Ginsenoside Rg3 attenuates tumor angiogenesis via inhibiting bioactivities of endothelial progenitor cells

Accumulating evidence suggests that Ginsenoside Rg3 appears to inhibit tumor growth including Lewis lung carcinoma, intestinal adenocarcinomas or B16 melanoma by inhibiting cell proliferation, tumor cell invasion and metastasis. Endothelial progenitor cells (EPCs) appear to play a key role in the growth of early tumors by intervening with the angiogenic switch promoting tumor neovessel formation by producing angiogenic cytokines during tumor progression. This paper reports a novel mechanism of Ginsenoside Rg3, a candidate anticancer bio-molecule, on tumor angiogenesis by inhibiting the multiple bioactivities of EPCs. When Ginsenoside Rg3 was applied to the ex vivo cultured outgrowth ECs, a type of EPCs, it inhibited the cell proliferation, cell migration and tubular formation of EPCs. Importantly, Ginsenoside Rg3 attenuated the phosphorylation cascade of the VEGF dependent p38/ERK signaling in vitro. The xenograft tumor model clearly showed that Ginsenoside Rg3 suppresses tumor growth and tumor angiogenesis by inhibiting the mobilization of EPCs from the bone marrow microenvironment to the peripheral circulation and modulates VEGF-dependent tumor angiogenesis. In conclusion, this study provides a potential therapeutic molecule, Ginsenoside Rg3, as an anticancer drug by inhibiting the EPC bioactivities.     

Comparison of the in vitro and in vivo effects of retinoids either alone or in combination with cisplatin and 5-fluorouracil on tumor development and metastasis of melanoma

Purpose  Retinoids have previously been reported to inhibit proliferation of melanoma cell lines in vitro. However, the relative antimetastatic efficacy of various retinoids on melanoma in vivo is unknown. Therefore, we investigated the effects of different retinoids on the invasion and metastasis of murine melanoma B16-F10 cells in vitro and in vivo. Based on the findings, the antitumor effects of a selected retinoid either alone or in combination with cisplatin were also investigated in a preclinical mouse melanoma model. Methods  Cell proliferation and invasion analyses of murine melanoma B16-F10 cells were assessed in the presence of different retinoids, either alone or in combination with cisplatin (CDDP) or 5-fluorouracil (5-FU). Experimental lung metastasis assay was performed in this study to investigate the antimetastatic efficacy of retinoids. Additionally, a mouse melanoma model was used to assess the antitumor efficacy of a selected retinoid in combination with cisplatin. Results  Retinoids showed significant antiproliferation and anti-invasion effects on murine melanoma B16-F10 cells. Pretreatment with retinoids increased the sensitivity to CDDP but not to 5-FU in in-vitro. Moreover, the number of metastatic colonies formed in the lungs of mice injected intravenously with B16-F10 cells was significantly reduced by injecting the respective retinoid once a day for 10 days. Treatment with a combination of cisplatin and 13-cis-retinoic acid resulted in a significant reduction in primary tumor size and the number of lung metastatic nodules in melanoma-bearing mice. Conclusion  These results suggest that retinoids not only exhibit antimetastatic effect, but also enhance the antitumor activity of cisplatin in vivo.     

20（S）-人参皂苷Rg3对血管内皮细胞增殖和迁移的抑制作用

 目的 探讨20（S）-人参皂苷Rg3（SPG-Rg3）抗肿瘤诱导新生血管生成的作用机制。方法 采用MTT法、PCNA免疫荧光染色和Boyden小室迁移实验,观察SPG-Rg3对B16黑色素瘤细胞条件培养液（Conditioned Medium of B16 Melanoma Cells, BMCM）诱导的人脐静脉内皮细胞增殖和迁移的影响;并通过免疫细胞化学染色法观察了SPG-Rg3对B16黑色素瘤细胞血管内皮细胞生长因子（Vascular Endothelial Growth Factor, VEGF）及金属基质蛋白酶-9（Matrix Metalloproteinase-9, MMP-9）表达的影响。结果SPG-Rg3组BMCM的促内皮细胞增殖和迁移作用均明显弱于对照组,且SPG-Rg3浓度为5μg/ml时能够降低B16黑色素瘤细胞VEGF及MMP-9的表达。结论SPG-Rg3通过减少肿瘤细胞分泌细胞因子VEGF和MMP-9,抑制肿瘤细胞对血管内皮细胞增殖和迁移的促进作用,从而间接发挥其抗肿瘤新生血管生成的作用。     

