抗HER-2工程抗体chA21对人卵巢癌SKOV3裸小鼠移植瘤血管生成的影响

目的 探讨抗HER-2工程抗体chA21对过表达HER-2的人卵巢癌细胞株SKOV3裸小鼠移植瘤血管生成的影响.方法 建立人卵巢癌SKOV3裸小鼠移植瘤模型,随机分成阴性对照组和chA21组,连续5周尾静脉注射给药,观察肿瘤生长变化;5周后处死裸鼠取下瘤体,利用组织芯片及免疫组化方法结合显微图像分析系统定量检测VEGF、DLL4表达情况,并用CD31免疫组化染色比较两组微血管密度(MVD)值.结果 chA21组肿瘤组织中VEGF、DLL4的表达及MVD值均显著低于阴性对照组(P<0.05).结论 抗HER-2工程抗体chA21能显著抑制人卵巢癌SKOV3裸小鼠移植瘤的血管生成.     

HOXB7 siRNA表达载体在裸鼠体内对人恶性黑色素瘤细胞株的影响

目的探讨转染同源盒第7基因(HOXB7)siRNA质粒表达载体对人恶性黑色素瘤细胞株A375在裸鼠体内生长的影响。方法裸鼠皮下接种人恶性黑色素瘤A375细胞,对2周后形成的瘤块进行分组干预。随机分为生理盐水对照组、阴性质粒组、HOXB7质粒组,观察转染后各组裸鼠移植瘤的生长情况;免疫组化法比较瘤体内微血管密度(MVD)。结果HOXB7质粒组的裸鼠移植瘤块生长慢、体积明显小于生理盐水对照组[(0.134±0.039)cm3比(1.006±0.235)cm3,P<0.05],而阴性质粒组瘤块体积大小与生理盐水对照组无统计学差异[(0.929±0.157)cm3比(1.006±0.235)cm3,P>0.05]。HOXB7质粒组裸鼠体内肿瘤MVD低于生理盐水对照组[(2.8±1.9)比(19.9±5.6),P<0.05],阴性质粒组与生理盐水对照组无统计学差异[(18.1±5.5)比(19.9±5.6),P>0.05]。结论针对HOXB7siRNA质粒表达载体可有效抑制A375细胞裸鼠体内肿瘤生长和瘤内血管生成。     

HOXB7 siRNA表达载体在裸鼠体内对人恶性黑色素瘤细胞株的影响

目的 探讨转染同源盒第7基因(HOXB7)siRNA质粒表达载体对人恶性黑色素瘤细胞株A375在裸鼠体内生长的影响.方法 裸鼠皮下接种人恶性黑色素瘤A375细胞,对2周后形成的瘤块进行分组干预.随机分为生理盐水对照组、阴性质粒组、HOXB7质粒组,观察转染后各组裸鼠移植瘤的生长情况;免疫组化法比较瘤体内微血管密度(MVD).结果 HOXB7质粒组的裸鼠移植瘤块生长慢、体积明显小于生理盐水对照组[(0.134±0.039)cm3比(1.006±0.235)cm3,P＜0.05],而阴性质粒组瘤块体积大小与生理盐水对照组无统计学差异[(0.929±0.157)cm3比(1.006±0.235)cm3,P＞0.05].HOXB7质粒组裸鼠体内肿瘤MVD低于生理盐水对照组[(2.8±1.9)比(19.9±5.6),P＜0.05],阴性质粒组与生理盐水对照组无统计学差异[(18.1±5.5)比(19.9±5.6),P＞0.05].结论 针对HOXB7 siRNA质粒表达载体可有效抑制A375细胞裸鼠体内肿瘤生长和瘤内血管生成.     

