题名的的撰写规范

题名应简明、具体、确切,能概括论文的特定内容,有助于选定关键词,符合编制题录、索引和检索的有关原则。题名应该避免使用公式和不常见的缩略词、字符、代号等。必要时,可使用本行业通用缩写词。题名一般不宜超过20字。若题名语意未尽,可以用副题名补充说明论文中的特定内容。避免使用陈述句,因为题名主要起标示作用,而陈述句容易使题名具有判断式的语义,且不够精炼和醒目。少数情况（评述性、综述性和驳斥性）下可以用疑问句做题名,因为疑问句有探讨性语气,易引起读者兴趣。同一篇论文的英文题名与中文题名内容上应一致,尽量减少冠词的使用。     

药物的诱变作用和它的DNA的圆二色谱的影响

一个药物若与DNA反应则往往有诱变作用。因此分析药物与DNA的关系是一个重要的课题。已有多种方法,从不同的角度分析药物与DNA之间的相互作用,其中园二色谱(circular dichroism,CD)是一种可靠、灵敏、简便的方法。DNA分子有它特有的CD谱,若药物分子嵌入DNA分子或与之形成复合物,这将改变DNA的构型而导致CD谱的变化。我们试图探索药物的诱变作用和它对DNA的CD谱影响之间的关系。小     

多拉的梦：谁的声音——斯垂彻的、弗洛依德的或多拉的?

通过梦发掘潜意识为弗洛依德的重大贡献,他首次从科学的角度对梦进行了系统性的研究。弗洛依德在1900年出版的《梦的解析》(Die Traumdeutung)一书至今仍是许多心理学家教学和临床运用的范本。分析梦是我们考察潜意识的绝佳途径,它已经成为精神分析的基本技术之一。本文不仅详细地描述了如何分     

肺癌的抗体治疗的研究进展

肺癌的传统疗法效果不够理想，用抗体治疗肺癌是一较为有效的方法。目前主要有5类抗体用于治疗肺癌：（1）西妥昔单抗(Cetuximab)、ABXEGF(Panitumumab)、Matuzumab（EMD72000）和曲妥珠单抗(Herceptin)等，这类抗体通过结合肿瘤细胞表面分子抑制细胞生长，具有较好的疗效，     

癌的光化学疗法的进展

1924年,有人发现血卟啉在动物及人的恶性肿瘤中聚集,并在光照后发生特异萤光。1960年Lipson研制成血卟啉衍生物(HPD)。1973年起Dougherty和早田义博等进行了大量基础理论研究工作。随着激光医学、光导纤维和纤维内窥镜的发展,已有效地应用于临床。     

关于数字的使用的要求

本刊执行GB／T15835-1995《关于出版物上数字用法的规定》。公历世纪、年代、年、月、日、时刻和计数、计量均用阿拉伯数字。书写百分数范围，前一个数字的百分符号不能省略，如：5％～30％，不要写成“5～30％”。     

上帝造的与人造的

我现在越来越喜欢使用类比这种思考方式，也越来越喜欢采用比喻的说法。我频繁使用上帝这个词，并不意味着我相信一个有人格的上帝，一个可以与人沟通的神。我只是采用了“上帝”这个比喻性的、拟人的说法。当然我也可以辩称，我所说的上帝是爱因斯坦或者斯宾诺莎的上帝，就是自然（规律）本身。     

直肠癌的辅助放化疗的临床研究

直肠癌是常见的消化道恶性肿瘤，手术是直肠癌的主要治疗手段，放化疗对可手术直肠癌是重要的辅助治疗手段。无论术前或术后放疗均可提高局部控制，术前放疗可增加保肛的机率，放疗的方式以常规分割较佳。术后放疗在中度复发危险的患者中对生存的影响与化疗相似，但需要两者对局控的资料。本文综述的是术前放疗、术后放疔以及术前与术后放疗的比较。     

肿瘤细胞来源的Exosomes的研究进展

目的：Exosomes是活细胞分泌的具有脂质双分子层结构、直径在40~100 nm之间的纳米级囊泡。肿瘤细胞来源的Exosomes含有mRNA、microRNA（miRNA)和蛋白质,其通过与受体（靶）细胞互动对话（cross talk）,将其携带的mRNA、miRNA和蛋白质传送至受体细胞,促进细胞间信息的交流和传递,进而调控受体细胞的生物学行为。肿瘤细胞来源的Exosomes不仅对肿瘤免疫、肿瘤的侵袭与转移及肿瘤耐药具有重要的调节作用,在肿瘤的诊断与治疗方面也具有重要价值。本文就近来肿瘤细胞来源的Exosomes研究进展进行阐述。     