阿维A酸和沙利度胺对鼠黑素瘤细胞株B16增殖和VEGF表达的影响

目的探讨阿维A酸和沙利度胺对鼠黑素瘤细胞株B16增殖的抑制作用。方法以B16细胞为研究对象，用不同浓度的阿维A酸和沙利度胺处理。（1）MTT比色法检测两药在不同的时间对B16细胞增殖的抑制作用；（2）倒置显微镜观察B16细胞形态的变化；（3）流式细胞术检测细胞周期和凋亡；（4）免疫细胞化学法测血管内皮生长因子（VEGF）的表达。结果（1）MTT法示两药对B16细胞的增殖有抑制效应。（2）倒置显微镜下可见阿维A酸组细胞不贴壁，沙利度胺组和对照组贴壁生长。（3）流式细胞术示两药处理后B16细胞G0／G1期比例增加，S期比例减少。（4）免疫细胞化学法示阿维A酸组VEGF表达受到抑制。结论两药均能抑制B16细胞增殖，抑制细胞从G0／G1期进入到S期；阿维A酸能影响B16细胞VEGF分泌，沙利度胺无此作用。     

人参皂甙Rg3和核糖核酸酶抑制因子转基因对小鼠黑色素瘤的抑制作用研究

目的观察人参皂甙Rg3和核糖核酸酶抑制因子(RI)转基因对小鼠B16黑色素瘤肺转移的抑制作用和影响,探讨人参皂甙Rg3和RI抗肿瘤生长和转移作用的分子机制。方法制备转RI基因的B16黑色素瘤肺转移小鼠模型,对野生型对照组(W组)、空质粒转染组(B组)和RI转基因组(RI组)以及给予Rg3的野生型对照组(Rg3/W组)、空质粒转染组(Rg3/B组)和RI转基因组(Rg3/RI组)中,荷瘤小鼠肺重量、肿瘤转移灶数目、生存期和肿瘤组织微血管密度进行检测和分析。结果Rg3和RI转基因使荷瘤小鼠肺重量降低,肿瘤转移灶数目减少,其肺重量降低和肿瘤转移灶数目减少的程度以Rg3/RI组最明显,Rg3/B组、Rg3/W组和RI组次之,与W组和B组差异有显著性(P<0.01),Rg3和RI有一定的协同性。Rg3和RI可延长荷瘤小鼠的生存期,Rg3/RI组小鼠在观察期(1.5个月)内均存活,W组和B组小鼠全部死亡(至26d),且出现死亡的时间较早。经HE染色和第Ⅷ因子相关抗原的免疫组化分析显示,Rg3和RI使肺内瘤组织的微血管密度降低,降低的程度为Rg3/RI组>Rg3/B组>Rg3/W组>RI组>B组>W组。结论人参皂甙Rg3可增强RI转基因对小鼠黑色素瘤肺转移的抑制作用,人参皂甙Rg3和RI基因在抗肿瘤生长、转移及血管生成方面有协同作用。     