碱性成纤维细胞生长因子与卵巢癌的关系

目的　探讨碱性成纤维细胞生长因子 (basic fibroblast growth factor,b FGF)对卵巢癌细胞增殖、浸润和肿瘤血管生成的影响 ,及 b FGF单克隆抗体 (b FGF monoclonal antibody,b FGF- MAb)的治疗作用。　方法　将人卵巢癌细胞株 SKOV3接种于 2 4孔板 ,加入不同浓度的 b FGF,每日行结晶紫染色后测定光密度 (D4 90 )值 ,绘制细胞生长曲线 ;将 SKOV3细胞团接种于铺设有细胞外基质凝胶的 4孔板 ,每日测定癌细胞在凝胶中的浸润距离 ;建立 SKOV3细胞裸鼠皮下移植瘤模型 ,每周两次分别将 b FGF、b FGF-MAb和生理盐水注射于移植瘤周围 ,8周后测量肿瘤体积 ;对移植瘤组织切片行 因子的免疫组化染色、测定肿瘤内微血管密度 (microvessel density,MVD)。　结果　 b FGF能促进 SKOV3细胞增殖并呈浓度依赖 ,实验第 5天 ,5 ng/ml、10 ng/ml组细胞 D4 90 值是对照组的 1.0 9倍和 1.2 1倍 ;b FGF能促进 SKOV3细胞浸润并呈浓度依赖 (P<0 .0 5 ) ,第 7天 ,5 ng/ml、10 ng/ml组细胞浸润距离分别是对照组的 1.5 3倍和2 .4 5倍 ;b FGF组移植瘤体积和 MVD分别是对照组的 1.80倍和 1.4 6倍 (P<0 .0 5 ) ,b FGF- MAb组移植瘤体积和 MVD分别是对照组的 6 3.7%和 6 2 .8% (P<0 .0 5 )。　结论　b FGF能明显促进卵巢癌细胞的增殖、     

RNA干扰沉默IGFBP2基因表达抑制裸鼠移植瘤的生长

目的：应用RNAi技术沉默胰岛素生长因子结合蛋白2基因（IGFBP2）,探讨其对人胃癌移植瘤生长的影响。方法：合成靶向IGFBP siRNA的表达质粒,于雌裸鼠皮下种植SGC7901胃癌细胞,肿瘤长至一定大小时,随机分为重组质粒实验组（A）,阴性质粒对照组（B）及盐水对照组（C）,于肿瘤局部分别注射重组质粒、阴性重组质粒、生理盐水。每3d给药一次,共8次,3d测量一次肿瘤体积,22d后处死全部动物,取肿瘤,测其大小和瘤重,RT-PCR检测各组IGFBP-2的表达。结果：A组肿瘤瘤块的体积和重量明显小于B、C组（P〈0.05）,RT-PCR显示,A组IGFBP-2的表达明显低于B、C组（P〈0.05）,B、C组IGFBP-2的表达差异无显著性（P〉0.05）。结论：靶向IGFBP-2siRNA瘤内注射能显著地延缓胃癌细胞裸鼠皮下移植瘤的生长,可能通过抑制IGFBP-2基因表达的机制抑制细胞增殖。     

siRNA对VEGF蛋白表达的影响及对裸鼠移植肾癌的抑制作用

目的探讨siRNA沉默血管内皮生长因子（VEGF）基因对人肾癌裸鼠移植瘤VEGF蛋白的表达水平及生长抑制作用的影响。方法化学合成针对VEGF的siRNA序列,通过脂质体将VEGF-siRNA转染到ACHN细胞中,将转染VEGF-siRNA的ACHN细胞（A组）、转染空质粒的ACHN细胞（B组）及未转染的ACHN细胞（C组）分别接种于裸鼠背部皮下。在SPF环境中饲养裸鼠并观察各组裸鼠移植瘤的生长情况,每隔5d测定移植瘤体积大小（肿瘤的长轴L,短轴W,肿瘤体积V=1/2LW2）,绘制肿瘤生长曲线,采用免疫组化及Western blot法测定裸鼠移植瘤组织切片中VEGF蛋白的表达水平。结果 A组小鼠移植瘤成瘤及生长明显缓慢,移植瘤的体积和质量均低于B、C组,差异有统计学意义（P〈0.05）;移植瘤组织切片免疫组化及Western blot法检测结果提示：与B、C组相比,A组中VEGF蛋白表达量降低,差异有统计学意义（P〈0.05）;而B、C组间瘤体的体积重量及VEGF蛋白表达差异均无统计学意义（P〉0.05）。结论 VEGF在肾癌的发生、发展中起着重要作用,化学合成的VEGF-siRNA可特异性抑制肾癌细胞中VEGF的表达,抑制肿瘤的生长增殖。     

