测转染效率、细胞周期及凋亡率;荧光定量PCR(FQ-PCR)检测PTEN、Survivin、Xiap、Smac mRNA水平变化,Western印迹检测PTEN蛋白表达水平的变化.(2)研究10例慢性粒细胞白血病慢性期(CML-CP)、10例慢性粒细胞白血病急变期(CML-BC)及10名健康人(NC)骨髓单个核细胞内PTEN、Survivin、Xiap、Smac mRNA表达水平变化.结果 以感染复数(MOI)=200转染K562细胞后,Ad-PTEN-GFP组K562细胞最大增殖抑制率为38.6％,转染3d后Ad-PTEN-GFP组K562细胞内Survivin、Xiap、Smac mRNA表达水平(0.0700±0.0059、0.0089±0.0006、0.0600±0.0039)均明显低于Ad-GPF组(0.4370±0.0790、0.0661±0.0072、0.1580±0.0078)和未转染组(0.4530±0.0810、0.0700±0.0079、0.1770±0.0085),转染Ad-PTEN-GFP组与转染Ad-GFP相比Survivin mRNA表达水平降低6.14倍、Xiap降低7.44倍,而Smac mRNA降低2.95倍(均P＜0.01).CML-BC患者中PTEN mRNA表达水平低于CML-CP及健康对照组,而Survivin、Xiap、Smac mRNA在CML-BC患者中均高于CML-CP及健康对照组(均P＜0.01).结论 Survivin、Xiap、Smac基因可能在PTEN介导的慢性粒细胞白血病细胞凋亡通路中参与抑制细胞增殖、促进细胞凋亡的作用.     

Anti-cancer Effects of Deguelin on Human Leukemia K562 and K562/ADM Cells In Vitro

In order to investigate the anti-cancer effects of deguelin and on K562 and K562/ADM cells in vitro and the underlying molecular mechanism and compare the cytotoxicity of deguelin on K562, K562/ADM cells and human peripheral blood mononuclear cells (PBMCs). The effects of de- guelin on cell proliferation were assessed by MTT assay. Apoptosis were detected by AnnexinⅤ/PI double-labeled cytometry. The effects of deguelin on the cell cycle were studied by a propidium io- dide method. Our study showed that deguelin inhibited the proliferation of K562 cell and K562/ADM cell in a time- and dose-dependent manner and had minimal effects on normal human peripheral blood mononuclear cells. The ratio of IC50 value of deguelin of 24 h on K562/ADM cells to K562 cells was only 1.27, which was significantly lower than the ratio of IC50 value of ADM (higher than 20). Deguelin could induce apoptosis of K562 cells and K562/ADM cells. K562 cells were arrested at G2/M phase while K562/ADM cells were arrested at G0/G1 phase. Our results suggested that deguelin was a novel anti-leukemia agents with high efficacy and low toxicity and it is also a promising agent for reversing drug resistance.     

As2O3诱导NB4、HL-60细胞凋亡的机制研究

目的探讨三氧化二砷(As₂O₃)在体外抑制急性早幼粒白血病(acute promyelocyticleukemia, APL)细胞NB4、HL-60细胞增殖,诱导细胞凋亡的分子机制。方法 通过WST-8法检测上述两个细胞株的增殖抑制曲线;用AnnexinV/PI流式细胞术检测细胞的凋亡;用Real time PCR检测凋亡相关基因Caspase-3、Caspase-8、Caspase-9、Bcl-2、Bax、p53、C-myc、Survivin在As₂O₃处理前后的表达变化,同时用Westernblot检测凋亡相关蛋白Caspase-3、Caspase-8、Caspase-9、Bcl-2、Bax、P53在As₂O₃处理前后的表达变化。结果 As₂O₃能够显著抑制两种细胞增殖, Westernblot检测及Realtime PCR结果显示,As₂O₃处理引起了两种细胞中Bax、Caspase-3、Caspase-8 、Caspase-9基因表达水平增加,且蛋白表达水平上都出现了活性形式的Caspases。NB4细胞中Survivin、C-myc、Bcl-2的基因表达水平都显著降低,突变型p53蛋白在细胞内的量同样显著下降;HL-60细胞的C-myc表达水平显著降低,但Survivin、Bcl-2表达水平无明显变化。结论 As₂O₃能在药物临床浓度范围内有效抑制急性早幼粒白血病细胞HL-60、NB4的细胞增殖, 但方式不同;1.5μmol/L浓度的As₂O₃对NB4细胞生长的抑制体现在诱导细胞分化并诱导细胞凋亡,对HL-60细胞生长的抑制只体现在诱导细胞分化。HL-60细胞中高表达的Survivin、Bcl-2抑制了细胞的凋亡。NB4、HL-60细胞株中P53基因的细胞遗传学变异的不同可能是As₂O₃对这两种细胞增殖抑制机制差异的主要原因之一。     