20(S)-人参皂苷Rg3对B16黑色素瘤生长的抑制作用

目的 :探讨 2 0 (S) 人参皂苷Rg3对B16黑色素瘤生长的影响。 方法 :体内建立B16实体瘤模型及PCNA免疫组织化学染色 ,体外应用MTT法、生长曲线观察Rg3对B16黑色素瘤生长影响。 结果 :实体瘤模型中 ,Rg3各组瘤重明显低于对照组 (P <0 0 1) ,且Rg3组PCNALI与对照组比较有差异 (P <0 0 5 ) ,随着Rg3给予浓度的增加 ,PCNALI逐渐降低。体外实验观察到Rg3对B16黑色素瘤细胞生长同样有抑制作用。 结论 :Rg3可以明显抑制B16黑色素瘤的生长及增殖活性     

蛇毒抗肿瘤应用及其机制的研究进展

蛇毒对多种恶性肿瘤细胞有抑制增殖、诱导细胞凋亡和(或)抑制细胞迁移等作用,且呈剂量效应和(或)时间效应关系;此外,蛇毒还具有抗肿瘤血管生成作用。蛇毒抗肿瘤机制如下:1)通过阻断某些信号通路抑制肿瘤转移;2)通过激活死亡信号通路诱导肿瘤细胞凋亡;3)通过调节抑(促)癌基因表达或阻滞细胞周期抑制肿瘤细胞生长和增殖;4)通过抑制肿瘤细胞表达血管内皮生长因子(vascular endothelial growth factor,VEGF)而抑制肿瘤血管生成。蛇毒在抗肿瘤应用方面具有较大的发展空间。本文对近年来国内外蛇毒抗肿瘤应用相关文献资料进行整理和归纳,总结了蛇毒抗肿瘤作用及其机制,以期为蛇毒抗肿瘤成分的研究、开发和应用提供参考。      

苦参碱衍生物M19对于肿瘤细胞转移的抑制作用

目的:探讨苦参碱衍生物M19对于肝细胞癌和黑色素瘤细胞转移的抑制作用。方法:肝癌细胞Hep3B、MHCC-LM3和黑色素瘤细胞B16F10经M19处理后,检测肿瘤细胞体外迁移能力。建立C57BL/6小鼠黑色素瘤B16F10和裸鼠肝细胞癌MHCC-LM3转移模型,经M19体内给药后,观察肿瘤细胞肝、肺转移情况。结果:M19能浓度依赖性地抑制肝癌细胞和黑色素瘤细胞迁移。M19体内给药使B16F10细胞在小鼠肺的转移减少,且还能抑制MHCC-LM3细胞在裸鼠肺和肝的转移。结论:M19能在体内外抑制肝细胞癌和黑色素瘤细胞的转移。     

反义STAT3对肿瘤细胞增殖抑制和诱导凋亡的作用

背景与目的：研究表明STAT3蛋白在多种肿瘤组织或细胞中高表达。STAT3蛋白可能参与了肿瘤的形成和发生。本文拟研究STAT3蛋白在鼠黑色素瘤细胞B16、人肝癌细胞SMMC-7721、人肝癌细胞HepG-2、人肺癌细胞A549、人宫颈癌HeLa细胞株中表达和活化情况,研究反义STAT3寡核苷酸对B16细胞的增殖抑制和促凋亡作用,为进一步反义药物设计及应用于辐射领域作前期研究。方法：利用Western blot检测所选几种肿瘤细胞的STAT3蛋白表达和磷酸化情况、反义干涉前后B16细胞中STAT3蛋白表达和磷酸化活化的变化情况,MTT法检测细胞增殖变化,利用Hoechst33258染色对细胞凋亡作形态学上的观察．用Annexin V／PI复染结合流式细胞仪检测细胞早期凋亡。结果：所研究的几种肿瘤细胞中均可检测到STAT3蛋白的高表达和磷酸化;反义STAT3转染后,B16细胞中STAT3蛋白的表达量及磷酸化水平均有下降;转染后48h,在0到200nmol／L范围内,反义核酸浓度越高。对B16细胞的增殖抑制效应越强,但是并不能够完全抑制肿瘤细胞的增殖（P〈0．01）。寡核苷酸浓度超过250nmol／L时．正义对照也表现出一定的增殖抑制作用（P〈0．05）;转染后不同时间内检测,结果表明转染后24h反义核酸即开始表现出一定的增殖抑制效应,48h起表现出明显的抑制效应;反义转染后,检测各组细胞早期凋亡率：对照组早期凋亡率为5．52％．反义400、800、2000nmol／L组早期凋亡率分别为8．22％、9．99％．16．97％,正义对照400、800、2000nmol／L组早期凋亡率分别为5．87％、5．36％、13．31％。统计分析表明反义寡核苷酸与B16细胞作用后能够促进细胞的早期凋亡（P〈0．01）,正义低浓度转染组（400、800nmol／L组）与对照组无明显差别（P〉0．05）,而对照组与正义2000nmol／L组相比,细胞的早期凋亡率也有统计学差异（P〈0．01）。结论：B16、SMMC-7721、HepG-2、A549、HeLa等恶性肿瘤细胞株中STAT3蛋白高表达并且可检测到磷酸化水平的增高;反义转染后B16细胞中STAT3蛋白的表达和磷酸化水平降低．细胞增殖受到明显抑制。细胞的凋亡增加．表明STAT3可能成为肿瘤治疗新的分子靶位。     