RNA干扰FABP5基因对人肝癌HepG2细胞裸鼠移植瘤生长的影响

目的:研究脂肪酸结合蛋白5(FABP5)基因沉默的慢病毒载体对人肝癌Hep G2细胞成瘤效应的影响。方法:采用RNA干扰技术构建重组逆转录慢病毒载体。Hep G2细胞分为3组:实验组以FABP5基因沉默慢病毒颗粒(LV-shRNA-FABP5)感染Hep G2细胞;阴性对照组以空载体慢病毒颗粒(LV-shRNA-NC)感染Hep G2细胞;空白对照组不做任何处理。将裸鼠随机分为3组,接种肿瘤细胞后观察裸鼠成瘤情况。4周后测量肿瘤的体积和重量,绘制移植瘤生长曲线。Real-time PCR、Western blot及免疫组织化学法检测裸鼠移植瘤中FABP5的表达。结果:LV-shRNA-FABP5可以降低Hep G2细胞FABP5的表达。3组裸鼠接种癌细胞后均有肿瘤形成。与空白对照组和阴性对照组相比,实验组肿瘤生长速度明显减慢,且体积及重量明显减小(P0.05);实验组裸鼠肝癌移植瘤组织的FABP5 mRNA和蛋白表达水平相比空白对照组和阴性对照组表达明显下降(P0.05)。结论:沉默FABP5基因表达能有效抑制人肝癌裸鼠移植瘤的生长。FABP5可能成为肝癌基因治疗的一个有效靶点。     

筛选鉴定Thy-1标记阳性肝癌细胞系中的卵圆细胞样干细胞:可能是肝肿瘤干细胞吗?

背景:肝癌的转移复发被认为可能存在有肿瘤干细胞,后者在肿瘤细胞中数目极少,使得临床鉴别存在一定困难。Thy-1是卵圆细胞的表面标记蛋白,通过特异性标记物间接证明肿瘤中存在肿瘤干细胞是目前研究的重点。目的:探讨肝癌细胞中是否存在Thy-1标记阳性的卵圆细胞,并进行筛选鉴定。方法:流式细胞仪检测卵圆细胞标记蛋白Thy-1在肝癌细胞HepG2,BEL7402及正常肝细胞QSG7701的阳性表达情况,免疫磁珠分选Thy-1标记阳性的肝癌细胞,免疫荧光鉴定分选效率。裸鼠皮下接种实验设立3组,Thy-1+细胞组裸鼠于背部皮下接种分选的Thy-1+细胞5×105/只,HepG2细胞阳性对照组同法接种HepG2细胞0.5×107/只,Thy-1-细胞阴性对照组同法接种分选的Thy-1-细胞0.5×107/只,1个月后观察各组成瘤性。结果与结论:卵圆细胞表面标记蛋白Thy-1在肝癌细胞HepG2,BEL7402中的表达明显高于正常肝细胞QSG7701(P0.05)。Thy-1+细胞组免疫荧光染色阳性率为85%,HepG2细胞阳性对照组为1%,Thy-1-细胞阴性对照组几乎无免疫荧光表达。HepG2细胞阳性对照组、Thy-1+细胞组5只裸鼠全部成瘤,且瘤体体积相对较大;而Thy-1-细胞阴性对照组仅有1只裸鼠成瘤,瘤体体积明显小于前2组(F=144.568,P0.05),提示肝癌细胞中存在Thy-1标记阳性的卵圆细胞样干细胞,其可能是肝癌细胞中的肿瘤干细胞。     

D-Limonene对小鼠移植瘤生长及淋巴管生成的影响

目的:观察右旋柠烯对小鼠移植瘤生长及淋巴管生成的影响,并探讨其作用机制。方法:皮下注射肉瘤(S180)腹水型瘤株构建小鼠移植瘤模型,给予D-Lim onene干预,免疫组化染色观察瘤细胞V EG F-C表达,LY V E-1标记淋巴管,观察其分布。结果:对照组瘤细胞V EG F-C表达较强,瘤周边部淋巴管较多,有淋巴结、肺转移。用药组瘤细胞V EG F-C表达较弱;瘤周边部淋巴管较少,未见淋巴结、肺转移。结论:D-Lim onene有抑制移植瘤内瘤细胞V EG F-C表达和淋巴管生成的作用,有可能降低肿瘤的淋巴道转移。     

