Manganese antagonizes iron blocking mitochondrial aconitase expression in human prostate carcinoma cells

Aim： To investigate the possible role of manganese in the regulation of mitochondrial aconitase （mACON） activity human prostate carcinoma cell line PC-3 cells. Methods： The mACON enzymatic activities of human prostate carcinoma cell line PC-3 cells were determined using a reduced nicotinamide adenine dinucleotide-coupled assay. Immunoblot and transient gene expression assays were used to study gene expression of the mACON. The putative response element for gene expression was identified using reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays. Results： In vitro study revealed that manganese chloride （MnCI2） treatment for 16 h inhibited the enzymatic activity of mACON, which induced the inhibition of citrate utility and cell proliferation of PC- 3 cells. Although results from transient gene expression assays showed that MnCI2 treatment upregulated gene translation by approximately 5-fold through the iron response element pathway, immunoblot and reporter assays showed that MnCl2 treatments inhibited protein and gene expression of mACON. This effect was reversed by cotreatment with ferric ammonium citrate. Additional reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays suggested that a putative metal response element in the promoter of the mACON gene was involved in the regulation of MnCh on the gene expression of mACON. Conclusion： These findings suggest that manganese acts as an antagonist of iron, disrupting the enzymatic activity and gene expression of mACON and citrate metabolism in the prostate.

Inhibitory effect of a new gossypol derivative apogossypolone (ApoG2) on xenograft of human prostate cancer cell line PC-3

Objective: To investigate the inhibitory effect of apogossypolone (ApoG2) on prostate cancer cell line PC-3 in vivo, and explore its mechanism. Methods: The models of transplantation tumors in Balb/c nu/nu mice were established via subcutaneous injection of PC-3 cells and the tumor-transplanted mice were divided into 4 groups: control group and three ApoG2 treatment groups, with 10 mice in each group. Volumes of the tumor were estimated every 2 d and the morphology of tumor tissues was observed. Immunohistochemistry was employed to observe the expression of Bcl-2, PCNA, CD31, caspase-3 and caspase-8 in tumor tissues. Results: ApoG2 (2.5 mg/kg-10 mg/kg) given intraperitoneally once a day can obviously inhibit the growth of subcutaneous prostatic carcinoma implant. The tumor volume decreased obviously when the treatment dosage was bigger than 5.0 mg/kg (P<0.01). Meanwhile, ApoG2 decreased the expression of PCNA and CD31, and enhanced the expression of caspases-3, caspase-8 in tumor tissues. Conclusion: ApoG2 exert an inhibitory effect on prostatic carcinoma possibly by inducing apoptosis and inhibiting tumor angiogenesis.

The multikinase inhibitor sorafenib induces caspase-dependent apoptosis in PC-3 prostate cancer cells

The present study investigated the effects of the multikinase inhibitor sorafenib on androgen-independent can- cer cells viability and intracellular signaling. Human androgen-independent PC-3 prostate cancer cells were treated with sorafenib. At concentration that suppresses extracellular signal-regulated kinase phosphorylation, sorafenib treatment reduced the mitochondrial transmembrane potential. Sorafenib also down-modulated the levels of mye- loid cell leukemia 1, survivin and cellular inhibitor of apoptosis protein 2. Sorafenib induced caspase-3 cleavage and the mitochondrial release of cytochrome c. However, no nuclear translocation of apoptosis inducing factor was detected after treatment and the pan-caspase inhibitor Z-VAD-FMK had an obvious protective effect against the drug. In conclusion, sorafenib induces apoptosis through a caspase-dependent mechanism with down-regulated antiapoptotic proteins in androgen-independent prostate cancer cells in vitro.