蟾蜍灵对B16细胞增殖及凋亡的影响

目的 研究中药蟾蜍灵对B16细胞增殖和凋亡的影响,探讨蟾蜍灵对黑色素瘤的抑制作用。方法 采用MTT法测定蟾蜍灵对B16细胞活力的影响;Hoechst 33342荧光染色检测细胞形态学变化;流式细胞术检测蟾蜍灵对细胞周期的影响。结果 蟾蜍灵对B16细胞的增殖有抑制作用,且呈浓度和时间的依赖性。蟾蜍灵作用24、48和72 h的IC50值分别为37.80、6.00和9.12 μmol/L。荧光染色显示蟾蜍灵作用于B16细胞24 h后,细胞呈现典型的凋亡形态特征;细胞周期分析显示,蟾蜍灵处理组S期细胞降低,蟾蜍灵可引B16细胞G0/G1期阻滞,而对G0/G1期阻滞随作用时间延长而增强。结论 蟾蜍灵可能通过阻滞B16细胞增殖周期进程而诱导凋亡。     

没食子酸诱导ROS积蓄介导黑色素瘤B16-F10细胞内源性凋亡及周期阻滞北大核心

目的:探究没食子酸诱导活性氧(reactive oxygen species,ROS)积蓄介导黑色素瘤B16-F10细胞凋亡及周期阻滞的作用机制。方法:以梯度浓度的没食子酸作用于黑色素瘤B16-F10细胞,采用MTT法检测没食子酸对细胞生长的影响,平板克隆技术检测细胞克隆形成率,Transwell实验检测细胞迁移及侵袭能力,ROS Assay Kit检测B16-F10细胞内ROS水平,线粒体膜电位检测试剂盒检测细胞膜电位的变化,Hoechst 33258荧光染色法进行细胞形态学检测,流式细胞术检测细胞凋亡及细胞周期阻滞水平,Western blot检测细胞内相关蛋白水平的变化。结果:结果显示,没食子酸明显抑制B16-F10细胞的生长,且具有浓度依赖性。没食子酸作用后,B16-F10细胞增殖、迁移及侵袭能力明显下降,细胞内ROS水平明显升高,线粒体膜电位明显下降;细胞数减少,细胞凋亡率增加,G_(0)/G_(1)期细胞数明显增多;细胞内凋亡相关蛋白Bax、Cytochrome C、Caspase-9以及Caspase-3表达量增加,而Bcl-2表达量减少;周期相关蛋白Chk2、p53、p21表达量明显增加,CyclinE1、CDK2表达量减少。结论:没食子酸作用于黑色素瘤B16-F10细胞后,通过诱导ROS积蓄,引起B16-F10细胞内源性凋亡及周期阻滞。     