姜黄素对裸鼠乳腺移植瘤p21及CD44V6表达的影响

目的: 研究姜黄素对裸鼠乳腺移植瘤p21及CD44V ₆表达的影响。方法: 选用人乳腺癌细胞株MCF-7对裸鼠进行异种移植,成瘤后随机分为2组：（1）阴性对照组；（2）姜黄素组。观测移植瘤的出瘤时间、成瘤率，测量瘤体大小并计算瘤表面积。同时应用RT-PCR，检测2组肿瘤组织中cyclin D1、p21及CD44V₆的表达。结果: 姜黄素组瘤表面积明显低于阴性对照组；姜黄素组p21表达量高于阴性对照组，CD44V₆表达量明显降低，2组的cyclin D1表达差异无显著。结论: 姜黄素抑制裸鼠MCF-7乳腺移植瘤CD44V₆的表达，增加p21的表达。     

靶向上皮性卵巢癌SKOV3细胞ZEB1-shRNA重组体构建及功能研究

目的:利用RNA干扰技术,降低人上皮性卵巢癌SKOV3细胞中锌指增强子结合蛋白1(ZEB1)基因的表达,观察ZEB1低表达对SKOV3细胞的生长影响。方法:用pSUPER-EGFP1载体构建针对人ZEB1基因的干扰质粒shZEB1,脂质体转染SKOV3细胞,G418筛选稳定转染细胞株,通过RT-PCR和Western blot检测ZEB1在SKOV3细胞中表达。用克隆形成、划痕试验、RT-PCR和致瘤试验分别检测转染细胞克隆能力、迁移力、miR-200c表达水平和在裸鼠的致瘤性。结果:成功构建shZEB1,稳定转染细胞株shZEB1-SKOV3内ZEB1表达下降,导致shZEB1-SKOV3细胞miR-200c表达增高,克隆能力、迁移力及致瘤性下降。结论:用RNA干扰技术可靶向降低卵巢癌细胞株SKOV3内ZEB1的表达,使其致瘤性降低,提示ZEB1可作为分子靶点用于上皮性卵巢癌靶向治疗。     

Systemic mesenchymal stem cells reduce growth rate of cisplatin-resistant ovarian cancer

Epithelial ovarian cancer is one of the most malignant cancers in women and resistant to chemotherapy is the major obstacle for the five-year survival rate. Cisplatin is one of the effective anticancer drug used in the ovarian cancer. To find a good strategy to cure the tumors which is resistant to cisplatin, the cisplatin-resistant 3SKOV3 cells were selected from SKOV-3 ovarian cancer cells. Furthermore, the isolated mesenchymal stem cells were infused systemically to try to cure the transplanted tumor induced by 3SKOV3 cells in nude mice. The morphology and cell membrane CD44 expression were investigated by microscope and flow cytometry. The biological behaviors of resistant 3SKOV3 and its parental SKOV3 cells, including proliferation, adhesion, and cell cycle were determined by CCK8, absorbance assay and FCM methods. The transplanted tumors were set up in nude mice with 3SKOV3 cells injection. The growth rate of transplanted tumors was detected following with MSCs injection. The 3SKOV3 cells have different morphologic manifestation and expressed high level of CD44 molecule. At the same time, 3SKOV3 cells have less adhesion ability and less S-phase ratio. The isolated MSCs from bone marrow could inhibit the growth of transplanted tumor via systemic injection. The cisplatin-resistant 3SKOV3 cells have the different biological behaviors as its parental SKOV3 cells. The present study indicated that systemic MSCs have the therapeutic role on ovarian cancer. However, further investigations are in progress to elucidate the underlying mechanism.     

NEK2基因沉默促进卵巢癌细胞SKOV3凋亡

目的研究siRNA干扰NEK2表达对卵巢癌细胞SKOV3增殖和凋亡的影响及其分子机制。方法设计合成3条对NEK2的siRNA,转染进SKOV3细胞,采用real-time PCR和Western blot技术筛选出抑制效率最高的NEK2-siRNA序列,进行后续实验;分别采用MTT和流式细胞学技术检测细胞增殖和凋亡,用Western blot检测BAD、BCL-2和caspase-3的表达。结果 1)RNA干扰序列2对SKOV3细胞NEK2的抑制效果最明显;2)与空白组和阴性对照组相比,NEK2-siRNA转染48 h后,SKOV3细胞增殖能力下降,发生凋亡的细胞增加(P<0.01);3)与空白组和阴性对照组相比,NEK2-siRNA转染48 h后,SKOV3细胞中BAD和caspase-3的蛋白表达上调,而BCL-2的蛋白表达下调(P<0.01)。结论 NEK2-siRNA可能通过沉默NEK2的表达,促进卵巢癌细胞SKVO3的凋亡。     

