流式细胞术对不同肿瘤细胞表面所表达血小板免疫相关抗原的检测

目的：研究不同肿瘤细胞表面血小板免疫相关抗原的表达。方法：利用流式细胞术观察了ＰＧＣＬ３、ＰＡａ、ＰＧ－３、ＰＣ－３Ｍ、ＭＧＣ８０３、ＥＳＣＬ、ＢｅＬ、ＴＣＴ、ＫＢ、Ａ２７８０、ＣＣＡ８０１共１１种人肿瘤细胞,其中包括二对高低不同转移能力的人肺癌（ＰＧＣＬ３和ＰＡａ）和人前列腺癌（ＰＧ－３和ＰＧ－３Ｍ）细胞阳性表达不同血小板免疫相关抗原的细胞数及其肿瘤细胞表面抗原表达的平均荧光强度。结果：１１种人肿瘤细胞膜表面均有ＣＤ９、ＣＤ６３、ＣＤ４２ａ和ＴＳＰ,等血小板免疫相关抗原不同程度的表达,在ＭＧＣ８０３细胞膜表面发现有ＣＬ８６较强的表达,ＣＤ４１、ＣＤ４２ｂ、ＣＤ６１和ＣＤ６２均未发现表达。１１种人肿瘤细胞系中ＣＤ９＋、ＣＤ４２ａ＋、ＣＤ６３＋、ＴＳＰ＋细胞所占的比例各不相同,不同肿瘤细胞系每个抗原阳性细胞抗原表达的荧光强度也不同。与高转移ＰＧＣＩ３和ＰＧ－３Ｍ细胞相比,ＣＤ９在低转移细胞系ＰＡａ和ＰＧ－３上有较高的表达,ＣＤ４２ａ、ＴＳＰ有相对低的表达。ＣＤ４２ａ＋和ＴＳＰ＋细胞数和表达强度在高转移ＰＧＣＬ３和ＰＧ－３Ｍ细胞系均要高于低转移的ＰＡａ和ＰＧ－３;ＣＤ６３＋细胞数高转移ＰＧ－３Ｍ细胞系要比低转移     

不同转移潜能的人肿瘤细胞系金属蛋白酶活性分析

目的探讨不同转移潜能的人类肿瘤细胞的金属蛋白酶（ＭＭＰｓ）活性与其侵袭转移潜能的相关性。方法分别选取具有不同转移潜能的人类肺癌细胞系（ＰＧ、ＰＡａ、ＢＥ１、ＣＬ３、ＬＨ７）、黑色素瘤细胞系（ＷＭ３５、ＷＭ１３４１ｂ、ＷＭ９８３ａ、ＷＭ４５１）及前列腺癌细胞系（ＰＣ，ＰＣ３Ｍ），经细胞培养，条件培养基的收集与浓缩，利用明胶Ｚｙｍｏｇｒａｐｈｙ法检测以上各组细胞ＭＭＰ２和ＭＭＰ９的产生及活性差异，并将这种差异与各自的转移潜能联系起来。结果转移能力相对较高的细胞系产生ＭＭＰｓ的能力相应强于转移能力相对较低者：ＰＧ高于ＰＡａ，ＢＥＩ高于ＣＬ３和ＬＨ７。在进展期黑色素瘤株ＷＭ９８３ａ和转移瘤株ＷＭ４５１出现了ＭＭＰ９的表达，早期瘤株则无。前列腺瘤细胞ＰＣ３的转移性克隆ＰＣ３Ｍ的条件培养基中有较高的ＭＭＰ９活性。结论肿瘤细胞的侵袭转移潜能与其产生ＭＭＰｓ的能力密切相关。     

全反式维甲酸对克隆化高转移人肺癌细胞浸润和转移的抑制作用

用５μｍｏｌ／Ｌ和１０μｍｏｌ／Ｌ全反式维甲酸（ＲＡ）处理克隆化高转移人肺癌细胞（ＰＧＣＬ３）５天后，细胞的体外生长速度、穿过Ｂｏｙｄｅｎ小室人工基底膜胶的浸润能力都受到一定的抑制，其中尤以１０μｍｏｌ／ＬＲＡ的作用明显。实验性转移显示，ＲＡ体外处理ＰＧＣＬ３细胞可在一定程度上降低其实验性转移的能力。此外通过ＤＮＡ－ＲＮＡ斑点杂交还发现ＰＧＣＬ３细胞经１０μｍｏｌ／ＬＲＡ处理５天后，人组织金属蛋白酶抑制剂基因（Ｔｉｍｐ－１和Ｔｉｍｐ－２）表达有一定水平的增高，这有助于进一步阐明ＲＡ抑制肿瘤细胞浸润和转移的机理。     