TAGLN基因过表达对乳腺癌细胞迁移和侵袭能力的影响

目的 研究TAGLN基因过表达对人乳腺癌细胞MDA-MB-231迁移能力和侵袭能力的影响及其分子机制.方法 对MDA-MB-231细胞采用慢病毒表达系统构建TAGLN基因稳定过表达细胞株,将MDA-MB-231细胞正常培养设为空白对照组,空载体慢病毒包装感染MDA-MB-231细胞后获得的稳定转染细胞株设为空载体对照组.Real time PCR和Western blot检测TAGLN mRNA和蛋白表达,划痕实验和Transwell侵袭实验检测细胞迁移和侵袭能力,Western blot检测TAGLN基因过表达后基质金属蛋白酶2(matrix metalloproteinase-2,MMP-2)和MMP-9蛋白表达变化.结果 MDA-MB-231细胞感染TAGLN基因过表达慢病毒载体后,细胞中TAGLN mRNA表达和蛋白表达升高(均P＜0.01),成功构建TAGLN基因过表达稳定细胞株(231-TAGLN).231-TAGLN细胞的体外迁移能力和侵袭能力下降,与空载体对照组和空白对照组细胞比较,差异均具有统计学意义(均P＜0.01),同时伴有MMP-2和MMP-9表达水平降低(均P＜0.01).结论 TAGLN基因过表达可以抑制乳腺癌细胞的迁移和侵袭,MMP-2和MMP-9基因表达下降可能参与这一过程.     

过表达RSK4m1对人乳腺癌细胞MDA-MB-231生长和侵袭的影响

目的 探讨过表达p90核糖体S6蛋白激酶4变异体1（ribosomal protein S6 kinase 4 variant 1,RSK4m1）对人乳腺癌MDA-MB-231细胞生长和侵袭的影响。方法 通过负载RSK4m1慢病毒在人乳腺癌MDA-MB-231细胞中稳定过表达RSK4m1。以MDA-MB-231亲本细胞为空白对照组（Con组）、转染空载病毒的MDA-MB-231细胞为阴性对照组（Mock组）、转染过表达RSK4m1的MDA-MB-231细胞为实验组（OE组）。采用qRT-PCR和Westen Blot法检测各组RSK4m1 mRNA及蛋白的表达;CCK-8法检测细胞增殖情况;细胞划痕实验检测细胞的迁移能力;Transwell小室侵袭实验检测细胞的侵袭能力。结果 OE组中RSK4m1 mRNA及蛋白的表达量均明显高于Con组及Mock组（P<0.05）。CCK-8实验显示,24 h、48 h、72 h和96 h时OE组细胞增殖均低于Mock组和Con组（P<0.05）;细胞划痕实验显示,细胞培养24 h后,OE组细胞迁移率显著低于Con组和Mock组［（14.53±0.64）% vs （25.67±2.44）%、（24.47±2.25）%,P<0.05］。Transwell小室侵袭实验显示,OE组细胞侵袭能力显著低于Con组和Mock组［（35.00±5.57）个 vs （66.70±5.86）个、（58.67±4.16）个,P<0.05］。结论 过表达RSK4m1可显著抑制人乳腺癌MDA-MB-231细胞增殖、迁移和侵袭能力,为RSK4m1可能成为乳腺癌的治疗新靶点提供了实验依据。     

Reduced expression of Toll-like receptor 4 inhibits human breast cancer cells proliferation and inflammatory cytokines secretion

Background

Tumor cell expression of Toll-like receptors (TLRs) can promote inflammation and cell survival in the tumor microenvironment. Toll-like receptor 4 (TLR4) signaling in tumor cells can mediate tumor cell immune escape and tumor progression, and it is regarded as one of the mechanisms for chronic inflammation in tumorigenesis and progression. The expression of TLR4 in human breast cancer cell line MDA-MB-231 and its biological function in the development and progression of breast cancer have not been investigated. We sought to characterize the expression of TLR1-TLR10 in the established human breast cancer cell line MDA-MB-231, and to investigate the biological roles of TLR4 in breast cancer cells growth, survival, and its potential as a target for breast cancer therapy.