Tumor-associated macrophages promote the metastasis of ovarian carcinoma cells by enhancing CXCL16/CXCR6 expression

This study investigated the underlying mechanism by which C-X-C motif chemokine ligand 16 (CXCL16)/C-X-C motif chemokine receptor 6 (CXCR6) signaling is activated by tumor-associated macrophages and assists in regulating the metastasis of ovarian carcinoma. Specimens of ovarian carcinoma tissue and adjacent tissue were collected from 20 ovarian carcinoma patients. Human THP-1 cells were induced to differentiate into macrophages, which were then co-cultured with SKOV3 cells and low concentrations of tumor necrosis factor-α (TNF-α) to simulate the inflammatory microenvironment of ovarian carcinoma. Additionally, small interfering RNA (siRNA) targeting CXCR6 was transfected into SKOV3 cells; after which, the levels of nuclear factor kappa B p65 (NF-κB p65) protein and phosphorylated PI3K and Akt were measured. The migration and invasion abilities of the SKOV3 cells were also tested. The levels of TNF-α, interluekin-6 (IL-6), NF-κB p65, CXCL16, and CXCR6 expression in the ovarian carcinoma tissues were higher than those in the precancerous tissues. CXCR6 expression was positively correlated with TNF-α, IL-6, and CXCL16 expression. Co-culture of SKOV3 cells with macrophages significantly promoted CXCL16, CXCR6, NF-κB, and p65 expression by the SKOV3 cells, increased their levels of phosphorylated PI3K and Akt, and increased the migration and invasion abilities of SKOV3 cells. Silencing of CXCR6 or blocking the PI3K/Akt signal pathway markedly attenuated the expression of NF-κB p65 and phosphorylation of PI3K and Akt, as well as the migration and invasion abilities of SKOV3 cells. These findings demonstrate that macrophages can promote the migration and invasion of ovarian carcinoma cells by affecting the CXCL16/CXCR6 pathway.     

长链非编码RNA PVT1调控miR-551通过Wnt信号通路对卵巢癌迁移和侵袭的影响

目的:探讨长链非编码RNA PVT1在卵巢癌组织中的表达情况及其在卵巢癌细胞迁移和侵袭过程中的作用及机制。方法:q PCR检测卵巢癌和正常卵巢组织及不同卵巢癌细胞中PVT1的表达情况;Transwell侵袭实验和细胞划痕实验分别检测沉默PVT1后卵巢癌细胞侵袭和迁移能力的变化;双萤光素酶报告基因检测PVT1与微小RNA(miR)-551的相互作用;Transwell侵袭实验和细胞划痕实验分别检测沉默PVT1后miR-551-inhibitor对卵巢癌细胞侵袭和迁移能力的影响;Western blot法检测沉默PVT1后Wnt信号通路相关蛋白的表达情况。裸鼠皮下成瘤实验检测沉默PVT1对卵巢癌成瘤重量及体积的影响。结果:与正常卵巢组织相比,卵巢瘤组织中PVT1表达明显增高(P0.05);卵巢癌细胞株ES-2中PVT1表达水平最高(P0.05);沉默PVT1可以抑制卵巢癌细胞侵袭和迁移能力;PVT1能与miR-551的位点特异性结合;沉默PVT1后,miR-551-inhibitor可以促进卵巢癌细胞侵袭和迁移能力;沉默PVT1后Wnt信号通路蛋白的表达相应下调;与阴性对照组相比,PVT1-siRNA组荷瘤小鼠肿瘤体积和重量都明显减小(P0.05)。结论:PVT1在卵巢癌发生发展过程中起重要作用,它可以靶向调节miR-551,通过Wnt信号通路调控卵巢癌细胞的侵袭和迁移能力。     