The effect of interleukin 6 on the growth of LNCaP and PC-3 prostatic carcinoma cells

Objective To investigate the effect of IL-6 on prostatic carcinoma cell lines, and differential effects on androgen-dependent and androgen-independent prostatic carcinoma cells. Methods The IL-6 producing capacities of LNCaP and PC-3 cells were determined, and effects of exogenous IL-6 and anti-IL - 6 antibodies on LNCaP and PC - 3 cells were examined. Results LNCaP produced a very small amount of IL-6, but PC-3 produced more, the concentraion of IL-6 being 190 pg/48 h per ml(1 × 106). The exogenous IL-6 inhibited LNCaP growth significantly,but had no obvious effect on PC -3 cells. Anti-IL-6 antibodies lowered PC-3 cells growth rate but had neutral effect on LNCaP. Conclusion PC-3 cells produces IL-6 massively in autocrine manner. IL-6 could be antagonized by anti-IL-6 antibodies,resulting in slowing PC-3 cells growth, and LNCaP cells growth could be inhibited by exogenous IL-6.7 refs,2 tabs.

Manganese antagonizes iron blocking mitochondrial aconitase expression in human prostate carcinoma cells

Aim:To investigate the possible role of manganese in the regulation of mitochondrial aconitase(mACON)activity human prostate carcinoma cell line PC-3 cells.Methods:The mACON enzymatic activities of human prostate carcinoma cell line PC-3 cells were determined using a reduced nicotinamide adenine dmucleotide-coupled assay. Immunoblot and transient gene expression assays were used to study gene expression of the mACON.The putative response element for gene expression was identified using reporter assays with site-directed mutagenesis and electro- phoretic mobility-shift assays.Results:In vitro study revealed that manganese chloride(MnCl2)treatment for 16h inhibited the enzymatic activity of mACON,which induced the inhibition of citrate utility and cell proliferation of PC- 3 cells.Although results from transient gene expression assays showed that MnCl_2,treatment upregulated gene translation by approximately 5-fold through the iron response element pathway,immunoblot and reporter assays showed that MnCl_2 treatments inhibited protein and gene expression of mACON.This effect was reversed by co- treatment with fenic ammonium citrate.Additional reporter assays with site-directed mutagenesis and electrophoretic mobility-shift assays suggested that a putative metal response element in the promoter of the mACON gene was involved in the regulation of MnCl_2 on the gene expression of mACON.Conclusion:These findings suggest that manganese acts as an antagonist of iron,disrupting the enzymatic activity and gene expression of mACON and citrate metabolism in the prostate.

The Effect of MMP-9 Inhibitors on the Biological Behavior of Human Oral Squamous Cell Carcinoma SCC15 Cell Line Through PI3K/Akt Signaling Pathway

Objective:To investigate the effect of MMP-9 inhibitor(Mki67)on the biology of human oral squamous cell carcinoma SCC15 cell line and to explore its mechanism of action through PI3K/Akt signaling pathway.Methods:SCC15 cells were extracted,and the supernatant was discarded.The cells were then rinsed twice with PBS,and 0,2.5,5,and 10μL of Mki67(50 mg/mL)were added to the culture respectively.The inhibition rate of cell proliferation was detected by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide(MTT)method,and the cell migration was measured by Transwell chamber test.The cell apoptosis rate was detected by cytometry,and the p-Akt protein content in the cells of each group was determined by a double-antibody sandwich enzyme-linked immunosorbent assay(ELISA)kit.Results:The cell proliferation rates of the 2.5μL,5μL,and 10μL dose groups were all lower than the 0μL group(P<0.05)before treatment,and the cell proliferation rates in the 2.5μL,5μL,and 10μL dose groups decreased overtime(P<0.05).After 24 h,with the increase of Mki67 concentration,the number of migration and invasion gradually decreased(P<0.05),and the number of apoptosis gradually increased(P<0.05);besides,the relative expression of MMP-9,PI3K,and Akt mRNA decreased gradually(P<0.05),and the expression level of Akt mRNA was not statistically significant(P>0.05).Conclusion:MMP-9 inhibitor(Mki67)can inhibit the proliferation and migration of SCC15 cell line and induce apoptosis,and its mechanism of action may be related to the inhibition of PI3K/Akt signaling pathway.