CD自杀基因联合GM-CSF基因治疗的抗肿瘤作用及免疫机理

目的研究自杀基因与粒细胞－巨噬细胞集落刺激因子（ＧＭ－ＣＳＦ）基因联合治疗抗肿瘤作用及免疫机理。方法小鼠皮下接种黑色素瘤Ｂ１６Ｆ１０细胞３天后,分别在肿瘤局部直接注射表达小鼠ＧＭ－ＣＳＦ的重组腺病毒ＡｄＧＭ－ＣＳＦ和表达大肠杆菌胞嘧啶脱氨酶（ＣＤ）基因的腺病毒Ａｄ－ＣＤ,然后连续１０天腹腔注射５氟胞嘧啶（５ＦＣ）（ＡｄＣＤ／５ＦＣ／ＡｄＧＭＣＳＦ组）、单用ＡｄＣＤ／５ＦＣ组、单用ＡｄＧＭ－ＣＳＦ组、注射对照病毒ＡｄｌａｃＺ／５ＦＣ组或ＰＢＳ组。结果与接受ＡｄＣＤ／５ＦＣ、ＡｄＧＭ－ＣＳＦ、ＡｄｌａｃＺ／５ＦＣ或ＰＢＳ治疗的荷瘤小鼠比较,经联合治疗后荷瘤小鼠皮下肿瘤结节的生长明显受到抑制,荷瘤小鼠的存活期明显延长（Ｐ＜０．０１）。经ＡｄＣＤ／５ＦＣ／ＡｄＧＭＣＳＦ联合基因治疗后,肿瘤瘤体内或瘤周有大量树突状细胞、ＣＤ８＋Ｔ细胞浸润,黑色素瘤细胞表达ＭＨＣ－Ⅰ和Ｂ７－１分子明显增加,荷瘤小鼠脾细胞对Ｂ１６Ｆ１０黑色素瘤细胞特异性杀伤功能增强。结论联合应用自杀基因和ＧＭ－ＣＳＦ基因转移可以直接杀伤肿瘤细胞,又可提高机体对肿瘤的免疫应答,两者可协同发挥抗肿瘤作用     

人B细胞系Raji细胞ClqR的特性

应用Ｃｅｌｌ－ＥＬＩＳＡ，ＦＡＣＳ，ＲＢＡ及ＷＢ等技术，对人Ｂ细胞系Ｒａｊｉ细胞ＣｌｑＲ的特性进行了研究。Ｒａｊｉ细胞可结合外源Ｃｌｑ，其与ＦＩＴＣ－ＣｌｑＲ的结合可为过量未标记Ｃｌｑ的阻断。在生理离子强度和温度条件下，＾１２５Ｉ－Ｃｌｑ与细胞的结合特异，剂量信号３，可饱和及可逆性，反应于５０－６０ｍｉｎ达平衡，服从假一级动力学；达平衡时，Ｃｌｑ结合位点数／细胞为１．６×１０＾６，Ｋａ值８．５×１     

肺癌细胞粘弹特性与超微结构的相关性研究

目的：肺癌是高恶性和高死亡率的肿瘤之一,作者力图从生物力学角度揭示肺 某些生物学特性。材料与方法：本文结合超微结构观察,采用微管吸吮技术定量测定体外培养的低转移人肺腺癌（ＰＡａ）细胞和高转移人肺巨细胞癌（ＰＧ）细胞在长春新碱（ＶＣＲ）作用下的是特性。结果：肺癌细胞粘弹性,在未使用ＶＣＲ前为ＰＡａ细胞大于ＰＧ细胞;随ＶＣＲ的使用和剂量增加,其在ＰＡａ细胞呈浓度依赖性下降,在ＰＧ细胞则表现为低ＶＣＲ浓     