B7-H4基因对SKOV3细胞生长功能的影响

目的： 初步探讨B7-H4基因对人卵巢癌细胞株SKOV3细胞生长和致瘤性的影响。方法：RT-PCR法扩增编码基因, 构建真核表达载体PEGFP-N1/B7-H4,以脂质体为载体将重组质粒PEGFP-N1和PEGFP-N1/B7-H4分别导入SKOV3细胞中,筛选建立高表达的细胞株。MTT法绘制体外培养细胞生长曲线,将转染前后的肿瘤细胞分别接种于SCID小鼠的腹部皮下观察其致瘤性。结果：成功构建了人B7-H4真核表达载体,SKOV3/B7-H4细胞高表达B7-H4,转染后肿瘤细胞体外生长速度明显增快。SKOV3/B7-H4细胞在小鼠体内的致瘤性较SKOV3/neo细胞和野生型SKOV3细胞明显升高。结论： B7-H4基因导入细胞后在体外和体内具有明显加快肿瘤生长的作用,可作为肿瘤基因治疗的靶向基因。     

Distinct role of fibroblast growth factor-2 and vascular endothelial growth factor on tumor growth and angiogenesis

Tumors express more than a single angiogenic growth factor. To investigate the relative impact of fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor (VEGF) on tumor growth and neovascularization, we generated tumor cell transfectants differing for VEGF and/or FGF-2 expression. Human endometrial adenocarcinoma HEC-1-B-derived Tet-FGF-2 cells that express FGF-2 under the control of the tetracycline-responsive promoter (Tet-off system) were further transfected with a VEGF(121) anti-sense (AS-VEGF) cDNA. Next, Tet-FGF-2 and AS-VEGF/Tet-FGF-2 cells were transplanted subcutaneously in nude mice that received tetracycline or not in the drinking water. Simultaneous expression of FGF-2 and VEGF in Tet-FGF-2 cells resulted in fast-growing lesions characterized by high blood vessel density, patency and permeability, and limited necrosis. Blood vessels were highly heterogeneous in size and frequently associated with pericytes. Inhibition of FGF-2 production by tetracycline caused a significant decrease in tumor burden paralleled by a decrease in blood vessel density and size. AS-VEGF expression resulted in a similar reduction in blood vessel density associated with a significant decrease in pericyte organization, vascular patency, and permeability. The consequent decrease in tumor burden was paralleled by increased tumor hypoxia and necrosis. A limited additional inhibitory effect was exerted by simultaneous down-regulation of FGF-2 and VEGF expression. These findings demonstrate that FGF-2 and VEGF stimulate vascularization synergistically but with distinctive effects on vessel functionality and tumor survival. Blockade of either one of the two growth factors results in a decrease in blood vessel density and, consequently, in tumor burden. However, inhibition of the expression of VEGF, but not of FGF-2, affects also vessel maturation and functionality, leading to tumor hypoxia and necrosis. Our experimental model represents an unique tool to investigate anti-neoplastic therapies in different angiogenic environments.     

BCYRN1 调控miR-503 通过Notch1 信号通路对肺癌迁移和侵袭的影响

目的:探讨BCYRN1 调控miR-503 通过Notch1 信号通路对肺癌迁移和侵袭的影响机制。方法:qPCR 检测不同肺癌细胞株中BCYRN1 和miR-503 的表达情况;免疫荧光和qPCR 检测慢病毒BCYRN1+siRNA 转染肺癌细胞的转染效率;双荧光素酶报告基因检测BCYRN1 与miR-503 的相互作用;Transwell 侵袭实验和划痕实验检测沉默BCYRN1 后肺癌细胞侵袭和迁移能力的变化;Western blot 检测沉默BCYRN1 后Notch1 信号通路蛋白的表达情况;裸鼠皮下成瘤检测沉默BCYRN1后肺癌细胞裸鼠体内成瘤能力的影响。结果:在肺癌细胞H1299 中BCYRN1 表达水平最高,miR-503 的表达水平相对较高;免疫荧光及mRNA 水平证明BCYRN1+siRNA 慢病毒可以有效转染进入H1299 细胞内;BCYRN19 能与miR-503 的3’-UTR 特异性结合;沉默BCYRN1 可以抑制肺癌H1299 细胞的侵袭和迁移能力;沉默BCYRN1 后Notch1 通路蛋白表达情况相应下调;与NC 组相比,BCYRN1-siRNA 组荷瘤小鼠肿瘤体积和重量都明显减小。结论:BCYRN1 可以靶向调节miR 503 通过Notch1 信号通路影响肺癌H1299 细胞的侵袭和迁移能力。