不同血液肿瘤细胞株survivin基因和蛋白表达及意义的研究

目的：研究survivin在不同血液肿瘤细胞株(Jurkat, Raji, EL 4, K562, K562/AO2)的表达，并探讨其与相关因素的关系。方法：应用RT PCR技术检测survivin mRNA在各细胞株的表达，用免疫组化法检测survivin 蛋白的表达，流式细胞仪检测细胞周期。结果：survivin mRNA在4种人源性细胞株(Jurkat, Raji, K562, K562/AO2)中均有表达，耐药株K562/AO2高于其他细胞株；免疫组化结果显示survivin蛋白在胞核与胞浆均有表达，且表达水平与mRNA水平一致；细胞周期结果显示，survivin表达较高的细胞株G2/M期细胞比例和增殖指数较高。结论：survivin基因在血液肿瘤细胞株中普遍表达，survivin 高表达可能与肿瘤细胞增殖及耐药有关。     

Effect of Ad-p16 combined with CDDP or As<Subscript>2</Subscript>O<Subscript>3</Subscript> on human bladder cancer cells

Summary To evaluate the therapeutic efficiency of combined use of p16-expressing adenovirus and chemotherapeutic agents CDDP or As₂O₃ on human bladder cancer cell line EJ, the human bladder cancer cell line EJ were transfected with adenovirus-mediated p16 gene (Ad-p16), with administration of cisplatin (CDDP) or arsenic trioxide (As₂O₃). The cell growth, morphological changes, cell cycle, apoptosis and molecular changes were measured using cell counting, reverse microscopy, flow cytometry, cloning formation, immunocytochemical assays andin vivo therapy experiments to evaluate the therapeutic efficacy of such combined regimen. Ad-p16 transfer and CDDP or As₂O₃ administration to EJ cells could exert substantially stronger therapeutic effects than the single agent treatment. Especially inin vivo experiments, combined administration of p16 and CDDP or As₂O₃ induced almost tumor diminish compared to the partial tumor diminish induced by single agent. Moreover, delivery of Ad-p16, or administration of minimal-dose CDDP or As₂O₃ or combined regimen could induce massive apoptosis of EJ cell. Cell cycle analysis demonstrated that administration of CDDP or As₂O₃ remarkably arrested EJ cell in G₁ prior to apoptotic cell death. When treated with combined regimen, cells were arrested in G₁ to a greater extent prior to apoptotic cell death. It is concluded that after introduction into EJ cell, Ad-p16 shows enhanced therapeutic efficacy for EJ cell when used in combination with CDDP or As₂O₃. ZHU Zhaohui, male, born in 1968, Doctor in Charge The project was supported by the grants from Project 863 (No. Z20-01-02).     

小分子酪氨酸激酶抑制剂AG-490对人慢性髓系白血病急变细胞株K562细胞增殖凋亡的影响

目的探讨酪氨酸激酶抑制剂AG-490对人慢性髓系白血病急变细胞株K562细胞的增殖及凋亡的影响。方法采用MTT法观察AG-490在体外对人慢性髓系白血病急变细胞株K562细胞增殖的影响,光学显微镜下观察AG-490对K562细胞形态的变化,流式细胞术检测AG-490对K562细胞凋亡及细胞周期的影响,逆转录-聚合酶链反应（RT-PCR）及实时荧光定量PCR技术检测AG-490作用后K562细胞bcr/abl融合基因及凋亡相关基因c-myc mRNA的表达水平。结果 AG-490可明显抑制K562细胞的增殖,并随药物作用时间的延长和浓度的增加,抑制作用越明显（P〈0.05）;AG-490可使细胞周期阻滞于G1期,促使其凋亡（P〈0.05）。AG-490作用于K562细胞48 h后bcr/abl融合基因的表达无明显改变（P〉0.05）,而c-myc的表达水平明显降低（P〈0.05）。结论 AG-490可能通过阻断JAK2信号通路而下调c-myc的表达,使K562细胞阻滞于G1期,从而抑制K562细胞增殖,促使其凋亡。     