Methods

TLRs mRNA and protein expressions were detected in human breast cancer cell line MDA-MB-231 by RT-PCR, real-time PCR and flow cytometry (FCM). RNA interference was used to knockdown the expression of TLR4 in MDA-MB-231. MDA-MB-231 transfected with the vector pGenesil-1 and the vector containing a scrambled siRNA were as controls. Recombinant plasmids named TLR4AsiRNA, TLR4BsiRNA and TLR4CsiRNA specific to TLR4 were transfected into human breast cancer cell line MDA-MB-231 with Lipfectamine™2000 reagent. TLR4 mRNA and protein expressions were investigated by RT-PCR, real-time PCR, FCM and immunofluorescence after silence. MTT analysis was performed to detect cell proliferation and FCM was used to detect the secretion of inflammatory cytokines in supernatant of transfected cells.

Results

The human breast cancer cell line MDA-MB-231 was found to express TLR1-TLR10 at both the mRNA and protein levels. TLR4 was found to be the highest expressed TLR in MDA-MB-231. TLR4AsiRNA, TLR4BsiRNA and TLR4CsiRNA were found to significantly inhibit TLR4 expression in MDA-MB-231 at both mRNA and protein levels as compared to vector control(vector transfected cells). TLR4AsiRNA mediated the strongest effect. Knockdown of TLR4 gene in MDA-MB-231 resulted in a dramatic reduction of breast cancer cell viability. The cytokines which were secreted by the TLR4 silenced cells, such as IL-6 and IL-8, also decreased significantly as compared with vector control. No significant difference was observed in siRNA control (Recombinant plasmid named ScrambledsiRNA transfected cells) compared to vector control.

Conclusions

These studies identified the expression levels of multiple TLRs in human breast cancer cell line MDA-MB-231 and demonstrated that knockdown of TLR4 could actively inhibit proliferation and survival of breast cancer cells. Taken together, our results suggest RNAi-directed targeting of TLR4 may be a beneficial strategy for breast cancer therapy.     

Effect of interference of MTA1 by shRNA on the biological behaviors and expression of related proteins in breast cancer MDA-MB-231 cells北大核心

Objective: To silence the expression of metastasis-associated gene 1 (MTA1) in breast cancer cell line MDA-MB-231 by using short hairpin small interfering RNA (shRNA) and observe its effects on expression of 15-lipoxygenase 2 (15-LOX-2), p53 and bcl-2 proteins. Methods: The shRNA-MTA1 plasmid was stably transfected into MDA-MB-231 cells and the cell proliferation was evaluated using MTT assay. The cell cycle distribution and apoptosis were analyzed using flow cytometry. The mRNA and protein expression levels of MTA1, 15-LOX-2, p53 and bcl-2 were determined using RT-PCR and Western blotting, respectively. Results: shRNA-MTA1 significantly suppressed the expression of MTA1 gene in MDA-MB-231 cells, inhibited the proliferation, induced apoptosis, and arrested the cells in G1 phase. The difference was significant compared with control group (P < 0.01). Expression levels of 15-LOX-2 and p53 were significantly up-regulated but MTA1 and bcl-2 were significantly down-regulated in MDA-MB-231 cells in shRNA-MTA1 group compared with the blank control group and negative control group (P <0.01). Conclusion: Silencing MTA1 gene inhibited the proliferation and induced the apoptosis of MDA-MB-231 cells. This effect may be related with up-regulation of the expression of 15-LOX-2 and p53 and down-regulation of bcl-2.     

NRP-1过表达对乳腺癌细胞MDA-MB-231、SK-BR-3生物学行为的影响

目的 通过上调乳腺癌细胞MDA-MB-231、SK-BR-3中NRP-1的表达,观察NRP-1对细胞增殖、凋亡、迁移及侵袭能力的影响。方法 构建pcDNA3.1-NRP-1表达载体,脂质体介导NRP-1 表达质粒转染MDA-MB-231、SK-BR-3细胞,用G418筛选出稳定转染的乳腺癌细胞株。利用RTqPCR、Western blot法分别检测NRP-1基因mRNA及其蛋白表达;CCK-8法、AnnexinⅤ-APC/7-AAD法、Transwell小室分别检测转染细胞增殖率、凋亡率及侵袭、迁移能力。结果 成功构建pcDNA3.1- NRP-1表达载体,转染MDA-MB-231、SK-BR-3细胞并筛选稳定表达系。与对照组相比,过表达组细胞的NRP-1 mRNA及蛋白表达水平明显升高（均P<0.05）;NRP-1过表达组的细胞较对照组增殖率增加、凋亡率降低、侵袭及迁移能力增强（均P<0.05)。结论 NRP-1在乳腺癌发展、浸润、转移中起着一定的作用,它可促进乳腺癌细胞增殖、迁移和侵袭,抑制其凋亡。     