Tumor Necrosis Factor-related Apoptosis Ligand Induces Apoptosis in Prostate Cancer PC-3M Cell Line

Summary： To study the effect of tumor necrosis factor-related apoptosis inducing ligand （TRAIL） on PC-3M cell line, PC-3M cell line was incubated with gradient concentrations of TRAIL for 4-24 h. Annixin-V fluorescence staining and TUNEL method were employed to detect the apoptosis of PC-3M cells. The morphology of apoptotic PC-3M cells was observed by electron microscopy. The relationship between TRAIL concentrations and the percentage of apoptotic cells was evaluated by flow cytometry. The proliferation inhibitory ratio was calculated by using MTT colorimetry. Our results showed that apoptosis of PC-3M cells could be induced by treatment with TRAIL for at most 4 h. The results of flow cytometry and MTT colorimetry demonstrated a time-and concentration-dependent relationship between cell apoptosis rate and TRAIL concentration. It is concluded that apoptosis of PC-3M cells can be induced by TRAIL. Because of the selective killing effect of TRAIL on tumor cells, it may become a potential alternative for the treatment of advanced prostate cancer.

Inhibitory effects of apogossypolone on subcutaneous implants of human LNCaP prostatic carcinoma cells

Objective:The aim of this study was to investigate the inhibitory effect of apogossypolone (ApoG2) on subcutaneous implants of human LNCaP prostatic carcinoma cells, and explore its mechanism. Methods:To establish human LNCaP prostatic carcinoma cell line subcutaneous xenograft models and observe the inhibitory effect of ApoG2 on the tumor model. Immunohistochemistry was employed to observe the expression of Bcl-2, PCNA, CD31, caspase-3 and-8 in tumor tissues. The microvessel density was calculated. Results:ApoG2 could obviously inhibit the growth of subcutaneous prostatic carcinoma implant. ApoG2 decreased the expression of PCNA and CD31, and increased the expression of caspases-3,-8 in tumor tissues. Conclusion:ApoG2 has an inhibitory effect on prostatic carcinoma implants.

Effect of hypoxia-inducible factor-1α on proliferation and invasion of prostate cancer PC-3 cell in hypoxic situation

Objective We transfected recombinant expression plasmid of pcDNA3. 1-HIF-1α into prostate cancer cells, to research effect of HIF-1α on proliferation of prostate cancer cell PC-3. Methods We selected a stable expression cell line with G418 we selected by transfection

DAPT Enhances the Apoptosis of Human Tongue Carcinoma Cells

Aim To investigate the effect of DAPT （γ-secretase inhibitor） on the growth of human tongue carcinoma cells and to determine the molecular mechanism to enable the potential application of DAPT to the treatment of tongue carcinoma. Methodology Human tongue carcinoma Tca8113 cells were cultured with DAPT. Cell growth was determined using Indigotic Reduction method. The cell cycle and apoptosis were analyzed by flow cytometry. Real-time PCR and Immuno-Fluorescence （IF） were employed to determine the intracellular expression levels. Results DAPT inhibited the growth of human tongue carcinoma Tca8113 cells by inducing G0-G1 cell cycle arrest and apoptosis, The mRNA levels of Hairy/Enhancer of Split-1 （Hes-1）, a target of Notch activation, were reduced by DAPT in a dose-dependent manner. Coincident with this observation, DAPT induced a dose-dependent promotion of constitutive Caspase-3 in Tca8113 cells. Conclusion DAPT may have a therapeutic value for human tongue carcinoma. Moreover, the effects of DAPT in tumor inhibition may arise partly via the modulation of Notch- 1 and Caspase-3.

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.

