Sulforaphane induces caspase-mediated apoptosis in cultured PC-3 human prostate cancer cells and retards growth of PC-3 xenografts in vivo

Sulforaphane (SFN), a constituent of cruciferous vegetables, is highly effective in affording protection against chemically induced cancers in animal models. Here, we report that SFN inhibited proliferation of cultured PC-3 human prostate cancer cells by inducing apoptosis that was characterized by appearance of cells with sub-G0/G1 DNA content, formation of cytoplasmic histone associated DNA fragments and cleavage of poly(ADP-ribose)polymerase (PARP). SFN-induced apoptosis was associated with up-regulation of Bax, down-regulation of Bcl-2 and activation of caspases-3, -9 and -8. SFN-induced apoptosis, and cleavage of procaspase-3 and PARP were blocked upon pre-treatment of cells with pan caspase inhibitor z-VADfmk, and specific inhibitors of caspase-9 (z-LEHDfmk) and caspase-8 (z-IETDfmk) suggesting involvement of both caspase-9 and caspase-8 pathways in SFN-induced cell death. Oral administration of SFN (5.6 micro mol, 3 times/week) significantly inhibited growth of PC-3 xenografts in nude mice. For instance, 10 days after starting therapy, the average tumor volumes in control and SFN-treated mice were 170 +/- 13 and 80 +/- 14 mm3, respectively, reflecting a >50% reduction in tumor volume due to SFN administration. To the best of our knowledge, the present study is the first published report to document in vivo anticancer activity of SFN in a tumor xenograft model.     

Ganoderma lucidum inhibits proliferation and induces apoptosis in human prostate cancer cells PC-3

Ganoderma lucidum (Reishi), an oriental medical mushroom, has been widely used in Asian countries for centuries to prevent or treat different diseases, including cancer. However, the mechanism(s) responsible for the effects of Ganoderma lucidum on cancer cells remain to be elucidated. We have previously demonstrated that Ganoderma lucidum down-regulated the expression of NF-kappaB-regulated urokinase plasminogen activator (uPA) and uPA receptor (uPAR), which resulted in suppression of cell migration of highly invasive human breast and prostate cancer cells. In this study, we investigated the effects of Ganoderma lucidum on cell proliferation, cell cycle, and apoptosis in human prostate cancer cells PC-3. Our data demonstrate that Ganoderma lucidum inhibits cell proliferation in a dose- and time-dependent manner by the down-regulation of expression of cyclin B and Cdc2 and by the up-regulation of p21 expression. The inhibition of cell growth was also demonstrated by cell cycle arrest at G2/M phase. Furthermore, Ganoderma lucidum induced apoptosis of PC-3 cells with a slight decrease in the expression of NF-kappaB-regulated Bcl-2 and Bcl-xl. However, the expression of proapoptotic Bax protein was markedly up-regulated, resulting in the enhancement of the ratio of Bax/Bcl-2 and Bax/Bcl-xl. Thus, Ganoderma lucidum exerts its effect on cancer cells by multiple mechanisms and may have potential therapeutic use for the prevention and treatment of cancer.     

UVB-activated indole-3-acetic acid induces apoptosis of PC-3 prostate cancer cells

Indole-3-acetic acid (IAA) has recently shown anticancer activity in combination with horseradish peroxidase. The current study demonstrated that IAA irradiated with ultraviolet B (IAA(UVB)) is able to generate free radicals and induce cell death in a time-dependent fashion in PC-3 prostate cancer cells, while PC-3 cells treated with IAA alone exhibited no toxic responses. It was also found through Western blot analysis that the cytotoxic effect of IAA(UVB) resulted from apoptosis. Treatment with IAA(UVB) for 24 hours showed a significant increase in phosphorylated p38 mitogen-activated protein kinase and c-Jun N-terminal kinase, the stress signaling proteins. Furthermore, pro-caspases (-3, -8, and -9) were clearly down-regulated and poly(ADP-ribose) polymerase cleavages were demonstrated in the group treated with IAA(UVB). Flow cytometric analysis also demonstrated the induction of apoptosis by IAA(UVB) in PC-3 cells. In conclusion, this study demonstrated that IAA induced cell death in combination with UVB irradiation by increasing apoptosis in PC-3 cells.     