人外周血树突状细胞在LAK抗HPBALL细胞中作用的研究

为探讨树突状细胞（ＤＣ）在ＬＡＫ抗ＨＰＢＡＬＬ细胞中的作用，采用多因素、多水平的杀伤试验，同时以光镜、电镜观察ＤＣ、ＬＡＫ、ＨＰＢＡＬＬ相互作用的形态特征及ＤＮＡ断端标记法检测瘤细胞是否凋亡。结果表明：（１）ＤＣ无直接杀伤ＨＰＢＡＬＬ作用。（２）５×１０５～１×１０７／ＬＤＣ有增强不同Ｅ／ＴＬＡＫ杀伤活性的趋势，而１×１０７～５×１０７／ＬＤＣ对ＬＡＫ活性有抑制趋势。（３）ＤＣ、ＬＡＫ杀伤ＨＰＢＡＬＬ的最佳组合条件为：ＤＣ培养４ｄ、浓度５×１０６／Ｌ，ＬＡＫＥ／Ｔ＝１０／１，ｒＩＬ－２＝０。（４）光镜、电镜下均可见ＤＣ的突起与ＬＡＫ、ＨＰＢＡＬＬ细胞紧密接触形成细胞簇。（５）ＤＮＡ断端标记法显示瘤细胞呈末端脱氧核糖核酸转移酶阳性反应。结论：ＤＣ对ＬＡＫ杀伤ＨＰＢＡＬＬ活性具有双向调节作用     

肺癌p53基因突变与临床病理关系的研究

目的；探讨肺癌Ｐ５３基因突变与临床之关系：方法：采用ＰＣＲ－限制性惩段长度多态性分析法（ＰＣＲ－ＲＦＬＰ）检测４７ 肺癌Ｐ５３基因２４９位密码为突变；结果：非小细胞肺癌（ＮＳＣＬＳ）Ｐ５３基因２４９位密码子突变率２４．２４％，小细胞肺癌（ＳＣＬＣ）突变率为０（０／１４）。Ｐ５３基因２４９位密码了点突变与肺癌分期、组织分化、吸烟无关，与ＮＳＣＬＣ淋巴结转移有关；结论：Ｐ５３基因２４９位密码子突变是Ｎ     

肝素增强血小板生成素对巨核细胞增殖的作用

目的和方法：为了探讨巨核细胞增殖调控,我们研究了肝素对重组人血小板生成素刺激ＢＡＬＢ／ｃ小鼠巨核系祖细胞（ＣＦＵ－ＭＫ）和人巨核细胞系－红白细胞白血病细胞 作用。采用固体和液体培养、ＣＦＵ－ＭＫ－乙酰胆碱脂酶染色和５－溴－２‘－脱氧尿嘧啶核苷（５－ＢｒｄＵ）－酶联免疫吸附等方法,观察了ＣＦＵＭＫ和ＨＥＬ细胞集落数以及ＨＥＬ细胞的吸光度。结果：在培养基中加入ｒｈＴｐｏ１００ｎｇ／ｍｌ和肝素２．５Ｕ／     

抗氧化剂PDTC抑制氧化的低密度脂蛋白诱导的人肾小球系膜细胞NF_(-k)B活化

目的 研究氧化的低密度脂蛋白（Ｏｘ－ＬＤＬ）对体外培养的人肾小球系膜细胞（ＨＭＣ）核因子－ＫＢ（ＮＦ－ＫＢ）活化的影响，以及抗氧化剂毗咯二硫氨基甲酸酯（Ｐ ＤＴＣ）对ＮＦ－ＫＢ活化的抑制作用，探讨ＯＸ－ＬＤＬ介导肾损害的基因调控机制及抗氧化剂ＰＤＴＣ防治脂质肾损害的可能性。方法 将Ｏｘ－ＬＤＬ或ＰＤＴＣ与ＨＭＣ共培养后，提取细胞核蛋白进行凝胶迁移率变动分析（ＥＭＳＡ）检测ＮＦ－ＫＢ的活化，用细胞ＥＬＩＳＡ法检测细胞内ＩＫＢα蛋白含量的变化，反映ＩＫＢα的降解及免疫组化染色检测细胞内的Ｐ６５向核转位。结果 正常对照组未见ＮＦ－ＫＢ活化，当用不同浓度（１０、２５、５０及１００ｍｇ／Ｌ）的Ｏｘ－ＬＤＬ，刺激肾小球系膜细胞 ｌｈ后，均可引起细胞 ＮＦ－ＫＢ活化及 ＩＫＢα降解。与对只组相卜较差异显著（ｐ＜０．０５），以５０ｍｇ／Ｌ 的ＯＸ－ＬＤＬ刺激ＨＭＣ１ｈ，ＮＦ－ＫＢ活化及 ＩＫＢα降解最明显。ＮＦ－ＫＢ活化的同时，伴有Ｐ６５由胞浆向胞核的转位。１００μｍｏｌ／Ｌ ＰＤＴＣ，能明显抑制 ＮＦ－ＫＢ的活化、ＩＫＢα降解（ｐ＜０．０１）及 Ｐ６５的核转位。结论Ｏｘ－ＬＤＬ。能诱导ＨＭＣ的ＩＫＢαａ降解、Ｐ６５的核转位，最终使Ｎ     

Comparison of the chemotactic responsiveness of two fibrosarcoma subpopulations of differing malignancy.