Simultaneous blockade of VEGFR-1 and VEGFR-2 activation is necessary to efficiently inhibit experimental melanoma growth and metastasis formation

Metastasis continues to be the major cause of morbidity and mortality in malignant melanoma. In our study, we explored whether inhibition of VEGFR-1 or VEGFR-2 signaling conveys distinct suppressive effects on B16 melanoma subcutaneous growth and metastasis formation. The inhibition of VEGFR-1 or -2 alone had no significant influence on both melanoma growth and metastasis formation. In contrast, simultaneous blockade of VEGFR-1 and -2 signaling strongly suppressed progression in both B16 tumor models. There was no expression of VEGFR-1 or -2 detectable on the B16 cells used, excluding the melanoma cells as direct therapeutic targets. Analyzing the contribution of progenitor-like cells during melanoma metastasis formation, we observed an enhanced proliferation and mobilization of VEGFR-1+ myeloid and VEGFR-2+ endothelial cells with progenitor potential by the induction of melanoma lung metastasis, which was not influenced by interference with VEGFR signaling. These results indicate that the antimetastatic effects exerted by combined inhibition of VEGFR-1 and -2 signaling were mediated via targeting cell populations other than progenitors only. Sole inhibition of VEGFR-1 signaling led to a strong reduction of the CD45-positive inflammatory infiltrate in the tumor tissue. However, the formation of lung metastasis was not affected, indicating that inhibition of the inflammatory response was not sufficient to efficiently block B16 melanoma metastasis development. Taken together, our data suggest that in the utilized B16 tumor models the blockade of both the inflammatory and the VEGFR-2-dependent angiogenic response are necessary to effectively inhibit solid tumor growth and formation of lung metastasis by B16 melanoma cells.     

How Do Bisphosphonates Inhibit Bone Metastasis In Vivo?

Bisphosphonates are potent inhibitors of osteoclast-mediated bone resorption and have demonstrated clinical utility in the treatment of patients with osteolytic bone metastases. They also exhibit direct antitumor activity in vitro and can reduce skeletal tumor burden and inhibit the formation of bone metastases in vivo. However, whether such effects are caused by a direct action of bisphosphonates on tumor cells or indirectly through inhibition of bone resorption remains unclear. To address this question, we used here a structural analog of the bisphosphonate risedronate, NE-58051, which has a bone mineral affinity similar to that of risedronate, but a 3000-fold lower bone antiresorptive activity. In vitro, risedronate and NE-58051 inhibited proliferation of breast cancer and melanoma cell lines. In vivo, risedronate and NE-58051 did not inhibit the growth of subcutaneous B02 breast tumor xenografts or the formation of B16F10 melanoma lung metastasis. In contrast to NE-58051, risedronate did inhibit B02 breast cancer bone metastasis formation by reducing both bone destruction and skeletal tumor burden, indicating that the antitumor effect of bisphosphonates is achieved mainly through inhibition of osteoclast-mediated bone resorption.     

Volatile isoprenoid constituents of fruits, vegetables and herbs cumulatively suppress the proliferation of murine B16 melanoma and human HL-60 leukemia cells.

Substantial evidence from epidemiological studies supports the inverse association between the intake of fruits, vegetables and other plant products and cancer incidence. Cancer-preventive constituents of fruits and vegetables may inhibit carcinogen activation, enhance carcinogen detoxification, prevent carcinogens from interacting with critical target sites, or impede tumor progression. These activities, however, are achievable only when levels of individual bioactive constituents reach beyond those attainable from a normal balanced diet. Isoprenoids, a broad class of mevalonate-derived phytochemicals ubiquitous in the plant kingdom, suppress the proliferation of tumor cells and the growth of implanted tumors. A search for volatile isoprenoid constituents of food products spanning seven plant families identified 179 isoprenoids. Of these, 41 purchased from commercial sources were screened for efficacy in suppressing the proliferation of murine B16 melanoma cells. Individual isoprenoids suppressed the proliferation of B16 and HL-60 promyelocytic leukemia cells with varying degrees of potency. Cell cycle arrest at the G(0)-G(1) phase and apoptosis account, at least in part, for the suppression. Blends of isoprenoids suppressed B16 and HL-60 cell proliferation with efficacies equal to the sum of the individual impacts. These findings suggest that the cancer-protective property of fruits, vegetables, and related products is partly conferred by the cumulative impact of volatile isoprenoid constituents.     