PTCSC3对谷氨酸诱导SH-SY5Y神经细胞凋亡的影响

目的探讨乳头状甲状腺癌易感性候选基因3(papillary thyroid carcinoma susceptibility candidate 3,PTCSC3)对谷氨酸(glutamicacid,Glu)诱导人神经母细胞瘤细胞(SH-SY5Y)凋亡的影响及其机制。方法体外培养SH-SY5Y细胞,谷氨酸损伤SH-SY5Y细胞24 h,转染技术对PTCSC3进行抑制及过表达,采用Hoechst 33258染色法、流式细胞技术、AO/EB染色及四甲基偶氮唑盐比色(methylthiazolyl tetrazolium,MTT)法检测抑制或过表达PTCSC3后对各组细胞凋亡、生存的影响;实时荧光定量PCR(quantitative real-time PCR,qPCR)技术检测各组细胞中PTCSC3、CCAAT/增强子结合蛋白β(CAAT/enhancer binding protein beta,C/EBP-β)及Cbp/p300结合转化激活因子4(Cbp/p300 interacting transactivator with Glu/Asp rich carboxy-terminal domain 4,CITED4)的基因表达情况;Western blot检测各组细胞中C/EBP-β、脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)、蛋白激酶B(protein kinase B,Akt)、B淋巴细胞瘤-2(B-cell lymphoma-2,Bcl-2)、Bcl-2相关X蛋白(Bcl-2 associated X protein,Bax)及CITED4、细胞周期蛋白D1(Cyclin D1)、原癌基因n-Myc的蛋白表达水平。结果2000μmol·L^(-1)Glu处理24 h对PTCSC3细胞有明显的损伤作用;与模型组比较,PTCSC3抑制剂可有效改善Glu诱导SH-SY5Y细胞凋亡率的增加和细胞存活率的下降;明显降低C/EBP-β基因及蛋白、Bax蛋白的表达,促进BDNF、p-Akt、Bcl-2蛋白的表达;增加CITED4、Cyclin D1和n-Myc的表达水平。反之,过表达PTCSC3则出现与上述结果相反的结果。结论PTCSC3可能通过调控C/EBP-β,进而调控下游信号通路BDNF/Akt和CITED4/Cyclin D1信号通路,改善Glu诱导SH-SY5Y神经细胞的凋亡和生存状态。

Effects of ATRA, Acitretin and Tazarotene on Growth and Apoptosis of Tca8113 Cells

Summary：To investigate the effects of ATRA, acitretin and tazarotene on the growth and apoptosis of human tongue squamous cell carcinoma cell line Tca8113. The effect of retinoids on growth of Tca8113 cells in vitro was examined by MTT assay and Trypan blue exclusion assay. Cell cycle analysis, early apoptosis analysis with double staining with Annexin V-FITC and PI, and active caspase-3 analysis with the staining of FITC-conjugated monoclonal rabbit anli-active caspase-3 antibody were made by flow cytometer. Streptavidin-biotin complex （SABC） immunocytochemical assays were employed for the detections of Bax/Bcl-2 proteins expressions. Our results showed that the retinoids inhibited growth of Tca8113 cells in a dose-and time-dependent manner with maximal inhibition 24 h after treatment of 10 5 mol/L. 10^-5 mol/L retinoids altered cell cycle distribution of Tca8113 cells, revealing an increase in G0/G1-phase population, a decrease in S-phase population and the inhibition of G1/S switching. 10^-5 mol/L retinoids significantly induced apoptosis of Tca8113 cells （all P〈0.05）, elevated the cells population with detectable active caspase-3 （P〈 0.05 for all）, increased the number of cells forming Bax and decreased the number of cells forming Bcl-2 significantly （all P〈0.05）. Acitretin played a most prominent role among the retinoids. It is concluded that the inhibition of cell cycle progress of Tca8113 cells by ATRA, acitretin and tazarotene is one of the possible mechanisms for proliferation arrest of TcaS113 cells elicited by the retinoids. The retinoids mediate apoptosis in TcaS113 cells that may be caspase-dependent through mitochondria pathway. High concentration retinoids inhibit growth of Tca8113 cells in vitro by interfering with proliferation and inducing apoptosis of cells. Acitretin may be an alternative medicine for the prevention and treatment of tongue squamous cell carcinoma.