Effect of Gambogic acid on the regulation of hERG channel in K562 cells <Emphasis Type="Italic">in vitro</Emphasis>

Overexpression of human ether-h-go-go （eag） related gene （bERG） has been found in a broad range of human leukemia cell lines and primary human leukemia. The block of hERG protein might be a potential therapeutic strategy for leukemia. Gambogic acid （GA） has recently exhibited marked anti-tumor potency on solid tumors of various derivations. Here, we investigated the anti-leukemia effects of GA and its relation to the regulation of hERG in K562 leukemia cells in vitro. K562 cells were treated with various concentrations of GA （0.125-8.0 μmol/L） for 0-72 h. MTT assay was used to evaluate the inhibition effect of GA on the growth of K562 cells. Cell apoptosis was measured through both Annexin-V FITC/PI double-labeled cytometry and transmission electron microscopy. Cell cycle regulation was studied by a propidium iodide method. RT-PCR and Western blot were applied to detect the expression level of hERG in K562 cells. GA presented striking growth inhibition and apoptosis induction potency on K562 ceils in vitro in a time- and dose-dependent manner. The IC50 value of GA for 24 h was 2.637±0.208 μmol/L. Moreover, GA induced K562 cells arrested in G0/G1 phase, accordingly, cells in S phase decreased gradually, and no obvious changes were found in G2/M phase cells. Under the transmission electron microscopy, apoptotic bodies containing nuclear fragments were found in GA-treated K562 cells. After treatment with GA of 2.0 μmol/L for 24 h, the percentage of apoptotic cells was increased from 4.09% to 18.47% （P〈0.01）. Overexpression of hERG channel was found in K562 cells, while GA could down-regulate it at both protein and mRNA levels （P〈0.01）. It was concluded that GA exhibited its anti-leukemia effects partially through down-regulating the expression level of hERG channel in K562 cells, suggesting that GA may be a potential agent against leukemia with a mechanism of blocking hERG channel.     

TBB对乳腺癌细胞miR-411表达及细胞凋亡的影响

目的 观察TBB作用下乳腺癌细胞中miR-411的表达,研究过表达miR-411对乳腺癌细胞凋亡和细胞周期改变的影响。方法 Real-time PCR验证生物芯片检测的差异miRNAs,流式细胞术分析转染前后细胞周期及细胞凋亡情况,针对miR-411进行下游靶基因预测,以real-time PCR验证预测结果。结果 TBB作用下MCF-7细胞株中miR-411显著升高;与对照组相比,转染组早期凋亡细胞比例升高;FoxO1 mRNA表达含量显著增高。结论TBB能够改变乳腺癌MCF-7细胞株中miR-411的表达,过表达miR-411能够抑制乳腺癌细胞株的凋亡,其机制可能与通过影响FoxO1表达有关。     

虫草素对人骨肉瘤MG-63细胞凋亡的影响及其机制研究

目的 研究虫草素对人骨肉瘤MG-63细胞凋亡的影响及其机制。方法 采用CCK-8实验检测不同浓度虫草素作用于MG-63骨肉瘤细胞24h和48h后对癌细胞增殖的抑制作用;采用流式细胞术分析虫草素对MG-63细胞周期分布及凋亡的影响;采用Western blot法检测虫草素对MG-63细胞凋亡相关蛋白Bax、Bcl-2、cleaved caspase-9、cleaved caspase-3及NICD1、Hes1蛋白表达的影响。结果 虫草素对人骨肉瘤MG-63细胞有明显的增殖抑制作用,导致MG-63细胞周期阻滞于G₀/G₁期并诱导细胞凋亡;虫草素可上调Bax、cleaved caspase-9和cleaved caspase-3蛋白的表达并下调Bcl-2,NICD1和Hes1蛋白的表达。结论 虫草素通过抑制骨肉瘤细胞增殖,诱导细胞周期阻滞于G₀/G₁期并通过线粒体凋亡途径诱导MG-63细胞凋亡从而发挥抗骨肉瘤作用,可能骨肉瘤细胞中Notch信号通路活性下调有关。     