Accelerated growth of B16BL6 tumor in mice through efficient uptake of their own exosomes by B16BL6 cells

Exosomes are extracellular vesicles released by various cell types and play roles in cell–cell communication. Several studies indicate that cancer cell‐derived exosomes play important pathophysiological roles in tumor progression. Biodistribution of cancer cell‐derived exosomes in tumor tissue is an important factor for determining their role in tumor proliferation; however, limited studies have assessed the biodistribution of exosomes in tumor tissues. In the present study, we examined the effect of cancer‐cell derived exosomes on tumor growth by analyzing their biodistribution. Murine melanoma B16BL6‐derived exosomes increased the proliferation and inhibited the apoptosis of B16BL6 cells, which was associated with an increase and decrease in the levels of proliferation‐ and apoptosis‐related proteins, respectively. GW4869‐induced inhibition of exosome secretion decreased the proliferation of B16BL6 cells, and treatment of GW4869‐treated cells with B16BL6‐derived exosomes restored their proliferation. Next, we treated B16BL6 tumors in mice with B16BL6‐derived exosomes and examined the biodistribution and cellular uptake of these exosomes. After the intratumoral injection of radiolabeled B16BL6‐derived exosomes, most radioactivity was detected within the tumor tissues of mice. Fractionation of cells present in the tumor tissue showed that fluorescently labeled exosomes were mainly taken up by B16BL6 cells. Moreover, intratumoral injection of B16BL6‐derived exosomes promoted tumor growth, whereas intratumoral injection of GW4869 suppressed tumor growth. These results indicate that B16BL6 cells secrete and take up their own exosomes to induce their proliferation and inhibit their apoptosis, which promotes tumor progression.     

Apoptosis Induced by Ginsenoside Rg3 in a Human Bladder Carcinoma Cell Line

OBJECTIVE This study was conducted to explore the effect of Rg3 on inhibition of proliferation and induction of apoptosis in bladder cancer cells. METHODS The EJ bladder cancer cell line was treated with Rg3 at various concentrations. Cell proliferation was measured by the MTT assay. Morphological changes in the cells were observed by fluorescent staining using Hoechst 33258. The cell cycle and apoptotic rate were analyzed by flow cytometry (FCM) and the expression of caspase-3 in cells was detected by immunocytochemistry. DMA ladder analysis was conducted by agarose gel electrophoresis. RESULTS Rg3 inhibited proliferation of EJ cells in a concentration-dependent manner, resulting in an IC50 for Rg3 at 48 h of 125.5μg/ml. When treated with 150μg/ml of Rg3 for 24 h and 48 h, the cells showed apoptotic morphological characteristics including condensed chromatin, nuclear fragmentation, apoptotic bodies and bright fluorescent granules as well as a higher caspase-3 expression. The FCM assay indicated that Rg3 altered the cell cycle and induced apoptosis of the EJ cells, when treated for 24 h and 48 h with 75μg/ml of Rg3 as well as for 48 h with 150μg/ml. The percentages of cells in the S phase and the G2/M transition were increased, whereas the percentages of cells in the G0-G1 transition were decreased. The apoptotic rates were increased from (1.05±0.17)% in the control group cells to (8.41±0.98)%,(18.57±2.20)% and (33.98±1.64)% respectively. Significant changes in the DNA ladders, showed that the effects of Rg3 were displayed in a dose and time dependent manner. CONCLUSION The results suggest that Ginsenoside Rg3 exerts an inhibitory effect on proliferation of EJ cells by inducing apoptosis.     