藤黄酸抑制前列腺癌PC-3细胞增殖并诱导其细胞凋亡

目的:研究中药藤黄的有效成分藤黄酸(gambogic acid,GA)对前列腺癌PC-3细胞增殖和凋亡的影响。方法:采用不同浓度的GA作用前列腺癌PC-3细胞后,在体外通过CCK-8比色法分析细胞的增殖情况,吖啶橙/溴化乙啶(acridine orange/ethidium bromide,AO/EB)双重染色法和FCM法分析细胞的凋亡情况;蛋白质印迹法检测细胞中凋亡相关蛋白P53、Bax和Bcl-2的表达变化。结果:GA不仅能抑制PC-3细胞的增殖,而且能有效诱导其细胞凋亡,与对照组比较差异有统计学意义(P<0.05),并且其抑制增殖和促凋亡作用呈浓度依赖性。CCK-8法检测结果表明,GA浓度>1μmol/L时,细胞的增殖能力受到明显抑制。AO/EB染色法显示,GA处理后的前列腺癌PC-3细胞核呈致密浓染橘红色,并伴有核浓缩和偏向。FCM法检测结果显示,GA处理后的前列腺癌PC-3细胞凋亡峰明显。蛋白质印迹法进一步表明,GA能够上调PC-3细胞中Bax和P53的表达水平,下调Bcl-2表达水平。结论:GA对前列腺癌PC-3细胞具有明显的抑制增殖和诱导凋亡作用。     

Neoxanthin and fucoxanthin induce apoptosis in PC-3 human prostate cancer cells

Neoxanthin and fucoxanthin, which have the characteristic structure of 5,6-monoepoxide and an allenic bond, were previously found to reduce the viability of human prostate cancer cells most intensively among 15 dietary carotenoids tested. In the present study, the induction of apoptosis in PC-3 cells by these two carotenoids was characterized by morphological changes, DNA fragmentation, an increased percentage of hypodiploid cells, and cleavages of caspase-3 and PARP. The ratio of apoptotic cells reached more than 30% after treatment for 48 h with 20 microM carotenoids. They reduced the expression of Bax and Bcl-2 proteins, but not Bcl-X(L). Fucoxanthin accumulated in the cells at the same level as neoxanthin. Moreover, fucoxanthinol, a deacetylated product of fucoxanthin, formed in the cells treated with fucoxanthin and reached a level comparable to that of fucoxanthin after incubation for 24 h. Treatment by fucoxanthinol alone also induced apoptosis in PC-3 cells. Thus, neoxanthin and fucoxanthin treatments were found to induce apoptosis through caspase-3 activation in PC-3 human prostate cancer cells.     

Geraniol induces cooperative interaction of apoptosis and autophagy to elicit cell death in PC-3 prostate cancer cells

Geraniol, an acyclic dietary monoterpene, suppresses prostate cancer growth and enhances docetaxel chemosensitivity in cultured cell or xenograft tumor models. However, the mechanisms of the geraniol action against prostate cancer are largely unknown. In this study, we investigated the cellular and molecular mechanisms of geraniol-induced cell death in PC-3 prostate cancer cells. Among the examined structurally and functionally similar monoterpenes, geraniol potently induced apoptosis and autophagy. Although independent processes, apoptosis and autophagy acted as cooperative partners to elicit geraniol-induced cell death in PC-3 cells. At a molecular level, geraniol inhibited AKT signaling and activated AMPK signaling, resulting in mTOR inhibition. Combined treatment of AKT inhibitor and AMPK activator markedly suppressed cell growth compared to either treatment alone. Our findings provide insight into future investigations that are aimed at elucidating the role of apoptosis and autophagy in prostate cancer therapy and at developing anticancer strategies co-targeting AKT and AMPK.     

Rapamycin-induced apoptosis is p53-independent in human prostate carcinoma PC-3 cells

We have investigated the mechanisms of rapamycin-induced growth inhibition and apoptosis in the PC-3 prostate carcinoma cell line. Rapamycin induced apoptosis as well as the expression of p21(waf1) mRNA and protein, independent of p53. Rapamycin treatment also resulted in: a decrease in cdk2 kinase activity; an increase in hypophosphorylated retinoblastoma protein (pRb); a dephosphorylation of p70 S6 kinase; and, growth-arrest in G(1)-phase of cell cycle. These data suggest that rapamycin-induced growth arrest and apoptosis occur through the p53-independent induction of p21(waf1). Since this induction occurred soon after rapamycin treatment, possibly, the early induction of p21(waf1) and G(1)-arrest are important components of the mechanism by which rapamycin induces apoptosis in PC-3 cells.     