三丁酸甘油酯对K562 白血病细胞的体外作用

目的观察组蛋白去乙酰化酶抑制剂三丁酸甘油酯(tributyrin，TB)对K562白血病细胞增殖、凋亡的影响，并进一步探讨其作用机制。方法用细胞计数及台盼兰拒染法观察TB对K562细胞增殖及活力的影响，通过细胞形态观察、流式细胞术分析观察TB对K562细胞体外诱导凋亡的情况，RT—PCR技术分析p2l^WAFl表达的改变。结果(1)TB抑制：K562细胞的增殖。(2)TB诱导K562白血病细胞的凋亡，影响细胞周期的进程，使细胞周期阻滞于G2／M期。(3)在TB引起的K562细胞增殖抑制及凋亡过程中，p2l^WAFl表达增加。结论TB抑制K562白血病细胞的增殖并诱导凋亡，阻滞细胞周期进程于G2／M期，p2l^WAFl在此过程中发挥作用。     

Effect of artesunate on human endometrial carcinoma HEC-1B cells

Objective： To observe the effect of the artesunate （ART） on cellular proliferation in vitro, to search for the possible anti-tumor mechanism of ART on endometrial carcinoma at the molecular level and to provide the experimental and theoretical foundations for the clinical applications of ART. Methods： The cell proliferation was observed by microscope; MTT was used to examine the effects of ART on proliferation of HEC-1B cells, and flow cytometric analysis was used to detect cell cycle and apoptosis. The human endometrial carcinoma HEC-1B cells were conventionally cultured; ART was administered with a concentration of 40 μg/ml before the total RNA were extracted, mRNA expression of Survivin, Caspase-3, N-Cadherin, E-Cadherin, Fibronectinl and Cox-2 were detected using RT-PCR. Results： ART reduced proliferation in human endometrial carcinoma cell line HEC-1B in a dose- and time-dependent effect. The cells of G0/G1 stage were significantly increased （P〈0.05）, but the cells of G2/M stages were significantly decreased （P〈0.05）, so it has shown that the cell cycle was probably blocked in G0/G1 stage. After intervention with ART at 20 and 80 μg/ml for 48 h, cellular apoptosis rate respectively was （36.42±0.77）% and （11.77±0.58）%, and the difference was statistically significant compared with the control （[6.64±0.191%, P〈0.01）. The expression of Cox-2 mRNA in the ART group was lower than those of control group, yet the expression of Caspase-3 and E-Cadherin mRNA in the ART group was higher than those of control group. Conclusion： ART can inhibit HEC-1B cell growth and proliferation in a dose- and time-dependent manner. Furthermore, ART can induce apoptosis in a dose-dependent manner. ART is able to downregulate Cox-2 mRNA expression and to upregulate E-Cadherin and Caspase-3 mRNA expression. So we can conclude that ART could induce the endometrial carcinoma HEC-1B cell apoptosis and inhibit tumor cell proliferation.     

新型靶向组蛋白去乙酰化酶抑制剂的抗肿瘤作用及其机制

探讨3种新型靶向组蛋白去乙酰化酶(HDAC)抑制剂D16,D22,D29的抗肿瘤活性作用及其抑制人宫颈癌细胞增殖的机制。MTT法检测D16,D22,D29对MCF-7、HCT-116、A549、HeLa以及K562的增殖抑制作用;测定D16,D22,D29对HDAC及其HDAC-1的酶活抑制作用;流式细胞术观察D16,D22,D29对HeLa细胞周期及凋亡诱导作用;Western blot测定D16,D22,D29对HeLa细胞中乙酰化组蛋白H3(Ac-H3),p21^cip/WAF的蛋白表达影响。结果显示,D16,D22,D29明显抑制多种肿瘤细胞株的增殖,有效抑制HDAC及其HDAC-1的活性,其效果优于阳性对照药Vorinostat(SAHA),并诱导HeLa细胞产生G₁期细胞周期阻滞及凋亡,Ac-H3及p21^cip/WAF的蛋白水平明显上升。D16,D22,D29具有一定的抗肿瘤活性,其机制与诱导细胞周期阻滞和凋亡产生,促进p21^cip/WAF的蛋白表达有关。     