There are several points of similarity between the processes of cancer metastasis and inflammation. In both, cells circulate in the vasculature, arrest, and cross vessel walls, thereby entering the extravascular tissues. In vitro, leukocytes and some, but not all, tumor cells exhibit chemotaxis. Since the chemotactic response of leukocytes effect their transvascular migration, we propose that chemotactic responsiveness contributes to the ability of circulating tumor cells to localize in extravascular tissues. This study was done to seek a relationship between chemotactic responsiveness of tumor cells and their behavior in vivo. Two subpopulations of cells were isolated from a methylcholanthrene-induced fibrosarcoma. The two cell lines were compared with regard to their biologic behavior in vivo and their chemotactic responsiveness in vitro. In vivo one subpopulation was highly malignant. An injection of 2.0 x 10(5) cells into the footpad of syngeneic mice led to the development of primary tumors in 87% of the animals and lung metastases in 61% of the animals with primary tumors. This line demonstrated chemotaxis to a factor that behaved similarly in gel filtration and showed immunologic reactivity similar to that of a previously described tumor cell chemotactic factor derived from the fifth component of complement. In contrast, an injection of the same number of cells from the second subpopulation of fibrosarcoma cells led to the development of primary tumors in only 12% of syngeneic mice, and lung metastases did not occur. Neither this subpopulation nor normal embryonic fibroblasts demonstrated chemotactic responsiveness. We postulate that the ability of tumor cells to respond to specific chemotactic stimuli may be one of the many unique properties which distinguish malignant from benign tumor cells. This is the first report documenting the chemotactic responsiveness of non-ascites tumors and fibrosarcomas.     

联胺对内皮细胞表达巨噬细胞炎性蛋白-1α的影响

目的观察联胺能否诱导培养的人脐静脉内皮细胞表达和分泌巨噬细胞炎性蛋白-1α (MIP-1α)及其意义.方法使内皮细胞暴露于不同浓度联胺4 h,以核酸酶S1保护分析法检测内皮细胞内MIP-1α mRNA,以细胞酶联免疫吸附实验测定内皮细胞的MIP-1α蛋白表达.同时收集内皮细胞条件培养基,用Boyden小室微孔滤膜法检测MIP-1α对外周血单核细胞的趋化活性.结果内皮细胞MIP-1α mRNA在5 μmol/L联胺组的表达是对照组的3.4倍, 差异具有显著性(t=8.70, P<0.05).1、5、10 μmol/L联胺组MIP-1α蛋白的表达分别是对照组的1.9倍、2.2倍、1.7倍,方差分析显示有统计学意义(F=35.65, P<0.05).趋化实验显示,5 μmol/L联胺组内皮细胞的条件培养基引起单核细胞的迁移距离[(99.50±4.31) μm]显著高于无联胺组[(66.47±3.25) μm]、化学促动组[(67.03±6.83) μm]和随机移动组[(65.40±3.36) μm,F=404.31, P<0.05],提示经联胺刺激的条件培养基内含有具趋化活性的物质.加入山羊抗人MIP-1α多克隆抗体后,联胺组条件培养基所致的单核细胞迁移距离降至(82.80±6.88) μm(F=192.25, P<0.05),说明经联胺刺激的条件培养基内含有具趋化活性的MIP-1α.结论脂质过氧化诱导剂联胺可促进内皮细胞产生高水平具趋化活性的MIP-1α, 并可能通过招引外周血单核细胞迁入动脉内膜, 而在动脉粥样硬化过程中发挥重要作用.     

The chemotactic response of tumor cells. A model for cancer metastasis.