Microarray analysis of survival pathways in human PC-3 prostate cancer cells

BACKGROUND: Insulin-like growth factor 1 (IGF-1), transforming growth factor beta 1 (TGFbeta1), and interleukin 6 (IL-6), act as survival factors inhibiting chemotherapy-induced apoptosis in PC-3 human prostate cancer cells, in vitro. MATERIALS AND METHODS: To study the intracellular pathways activated by these survival factors we performed a comparative genomic analysis using oligonucleotide microarray chips. A validation by real time-PCR was also performed for the genes of interest. RESULTS: The expression data derived were analysed using various normalization algorithms. The differentially expressed genes were clustered and their ontological annotations were statistically tested to provide evidence for possible deregulated biological processes on the action of the aforementioned survival factors. Emphasis was given on the regulation and the role of the genes AKR1C1, SDPR and GADD45B in the survival pathways of prostate cancer cells, whose expression was also validated by real time-PCR. CONCLUSION: The overall analyses reveal an overrepresentation of differentially expressed genes related to cellular processes such as cell cycle regulation, lipid metabolism and steroid biosynthesis.     

Alisol B acetate, a triterpene from Alismatis rhizoma, induces Bax nuclear translocation and apoptosis in human hormone-resistant prostate cancer PC-3 cells

The anti-tumor potential of components from Chinese herbal medicines has been greatly concerned. Alisol B acetate, a triterpene from Alismatis rhizoma, induced apoptotic cell death in human hormone-resistant prostate cancer PC-3 cells in a time- and concentration-dependent manner. A good correlation between loss of mitochondrial membrane potential and apoptotic cell death was apparent indicating the participation of mitochondria-related mechanism. Alisol B acetate induced Bax up-regulation and nuclear translocation; it also induced the activation of initiator caspase-8 and caspase-9, and executor caspase-3, suggesting the involvement of both extrinsic and intrinsic apoptosis pathways. Taken together, it is suggested that alisol B acetate induces apoptosis in PC-3 cells via a mitochondria-mediated mechanism with activation of caspase-8, -9 and -3. Furthermore, the Bax activation and translocation from the cytosol to nucleus might be a crucial response to the apoptotic effect.     

Incadronate induces cell detachment and apoptosis in prostatic PC-3 cells

BACKGROUND: Bisphosphonates are widely used for the treatment and prevention of osteoporosis and are also effective in the treatment of bone metastasis of prostate cancer. Several mechanisms underlying the antitumor effect of bisphosphonates have been proposed, including direct effects on tumor cells, such as induction of apoptosis and inhibition of invasion. MATERIALS AND METHODS: The detached and adherent cells after incadronate treatment were collected separately and stained with trypan blue solution. RESULTS: It was found that incadronate induced cell detachment with dephosphorylation of focal adhesion kinase (FAK). The induction of cell detachment by incadronate was prevented by coincubation with geranylgeraniol. The activation of caspase-3 was observed in incadronate-treated floating cells, but not in the adherent cells. A caspase inhibitor did not inhibit cell detachment by incadronate but it markedly prevented cell death. Conclusion: These results suggest that incadronate induces cell detachment, followed by caspase-dependent apoptosis.     

Artemisinin induces apoptosis in human cancer cells

BACKGROUND: Artemisinin is a chemical compound extracted from the wormwood plant, Artemisia annua L. It has been shown to selectively kill cancer cells in vitro and retard the growth of implanted fibrosarcoma tumors in rats. In the present research, we investigated its mechanism of cytotoxicity to cancer cells. MATERIALS AND METHODS: Molt-4 cells, in complete RPMI-1640 medium, were first incubated with 12 microM of human holotransferrin at 37 degrees C in a humid atmosphere of 5% CO2 for one hour. This enhanced the iron supply to the cells. The cells were then pelleted and transferred to a complete RPMI-1640 containing 200 microM of an analog dihydroartemisinin (DHA) and incubation was started (0 h). In addition, some culture samples were treated with holotransferrin alone and some (controls) were assayed without neither holotransferrin nor DHA treatment. Cells were counted and DNA diffusion assay was used to evaluate apoptosis and necrosis in each sample at 0 h and at 1, 2, 4 and 8 h of incubation. RESULTS: DHA treatment significantly decreased cell counts and increased the proportion of apoptosis in cancer cells compared to controls (chi2=4.5, df=1, p<0.035). Addition of holotransferrin significantly further decreased cell counts (chi2=4.5, df=1, p<0.035) and increased apoptosis (chi2=4.5, df=1, p<0.035). No necrotic cells were observed. CONCLUSION: This rapid induction of apoptosis in cancer cells after treatment with DHA indicates that artemisinin and its analogs may be inexpensive and effective cancer agents.     