Norcantharidin induces melanoma cell apoptosis through activation of TR3 dependent pathway

Norcantharidin (NCTD) has been reported to induce tumor cell apoptosis. However, the underlying mechanism behinds its antitumor effect remains elusive. We have previously shown that TR3 expression is significantly decreased in metastatic melanomas and involved in melanoma cell apoptosis. In this study, we showed that NCTD inhibited melanoma cell proliferation and induced apoptosis in a dose related manner. NCTD induced translocation of TR3 from nucleus to mitochondria where it co-localized with Bcl-2 in melanoma cells. NCTD also increased cytochome c release from mitochondria to the cytoplasm. These changes were accompanied by increased expression of Bax and cleaved caspase-3 along with decreased expression of Bcl2 and NF-κB2. The effects of NCTD were inhibited by knockdown of TR3 expression using TR3 specific shRNA in melanoma cells. Furthermore, NCTD significantly decreased tumor volume and improved survival of Tyr::CreER; BRAF(Ca/+); Pten(lox/lox) transgenic mice. Our data indicates that NCTD inhibits melanoma growth by inducing tumor cell apoptosis via activation of a TR3 dependent pathway. These results suggest that NCTD is a potential therapeutic agent for melanoma.     

RNA干扰抑制高迁移率族蛋白-1表达对人视网膜母细胞瘤细胞增殖和凋亡的影响

目的:研究siRNA抑制高迁移率族蛋白-1(high mobility group protein box-1, HMGB1)表达对人视网膜母细胞瘤细胞增殖和凋亡的影响。方法:RT-PCR和Western blot检测HMGB1在人视网膜母细胞瘤中的表达。体外化学合成靶向HMGB1 siRNA,RT-PCR和Western blot检测其抑制效率。MTT法检测HMGB1沉默后Y79细胞的增殖情况。Caspase-3活性检测试剂盒检测HMGB1沉默后Y79细胞的凋亡情况。采用流式细胞仪来分析细胞周期的分布以及细胞凋亡率的变化。结果:HMGB1 mRNA和蛋白在人视网膜母细胞瘤细胞中高表达,siRNA抑制HMGB1表达后,Y79细胞增殖抑制,促进凋亡。结论:抑制HMGB1的表达可以降低人视网膜母细胞瘤细胞的增殖,并促进其凋亡,为人视网膜母细胞瘤的生物学治疗提供新的思路。     

小剂量X线全身照射对不同荷瘤时间小鼠的抗肿瘤转移效应

采用肿瘤血道转移模型，选用Ｂ１６黑色素瘤和Ｌｅｗｉｓ肺癌（ＬＬＣ）两种类型细胞，就小剂量Ｘ线全身照射对不同荷瘤时间小鼠的抗肿瘤转移效应进行研究。结果发现，于静脉注射Ｂ１６黑色素瘤或ＬＬＣ细胞后２４ｈ（Ｂ组）或第１３天（Ｃ组）接受７５ｍＧｙＸ线全身照射小鼠的肿瘤肺转移结节数明显低于未照射组（Ａ组）（Ｐ＜０．０５～０．００２）。比较不同照射时间的抗肿瘤转移效果时发现，静注Ｂ１６黑色素瘤的Ｂ组肺转移结节数仅为Ｃ组的５９％，而ＬＬＣ的Ｂ组则为其Ｃ组的７１％。检测注射Ｂ１６黑色素瘤第１４天各组小鼠的免疫功能时发现，Ｂ、Ｃ两组ＮＫ、ＬＡＫ细胞活性及脾细胞对ＩＬ－２反应性明显高于Ａ组（Ｐ＜０．０５～０．００１）。上述结果提示：小剂量Ｘ线全身照射提高荷瘤小鼠的免疫功能可能是其抗肿瘤转移作用的主要机制之一。