Injection of a C5-derived chemotactic factor for tumor cells into the peritoneal cavities of Sprague-Dawley rats induced diffuse mesenteric metastasis following the intravenous injection of Walker carcinosarcoma cells. Intraperitoneal injections of culture medium, histamine, or of trypsin-treated albumin resulted in many fewer metastases. Intraperitoneal injections of the chemotactic factor, unlike histamine, did not alter mesenteric vasopermeability as measured by the exudation of Evans blue into the mesentery. In vitro, tumor cells responded to the chemotactic factor by demonstrating directed migration in the Boyden chamber, by volume changes, measurable in the Coulter counter, and by demonstrating an increased adherence to nylon fibers. These phenomena are similar to the behavior of neutrophils in the presence of their chemotactic factors. All the responses in vitro were markedly depressed by the addition of 2-deoxyglucose, while the cell swelling response was slightly enhanced by cytochalasin B (again similar to the responses of leukocytes). The data suggest that movement of tumor cells from the circulation may be under chemotactic influence in the manner similar to the responsiveness of neutrophils to leukotactic stimuli in vivo.     

RAB5A反义RNA对人肺腺癌细胞系侵袭转移影响的体外研究

目的　已知RAB5A基因过表达与人非小细胞肺癌恶性表型形成相关,本研究在此基础上进一步探 讨该基因过表达在人肺腺癌恶性演进中的作用。　方法　将RAB5A反义表达载体稳定转染入高浸润人肺腺癌细 胞系L18和高转移人肺腺癌细胞系95D中,采用重组基底膜侵袭、与基底膜成分黏附能力测定、趋化运动能力测 定、明胶酶分泌与活性检测等体外实验方法观察转染前后细胞生物学特性的改变。　结果　RAB5A反义RNA稳 定转染后L18细胞趋化运动和侵袭基底膜能力显著降低(P<0.05),明胶酶活性检测发现转染后细胞MMP 2的分 泌能力明显减弱;稳定转染后95D细胞趋化运动和侵袭基膜能力显著降低(P<0.05)。　结论　体外实验显示, RAB5A基因过表达对肿瘤细胞的趋化运动能力和侵袭重组基底膜能力起重要作用,进一步提示RAB5A基因过表 达在人肺腺癌的侵袭转移过程中发挥一定作用。     

瘤内注射新城鸡瘟病毒的抗癌效应及其机理研究

本文报道了瘤内注射新城鸡瘟病毒（ＮＤＶ）对６１５系小鼠乳腺癌（Ｃａ７６１）治疗作用，并初步探讨了其抗瘤机理。结果表明：单纯ＮＤＶ瘤内注射有一定抑瘤作用，抑瘤率达３５．３％；联合环磷酸胺化疗，可使其抑瘤率提高至７４．１％，明显优于化疗对照组（Ｐ＜００１），而该病毒腹腔注射则无效。治疗后带瘤小鼠的瘤细胞电镜显示：ＮＤＶ颗粒主要位于瘤细胞的胞浆内及胞膜上。Ｗｅｓｔｅｒｎ印迹检测细胞膜上有该病毒相关抗原的表达，其分子量分别是：８０ｋＤ、５５ｋＤ、４９ｋＤ、３８ｋＤ、２９ｋＤ。进一步以ＭＴＴ比色分析法证实：治疗后小鼠脾细胞的ＣＴＬ杀伤活性明显增强，且具有一定的肿瘤特异性，提示ＮＤＶ瘤内注射可能通过肿瘤细胞“体内异种化”而增强机体的主动特异性抗癌免疫反应。     

IFN-γ production by lung NK cells is critical for the natural resistance to pulmonary metastasis of B16 melanoma in mice

NK cells are effector lymphocytes playing a critical role in the natural resistance against tumors. However, the precise mechanisms underlying NK cell-mediated natural resistance against tumor metastasis are still unrevealed. B16 cells, mouse melanoma cells, were resistant to freshly isolated NK cell-mediated killing; nevertheless, NK cells were critical for natural resistance against experimental lung metastasis of B16 cells. We found that lung metastasis was increased significantly in IFN-γ(-/-) mice but not pfp(-/-), IFN-αR(-/-), or IL-12/IL-18(-/-) mice. Interestingly, freshly isolated lung NK cells, but not spleen or liver NK cells, displayed augmented IFN-γ production after B16 inoculation. Adoptive transfer of pfp(-/-) NK cells, but not IFN-γ(-/-) NK cells, significantly decreased B16 lung metastasis in IFN-γ(-/-) and pfp/IFN-γ(-/-)mice. Lung metastases of IFN-γRDN B16 was also increased in NK cell-depleted or IFN-γ(-/-) mice, suggesting that the IFN-γ response of host cells was required in the NK cell and IFN-γ-mediated antimetastatic effect. Our results demonstrate that IFN-γ production from lung resident NK cells is a key response in the natural resistance to the experimental lung metastasis of NK cell-resistant tumor cells.     