雷帕霉素对人前列腺癌PC-3细胞的作用及其机制

背景与目的：哺乳动物细胞中雷帕霉素靶蛋白（mammalian target of rapamycin,mTOR）信号途径调节细胞生长、增殖、存活和凋亡。本实验是研究雷帕霉素对前列腺癌PC-3细胞的作用及其机制。方法：培养前列腺癌PC-3细胞,采用MTT法检测雷帕霉素1nmol／L作用24h、36h、48h、72h后PC-3细胞增殖的改变,流式细胞术检测作用不同时间细胞周期的改变,Western blot检测雷帕霉素作用PC-3细胞24h、36h、48h、72h后raptor、rietor、Akt、pS6k1-T389、pAkt-s473的表达情况。结果：MTT结果显示雷帕霉素在作用24h时,促进了PC-3细胞增殖,但在36h显著抑制PC-3细胞增殖（P〈0．01）,72h时抑制作用更明显。FCM结果显示雷帕霉素作用24h时S期细胞有所增加,但作用36、48、72h后PC-3细胞的G1期细胞逐渐增加,使PC-3细胞周期主要阻滞在G。期。Western blot检测结果显示雷帕霉素作用24h时显著抑制raptor和pS6k1-T389的表达（P〈0．01）;rictor、Akt表达并没有显著变化;pAkt-s473表达在雷帕霉素作用24h时反而显著增加（P〈0．01）,但在36h后即被显著抑制,72h几乎完全被抑制（P〈0．01）。结论：延长雷帕霉素作用时间可抑制PC-3细胞增殖,其机制可能与雷帕霉素阻滞细胞周期、抑制Akt磷酸化有关。     

左旋棉酚体外诱导人前列腺PC-3细胞凋亡的研究

目的:研究左旋棉酚对人前列腺癌PC-3细胞体外增殖和凋亡的影响。方法:MTT法检测左旋棉酚对PC-3细胞增殖的影响,透射电镜观察细胞超微结构的改变,TUNEL染色观察细胞凋亡,流式细胞术检测细胞周期的改变,半定量RT-PCR检测Bcl-2及Bak mRNA的表达水平。结果:左旋棉酚能显著抑制PC-3细胞的体外增殖,并呈浓度-时间依赖性。左旋棉酚可以诱导PC-3细胞发生典型的凋亡形态学改变和G0/G1期阻滞,RT-PCR显示Bcl-2 mRNA表达水平降低,Bak mRNA表达水平升高。结论:左旋棉酚能诱导前列腺癌细胞的体外凋亡,主要可能与Bak mRNA的表达升高及Bcl-2 mRNA的表达下调有关。     

Lysosomotropic acid ceramidase inhibitor induces apoptosis in prostate cancer cells

Purpose Alterations in ceramide metabolism have been reported in prostate cancer (PCa), resulting in escape of cancer cells from ceramide-induced apoptosis. Specifically, increased expression of lysosomal acid ceramidase (AC) has been shown in some primary PCa tissues and in several PCa cell lines. To determine if this represents a novel therapeutic target, we designed and synthesized LCL204, a lysosomotropic analog of B13, a previously reported inhibitor of AC Methods Prostate cancer cell lines were treated with LCL204 for varying times and concentrations. Effects of treatment on cytotoxicity, sphingolipid content, and apoptotic markers were assessed. Results Treatment of DU145 PCa cells resulted in increased ceramide and decreased sphingosine levels. Interestingly, LCL204 caused degradation of AC in a cathepsin-dependent manner. We also observed rapid destabilization of lysosomes and the release of lysosomal proteases into the cytosol following treatment with LCL204. Combined, these events resulted in mitochondria depolarization and executioner caspase activation, ultimately ending in apoptosis Conclusions These results provide evidence that treatment with molecules such as LCL204, which restore ceramide levels in PCa cells may serve as a new viable treatment option for PCa.     