澳洲茄胺诱导肠癌HCT-116细胞凋亡的实验研究

目的?通过研究中药灌肠方中的有效成分澳洲茄胺对肠癌HCT-116细胞凋亡及相关基因表达的影响,探讨澳洲茄胺抑制肠癌细胞增殖的作用机制。方法?通过实时无标记细胞分析仪检测澳洲茄胺对HCT-116细胞增殖的影响;流式细胞仪检测HCT-116细胞凋亡;qPCR法检测凋亡相关基因Bax、Survivin的mRNA表达水平;Western blot实验检测凋亡相关蛋白Bcl-2、Bax、Bcl-xl、Caspase-3、Caspase-8、Caspase-9、PARP以及PI3K/Akt信号通路蛋白PI3K、Akt表达情况。结果?实时无标记细胞分析检测法证实澳洲茄胺对肠癌HCT-116细胞的生长有抑制作用,且随药物浓度、给药时间的增加而增强;流式检测发现随药物浓度的增加,其凋亡增多;qPCR法证实澳洲茄胺能上调Bax、下调Survivin的mRNA表达;Western blot法检测证实澳洲茄胺上调Bax蛋白,促进Caspase-3、Caspase-8、Caspase-9、PARP蛋白活化,下调Bcl-2、Bcl-xl蛋白表达,升高Bax/Bcl-2表达比值,并且抑制PI3K、Akt蛋白活化。结论?澳洲茄胺抑制肠癌HCT-116细胞增殖,通过抑制PI3K/Akt信号通路及调控Caspase家族、Bcl-2家族、Survivin、PARP的表达,诱导细胞凋亡,对凋亡的2条途径均有作用,即线粒体途径和死亡受体途径。      

汉防己甲素对人神经母细胞瘤SH-SY5Y增殖和凋亡的影响

目的 探讨汉防己甲素对神经母细胞瘤SH-SY5Y细胞株的增殖抑制和诱导凋亡的作用。方法 通过CCK-8实验检测汉防己甲素对于细胞生长的抑制率,流式细胞术检测Tet作用于细胞后,对细胞活性氧、线粒体膜电位、凋亡和周期的影响。结果 汉防己甲素能显著抑制SH-SY5Y细胞生长,基本呈时间－剂量依赖性。流式细胞术检测显示不同浓度汉防己甲素处理后,活性氧明显升高,线粒体膜电位明显下降,细胞凋亡比例明显升高,G₀/G₁期细胞占比明显增高。结论 汉防己甲素能够抑制SH-SY5Y细胞增殖并且诱导其发生凋亡。     

Survivin反义寡核苷酸诱导肺癌细胞株凋亡的研究

目的: 探讨生存素(Survivin)的反义寡核苷酸(A SO DN)对肺癌细胞株的作用。方法: 在脂质体介导下,分别以100 nmol/L、300 nmol/L和500 nmol/L的Survivin A SO DN作用于小细胞肺癌细胞株NCI-H446和肺腺癌细胞株SPC-A1,于24 h、48 h、72 h用逆转录聚合酶链反应(RT-P CR)检测Survivin mRNA表达,Western blot检测Survivin蛋白,流式细胞仪检测凋亡。结果: NCI-H446和SPC-A1皆表达Survivin基因和蛋白。随着ASODN浓度增加,Survivin mRNA明显下调,其差异有显著性,其中ASODN 500 nmol/L作用72 h时两种细胞Survivin mRNA抑制率分别达62.72%和67.43%;Survivin蛋白表达也有类似的变化;ASODN对两种细胞生长抑制和诱导凋亡作用随浓度增大和作用时间延长而增强。结论: Survivin ASODN能够抑制肺癌细胞株Survivin基因和蛋白表达,呈时间、浓度依赖性,诱导凋亡的效果也呈剂量、时间依赖性,500 nmol/L的浓度作用72 h效果最佳。     