人鼻咽癌CNE－2Z细胞的不同转移潜能克隆株在严重联合免疫缺陷小鼠体内的检验和比较研究

将人类鼻咽癌不同克隆株的细胞悬液移植在严重联合免疫缺陷（ＳＣＩＤ）小鼠和ＢＡＬＢ／ｃ（ｕｎ／ｕｎ）裸小鼠的颈背侧皮下，５６ｄ后处死全部动物进行观察。结果发现，在ＳＣＩＤ小鼠体内移植后ＣＮＥ２Ｌ２为高转移克隆株，其淋巴结转移率为１００％，肺转移率为７１％；而ＣＮＥ２Ｌ４为低转移克隆株，其肺转移率为１３％，淋巴结未见癌转移。这是从１个细胞母系中新筛选出的１个高转移和１个低转移的癌细胞克隆株。实验结果还显示，同ＢＡＬＢ／ｃ（ｕｎ／ｕｎ）裸小鼠相比，ＳＣＩＤ小鼠的恶性表型的表达能力高。另外，皮下移植时肿瘤细胞的数量可能与转移表型的表达有相关性，移植的瘤细胞数越多，转移率越高，反之亦然。     

Bronchial epithelial cells produce lung fibroblast chemotactic factor: fibronectin

The interaction between the epithelial cells and the subjacent mesenchymal cells in the airway is thought to play a major role during tissue repair after airway injury and lung morphogenesis. To evaluate this interaction, we cultured human lung fibroblasts, and bovine and human bronchial epithelial cells, and determined that bronchial epithelial cell-conditioned medium has a chemotactic activity for lung fibroblasts. This activity had the characteristics of protein: it was nondialyzable, heat-labile, pepsin-labile, acid-stable, and lipid-inextractable. Molecular sieve chromatography on Sephadex G-150 and affinity chromatography on gelatin-Sepharose revealed that there was one peak of chemotactic activity in high molecular weight range, which bound to gelatin, thus suggesting that the chemotactic factor might be fibronectin. Production and secretion of fibronectin into the culture media were demonstrated by biosynthetic incorporation of radioactive amino acid into fibronectin followed by immunoprecipitation on SDS-PAGE and autoradiography. Release into the culture medium was confirmed by ELISA. The identity of fibronectin as the chemotactic activity was confirmed by the addition of antifibronectin antibody to the conditioned medium, which inhibited chemotaxis in dose-dependent manner. Thus, bronchial epithelial cells produce fibronectin which can function as a chemotactic factor for lung fibroblasts. This production of fibronectin by bronchial epithelial cells may play an important role in regulating interaction between the bronchial epithelial cells that line the lumenal surface of the bronchial epithelial wall and the mesenchymal fibroblasts that underlie the bronchial epithelial basement membrane.     

Salmonella reduces tumor metastasis by downregulation C-X-C chemokine receptor type 4

Tumor metastasis is the main reason for the death of most cancer patients. C-X-C chemokine receptor type 4 (CXCR4) has been demonstrated to be overexpressed in numerous types of cancer. CXCR4 selectively binds with stromal cell-derived factor 1 (SDF1), also known as C-X-C family chemokine ligand 12 (CXCL12) (CXCL12/SDF-1), which induced tumor proliferation and metastasis. Recently, the use of conventional cancer treatments had some limitation; bacteria treatment for cancer becomes a trend that overcomes these limitations. Plenty of studies show that Salmonella has anti-tumor and anti-metastatic activity. The current study aimed to investigate Salmonella suppresses CXCR4 protein expression and tumor cell migration ability in B16F10 melanoma and LL2 lung carcinoma cells. Salmonella reduced CXCR4 protein expression through downregulating Protein Kinase-B (Akt)/Mammalian Target of Rapamycin (mTOR) signaling pathway. In cells transfected with constitutively active Akt plasmids, a reverse effect of Salmonella-induced inhibition of CXCR4 was observed. Tumor cells have chemotactic response to CXCL12 in migration assay, and we found that Salmonella reduced tumor chemotactic response after CXCL12 treatment. The C57BL/6 mice were intravenously injected with B16F10 and LL2 cells pre-incubated with or without Salmonella, the tumor size and lung weight of Salmonella group had obviously decreased, indicating anti-metastatic effect that confirmed the findings from the in vitro experiments.