Pancratistatin induces apoptosis and autophagy in metastatic prostate cancer cells

The Amaryllidaceae alkaloid pancratistatin has been proven to selectively induce apoptotic cell death in a variety of human cancer cells with an insignificant effect on non-cancerous cells. In this study we report, for the first time, the effects of pancratistatin (PST) on models of metastatic prostate cancer. The effects of pancratistatin on prostate cancer DU145 and LNCaP cell lines was assessed by microscopy, enzymatic activity assays and Western blotting. Apoptosis was determined by nuclear condensation and caspase activation, and autophagy was observed by MDC staining and LC3 expression levels. Human prostate xenografts were used to test the potential therapeutic efficacy of intra-tumor administration of pancratistatin in vivo. Pancratistatin treatment reduced cell viability and induced apoptosis in androgen-responsive (LNCaP) and androgen-refractory (DU145) prostate cancer cell lines in a dose- and time-dependent manner, but with an insignificant effect on normal human fibroblast (NHF) cells at the effective dose. Increased reactive oxygen species production and collapse of mitochondrial membrane potential resulted from treatment with pancratistatin in both cancer cell lines. This study presents the novel finding that pancratistatin treatment caused decreased migration capacity and increased autophagy levels in metastatic prostate cancer cells. Importantly, in this proof-of-concept study, pancratistatin reduced the volume of xenograft tumors compared to control-treated animals, and was well-tolerated. Our results highlight the potential of pancratistatin for clinical development as a selective therapeutic for treatment of metastatic prostate cancer.     

Overexpression of 15-lipoxygenase-1 in PC-3 human prostate cancer cells increases tumorigenesis.

The effect of overexpression of 15-lipoxygenase-1 (15-LO-1) was studied in the human prostate cancer cell line, PC-3. Stable PC-3 cell lines were generated by transfection with 15-LO-1-sense (15-LOS), 15-LO-1-antisense (15-LOAS) or vector (Zeo) and selection with Zeocin. After characterization by RT-PCR, western and HPLC, a PC3-15LOS clone was selected that possessed 10-fold 15-LO-1 enzyme activity compared with parental PC-3 cells. The PC3-15LOAS clone displayed little or no 15-LO-1 activity. These PC-3 cell lines were characterized for properties of tumorigenesis. The proliferation rates of the cell lines were as follows: PC3-15LOS > PC-3 = PC3-Zeo > PC3-15LOAS. Addition of a specific 15-LO-1 inhibitor, PD146176, caused a dose-dependent inhibition of proliferation in vitro. Overexpression of 15-LO-1 also caused [(3)H]thymidine incorporation to increase by 4.0-fold (P < 0.01). Compared with parental and PC-3-Zeo cells, PC3-15LOS enhanced whereas PC3-15LOAS reduced the ability of PC-3 cells to grow in an anchorage-independent manner, as assessed by colony formation in soft agar. These data suggested a pro-tumorigenic role for 15-LO-1 in PC-3 cells in vitro. Therefore, to clarify the role of 15-LO-1 in vivo, the effect of 15-LO-1 expression on the growth of tumors in nude mice was investigated. The PC-3 cell lines were inoculated subcutaneously into athymic nude mice. The frequency of tumor formation was increased and the sizes of the tumors formed were much larger in the PC3-15LOS compared with PC3-15LOAS, parental PC-3 and PC-3-Zeo cells. Immunohistochemistry for 15-LO-1 confirmed expression throughout the duration of the experiment. The expression of factor VIII, an angiogenesis marker, in tumor sections was increased in tumors derived from PC3-15LOS cells and decreased in those from PC3-15LOAS cells compared with tumors from parental or Zeo cells. These data further supported the evaluation by ELISA of vascular endothelial growth factor (VEGF) secretion by PC-3 cells in culture. Secretion of this angiogenic factor was elevated in PC3-15LOS cells compared with the other cell lines. These results support a role for 15-LO-1 in a novel growth-promoting pathway in the prostate.     