胃祺饮乙醇提取物可诱导AGS细胞G2/M 期阻滞及凋亡

Objective:To evaluate the effects of the ethanol extract isolated from Weiqi Decoction(胃祺饮,WQD-EE)on AGS cell proliferation and apoptosis.Methods:By using high-performance liquid chromatography with ultraviolet detectors(HPLC-UV)assay and MTT method,the main compounds in WQD-EE and cell viability were detected.And cell cycle distributions were determined by flow cytometry with propidium iodine(PI)staining while apoptosis was detected by flow cytometry with annexin V/Pl double staining.Finally,caspase-3 activities were measured by calorimetric method and protein expression was determined by Western blotting.Results:HPLC analysis showed that naringin(35.92μg/mg),nobiletin(21.98μg/mg),neohesperidin(17.98μg/mg)and tangeretin(0.756μg/mg)may be the main compounds in WQD-EE.WQD-EE not only inhibited AGS and MCF7 cell proliferation in a dose-dependent manner,but also blocked cell cycle progression at G_2/M stage as well as inducing cell apoptosis at concentrations triggering significant inhibition of proliferation and cell cycle arrest in AGS cells.While at 0.5 mg/mL,WQD-EE significantly increased caspase-3 activity by 2.75 and 7.47 times at 24 h and 48 h,respectively.Moreover,WQD-EE in one hand reduced protein expressions of p53 and cyclin B1,and in other hand enhanced protein expressions of cytochrome c and Bax.Protein levels of Bcl-2,Fas L and Fas were not significantly affected by WQD-EE.Conclusions:WQD-EE inhibits AGS cell proliferation through G_2/M arrest due to down-regulation of cyclin Bi protein expression,and promotes apoptosis by caspase-3 and mitochondria-dependent pathways,but not by p53-dependent pathway.     

辛伐他汀依赖p53通路对K562细胞G1期调节的分子机制

目的探讨辛伐他汀体外处理后的K562细胞p53通路和K562细胞G1期的分子水平的变化,以说明辛伐他汀是否依赖p53通路参与K562细胞细胞周期G0／G1期停滞的调控和抑制K562细胞增殖。方法体外培养和用辛伐他汀处理K562细胞,用流式细胞术检测辛伐他汀作用后细胞周期和凋亡率的变化,用RT-PCR检测K562细胞p53通路和细胞周期G1期相关基因表达的变化。结果辛伐他汀能使K562细胞停滞在G1／G0期,明显诱导K562细胞凋亡,大多数p53通路基因和细胞周期相关基因的变化出现差异表达。结论辛伐他汀可能通过作用于参与细胞增殖和凋亡的p53通路,抑制K562细胞增殖并诱导细胞凋亡。     

miR-370-5p对前列腺癌细胞周期及增殖的影响

目的 研究miR-370-5p导入对前列腺癌细胞株DU-145和LNCaP细胞周期和增殖的影响。方法 合成miR-370-5p（实验组）和dsControl（阴性对照组）,分别转染至两个细胞株。利用Real-time PCR和Western blot法分别检测细胞转染后p21、CDK4、Cyclin D1 mRNA和蛋白的表达变化。流式细胞术分析细胞周期变化,利用MTT法和集落形成实验分析细胞活力和增殖能力。结果 Real-time PCR结果提示,转染miR-370-5p后DU-145和LNCaP细胞中p21 mRNA水平分别上调3.43倍（P<0.01）和3.06倍（P<0.01）,CDK4 mRNA水平分别下调0.51倍（P<0.01）和0.43倍（P<0.01）,Cyclin D1 mRNA水平分别下调0.31倍（P<0.01）和0.35倍（P<0.01）。Western blot法检测结果符合这一趋势。流式细胞术检测结果显示,转染miR-370-5p后,位于S期和G₂/M期的细胞比例下降,位于G₀/G₁期的细胞比例则上升,说明细胞周期被阻滞在G₀/G₁期。MTT分析结果显示,与dsControl组相比,转染miR-370-5p后,DU-145和LNCaP细胞活力明显降低。集落形成实验显示,miR-370-5p组的集落数数量明显较少,细胞增殖能力降低。结论 miR-370-5p能显著激活前列腺癌细胞中p21蛋白的表达,抑制前列腺癌细胞周期的进展和增殖。