Ad-ING4对人前列腺癌细胞PC-3体内外抑癌效应的研究

背景与目的:腺病毒作为载体已被广泛用于肿瘤的基因治疗。ING4是生长抑制因子家族中的一个成员,是一种潜在的抑癌基因。本研究旨在探讨腺病毒介导的人ING4基因(Ad-ING4)对人前列腺癌细胞PC-3的体内外抑癌效应及其分子机制。方法:将扩增的Ad-ING4重组腺病毒感染PC-3细胞,用RT-PCR法检测ING4在PC-3细胞中的转录;MTT法检测ING4基因对PC-3细胞增殖的影响;流式细胞术和Hoechst33258染色法检测细胞凋亡的变化;半定量RT-PCR法检测ING4基因的表达对PC-3细胞中的bcl-2、bax、p53和caspase-3凋亡相关基因表达的影响。用Ad-ING4重组腺病毒在裸鼠PC-3移植瘤的瘤体内注射治疗,观察肿瘤生长变化,15d后处死裸鼠,摘除瘤体,称瘤重;用免疫组化法检测瘤组织中Bcl-2、Bax、Caspase-3和CD34蛋白的表达。结果:腺病毒介导的人ING4基因在PC-3细胞中成功转录,明显抑制PC-3细胞增殖,上调p53、bax、caspase-3基因表达和下调bcl-2基因表达,并诱导细胞凋亡。Ad-ING4重组腺病毒能显著抑制裸鼠PC-3移植瘤的生长,瘤重的抑制率达37%,与空病毒载体Ad-GFP组和细胞对照PBS组比较差异有统计学意义(P<0.05);免疫组化结果显示Ad-ING4重组腺病毒能明显上调Bax和Caspase-3蛋白的表达水平,下调Bcl-2和CD34蛋白的表达水平。结论:腺病毒介导的ING4基因在体内外均可明显抑制人前列腺癌细胞PC-3的生长,诱导其凋亡,其机制可能是上调P53、Bax、Caspase-3蛋白和下调Bcl-2蛋白表达水平。

沙棘黄酮制备及体外抑制人前列腺癌PC-3细胞作用研究

采用AB-8大孔树脂纯化沙棘黄酮初提物,用10%、30%、50%乙醇溶液梯度洗脱,以总黄酮含量和黄酮苷元含量为指标,筛选纯化样品;采用MTT法、实时无标记细胞分析技术检测沙棘黄酮样品体外对人前列腺癌PC-3细胞的增殖抑制作用,流式细胞技术检测细胞凋亡和细胞周期情况,Western blot检测Bax和Bcl-2蛋白表达情况。实验结果表明50%乙醇梯度洗脱样品(S50)中,总黄酮含量达到25.42%;水解后得到SH50样品,其槲皮素、异鼠李素含量分别达到5.03%、18.64%;25μg/m L的SH50样品对PC-3细胞即有增殖抑制作用,且呈剂量和时间依赖性;同时25μg/m L的SH50样品作用48 h即可显著诱导细胞凋亡(P<0.01),并将细胞周期阻滞在G2/M期,此外,样品可提高Bax蛋白和降低Bcl-2蛋白的表达。说明沙棘黄酮SH50样品对体外人前列腺癌PC-3细胞具有抑制增殖并诱导细胞凋亡作用,其机制可能与阻滞细胞周期,调节Bax和Bcl-2蛋白的表达有关。

蕃茄汁对人前列腺癌PC-3细胞增殖的影响

目的 研究番茄汁对人前列腺癌PC 3细胞增殖的影响及其可能的机制。方法 体外培养人前列腺癌PC 3细胞,分别加入不同浓度的番茄汁;用彗星试验测定经番茄汁处理的人前列腺癌PC 3细胞DNA链断裂情况,分析DNA的损伤作用;采用MTT法测定细胞的增殖情况。结果 番茄汁对人前列腺癌PC 3细胞的DNA具有损伤作用,可使DNA链断裂,DNA的迁移长度与彗星细胞拖尾率显著增高,与对照组相比,差异有非常显著性;能抑制PC 3细胞的增殖,与对照组相比,各实验组的吸光度逐渐降低,差异有非常显著性,且随着浓度的增加抑制作用逐渐加强。结论 番茄汁可诱导人前列腺癌PC 3细胞的DNA损伤,从而抑制其生长。

新型棉酚衍生物ApoG2对人前列腺癌PC-3移植瘤生长的抑制

目的:探讨棉酚衍生物ApoG2对前列腺癌的抑制作用,并了解其作用机理。方法:建立人前列腺癌细胞的裸鼠皮下移植瘤模型,在ApoG2作用下观察其对皮下移植瘤生长的抑制作用,通过免疫组化方法检测肿瘤组织中bcl-2、PCNA及caspase-3、-8的表达。结果:ApoG2可明显抑制前列腺癌皮下移植瘤生长速度,肿瘤体积明显减小,ApoG2能增加肿瘤组织中caspase-3、8的表达,减少PCNA表达。结论:ApoG2对人前列腺癌有显著的生长抑制作用。