浅蓝菌素对前列腺癌细胞株PC-3生长抑制的研究

目的：探讨脂肪酸合成酶（FAS）的抑制剂浅蓝菌素对前列腺癌细胞株PC-3的生长抑制作用。方法：采用人前列腺癌细胞株PC-3在体外实验中用MTT法观察浅蓝菌素对细胞株的生长抑制作用;流式细胞术（FCM）对细胞株的凋亡及细胞周期的变化进行检测;蛋白免疫印迹（W estern b lotting）法检测浅蓝菌素对PC-3细胞中FAS蛋白水平表达的影响。结果：PC-3细胞在浅蓝菌素的作用下,细胞增殖被明显阻遏,并呈现剂量效应关系,在浓度为2.5mg/L、5.0mg/L、10.0mg/L、20.0mg/L的浅蓝菌素作用下,PC-3细胞24h的抑制率分别为（34.78±2.47）%、（46.76±3.18）%、（58.13±3.55）%、（65.31±2.81）%,与对照组比较有统计学意义（P〈0.05）。流式细胞仪显示,细胞经浅蓝菌素作用后,细胞凋亡增多,PC-3细胞在浅蓝菌素浓度5.0mg/L三个时间组（24h,48h,72h）的细胞凋亡率分别为（28.29±1.88）%、（44.73±2.69）%、（61.25±1.43）%;且G0/G1期细胞比例增加,S期和G2/M期细胞比例减少。蛋白免疫印迹实验中,随着浅蓝菌素作用时间的延长,PC-3细胞中的FAS蛋白水平表达量明显减少,药物作用时间与细胞中蛋白水平表达量呈负相关。结论：浅蓝菌素能抑制PC-3细胞生长,且其呈现时间和浓度依赖性。     

Fatty acid regulates gene expression and growth of human prostate cancer PC-3 cells

It has been proposed that the omega-6 fatty acids increase the rate of tumor growth. Here we test that hypothesis in the PC-3 human prostate tumor. We found that the essential fatty acids, linoleic acid (LA) and arachidonic acid (AA), and the AA metabolite PGE(2) stimulate tumor growth while oleic acid (OA) and the omega-3 fatty acid, eicosapentaenoic acid (EPA) inhibited growth. In examining the role of AA in growth response, we extended our studies to analyze changes in early gene expression induced by AA. We demonstrate that c-fos expression is increased within minutes of addition in a dose-dependent manner. Moreover, the immediate early gene cox-2 is also increased in the presence of AA in a dose-dependent manner, while the constitutive cox-1 message was not increased. Three hours after exposure to AA, the synthesis of PGE(2) via COX-2 was also increased. Previous studies have demonstrated that AA was primarily delivered by low density lipoprotein (LDL) via its receptor (LDLr). Since it is known that hepatomas, acute myelogenous leukemia and colorectal tumors lack normal cholesterol feedback, we examined the role of the LDLr in growth regulation of the PC-3 prostate cancer cells. Analysis of ldlr mRNA expression and LDLr function demonstrated that human PC-3 prostate cancer cells lack normal feedback regulation. While exogenous LDL caused a significant stimulation of cell growth and PGE(2) synthesis, no change was seen in regulation of the LDLr by LDL. Taken together, these data show that normal cholesterol feedback of ldlr message and protein is lost in prostate cancer. These data suggest that unregulated over-expression of LDLr in tumor cells would permit increased availability of AA, which induces immediate early genes c-fos and cox-2 within minutes of uptake.     

浅蓝菌素对前列腺癌细胞株PC-3生长抑制的研究

目的:探讨脂肪酸合成酶(FAS)的抑制剂浅蓝菌素对前列腺癌细胞株PC-3的生长抑制作用。方法:采用人前列腺癌细胞株PC-3在体外实验中用MTT法观察浅蓝菌素对细胞株的生长抑制作用;流式细胞术(FCM)对细胞株的凋亡及细胞周期的变化进行检测;蛋白免疫印迹(W estern b lotting)法检测浅蓝菌素对PC-3细胞中FAS蛋白水平表达的影响。结果:PC-3细胞在浅蓝菌素的作用下,细胞增殖被明显阻遏,并呈现剂量效应关系,在浓度为2.5mg/L、5.0mg/L、10.0mg/L、20.0mg/L的浅蓝菌素作用下,PC-3细胞24h的抑制率分别为(34.78±2.47)%、(46.76±3.18)%、(58.13±3.55)%、(65.31±2.81)%,与对照组比较有统计学意义(P<0.05)。流式细胞仪显示,细胞经浅蓝菌素作用后,细胞凋亡增多,PC-3细胞在浅蓝菌素浓度5.0mg/L三个时间组(24h,48h,72h)的细胞凋亡率分别为(28.29±1.88)%、(44.73±2.69)%、(61.25±1.43)%;且G0/G1期细胞比例增加,S期和G2/M期细胞比例减少。蛋白免疫印迹实验中,随着浅蓝菌素作用时间的延长,PC-3细胞中的FAS蛋白水平表达量明显减少,药物作用时间与细胞中蛋白水平表达量呈负相关。结论:浅蓝菌素能抑制PC-3细胞生长,且其呈现时间和浓度依赖性。