番茄汁对人前列腺癌PC-3细胞增殖和凋亡的影响

目的:探讨番茄汁对人前列腺癌PC-3细胞生长抑制作用及其机理研究。方法:番茄红素及不同浓度番茄汁作用于人前列腺癌PC-3细胞48h;采用生长曲线及噻唑蓝(MTT)法检测番茄汁、番茄红素对人前列腺癌PC-3细胞的生长抑制作用,通过原位(缺口)末端标记法(TUNEL)法观察凋亡细胞的形态结构变化,流式细胞仪检测细胞凋亡峰。结果:番茄汁、番茄红素能显著抑制人前列腺癌PC-3细胞生长;TUNEL方法检测呈阳性;流式细胞仪分析图上出现典型的凋亡细胞峰。以上各指标中,番茄汁随着浓度增大其作用加强;低剂量组的作用虽比番茄红素组差,中剂量组的作用与番茄红素组相比无差别,高剂量组的作用比番茄红素组强。结论:番茄汁对抗人前列腺癌PC-3细胞的作用,除番茄红素外,可能还存在其他抗癌成分的交互作用。番茄汁、番茄红素对PC-3细胞生长抑制作用的机理可能与其诱导人前列腺癌PC-3细胞细胞凋亡有关。

葡萄汁对人前列腺癌PC-3细胞增殖和凋亡的影响

目的:探讨葡萄汁对人前列腺癌PC-3细胞生长抑制的作用及其机制。方法:白藜芦醇及不同浓度葡萄汁作用于人前列腺癌PC-3细胞48h;采用生长曲线及噻唑蓝(MTT)法检测葡萄汁、白藜芦醇对人前列腺癌PC-3细胞的生长抑制作用,通过原位(缺口)末端标记法(TUNEL)观察凋亡细胞的形态结构变化,流式细胞仪检测细胞凋亡峰。结果:葡萄汁、白藜芦醇能显著抑制人前列腺癌PC-3细胞生长;TUNEL方法检测呈阳性;流式细胞仪分析图上出现典型的凋亡细胞峰。以上各指标中,葡萄汁随着浓度增大作用加强;低剂量组的作用比白藜芦醇组差,中、高剂量组的白藜芦醇浓度低,但作用比白藜芦醇组强。结论:葡萄汁对抗人前列腺癌PC-3细胞的作用,除白藜芦醇外,可能还存在其他抗癌成分的作用。葡萄汁、白藜芦醇对PC-3细胞生长抑制作用的机制可能与其诱导人前列腺癌PC-3细胞凋亡有关。

昆布多糖硫酸酯对非激素依赖型人前列腺癌细胞PC-3的作用研究

目的研究昆布多糖硫酸酯(LAMS)对体外培养的非激素依赖型人前列腺癌细胞株PC-3的作用。方法利用WST-8法检测LAMS对体外培养的非激素依赖型人前列腺癌细胞株PC-3细胞生长的抑制作用,利用流式细胞术(FCM)分析LAMS对细胞周期和凋亡的影响,利用荧光显微镜观察PC-3细胞形态。结果随着LAMS浓度的增加和作用时间的延长,对非激素依赖型人前列腺癌细胞株PC-3细胞的生长抑制率逐渐增高,呈时间-剂量效应;流式细胞仪分析,PC-3细胞凋亡率逐渐增高;但PC-3细胞的凋亡率与作用时间的延长无明显关系;荧光显微镜观察,PC-3细胞凋亡小体逐渐增多,甚至出现细胞死亡;随着LAMS浓度增加PC-3细胞G1期细胞比例逐渐减少,S+G2期细胞比例呈剂量依赖性增加,表明存在S+G2期阻滞。结论LAMS能抑制体外PC-3细胞的生长,并促进其S+G2期阻滞和凋亡,可能是其抑制前列腺癌的机制之一。