雌激素受体β1对乳腺癌MDA-MB-231细胞上皮间质转化影响的初步研究

目的将雌激素受体ERβ1真核表达质粒转染到人乳腺癌MDA-MB-231细胞中,观察外源性ERβ1基因转染MDA-MB-231细胞后对E-cadherin、Vimentin等基因表达和细胞上皮间质转化的影响,探讨ERβ1在乳腺癌发生发展中的生物学作用机制。方法应用脂质体法将ERβ1真核表达质粒转染至乳腺癌MDA-MB-231细胞中,分别用实时荧光定量PCR、Western Blot检测转染前后细胞中ERβ1、E-cadherin、Vimentin mRNA和蛋白表达的变化;并用细胞增殖曲线显示转染后细胞增殖能力的改变。所有数据以±s表示,多个样本均数间的比较用单因素方差分析,组间比较采用SNK法。细胞生长曲线变化采用重复测量方差分析。结果外源性ERβ1真核表达质粒转染组MDA-MB-231细胞较未转染组ERβ1、E-cadherin mRNA和蛋白水平明显增强（P〈0.010）,Vimentin mRNA水平明显减少（P〈0.010）,细胞增殖能力明显减弱。结论 ERβ1可能参与抑制乳腺癌MDA-MB-231细胞的上皮间质转化过程。     

BTG2 inhibits the proliferation, invasion, and apoptosis of MDA-MB-231 triple-negative breast cancer cells

The purposes of this study were to investigate the effects of B cell translocation gene 2 (BTG2) on the proliferation, apoptosis, and invasion of triple-negative breast cancer and to provide an experimental basis for the future treatment of human triple-negative breast cancer. A pcDNA3.1-BTG2 eukaryotic expression vector was constructed and transfected into the MDA-MB-231 human triple-negative breast cancer cell line using lipofection. Then, relevant changes in the biological characteristics of the BTG2-expressing cell line were analyzed using MTT (tetrazolium blue), flow cytometry, and Transwell invasion chamber assays. Additionally, the effects of BTG2 expression on cyclin D1, caspase 3, and matrix metalloproteinases 1/2 (MMP-1/-2) expression were analyzed. Cell proliferation was significantly lower in the pcDNA3.1-BTG2-transfected group compared to the empty vector and blank control groups (p?<?0.05). There was no significant difference between the empty vector and blank control groups. FCM results demonstrated that there were significantly more cells in the G1 phase of the cell cycle and fewer S phase cells in the pcDNA3.1-BTG2 group than in the empty vector and blank control groups (p?<?0.05). Additionally, the proportion of cells that migrated across the membrane was significantly lower in the pcDNA3.1-BTG2 group than in the empty vector and blank control groups (p?<?0.05). Cyclin D1 and MMP-1/-2 expression were significantly lower in MDA-MB-231 cells transfected with pcDNA3.1-BTG2 as compared to the empty vector and blank control groups (p?<?0.05). Caspase 3 expression was significantly higher in MDA-MB-231 cells from the pcDNA3.1-BTG2 group compared to the empty vector and blank control groups (p?<?0.05). In conclusion, BTG2 may inhibit MDA-MB-231 proliferation and promote apoptosis. Additionally, BTG2 may also inhibit the invasion of MDA-MB-231 human triple-negative breast cancer cells.     

雌激素受体β1上调p21基因表达抑制乳腺癌细胞MDA-MB-231的增殖

目的将雌激素受体(ER)β1真核表达质粒转染人乳腺癌MDA-MB-231细胞中,观察外源性ERβ1基因转染MDA-MB-231细胞后对p21基因表达和细胞增殖能力的影响,探讨ERβ1在乳腺癌中的生物学作用机制。方法应用脂质体法将ERβ1真核表达质粒转染至乳腺癌MDA-MB-231细胞中,流式细胞仪观察细胞凋亡率的变化;分别用实时聚合酶连锁反应(RT-PCR)、Western Blot检测转染前后细胞中ERβ1、p21mRNA和蛋白表达的变化;细胞增殖曲线显示转染后细胞增殖能力的改变。统计分析采用t检验和单因素方差分析。结果外源性ERβ1真核表达质粒转染组MDA-MB-231细胞较未转染组ERβ1、p21mRNA和p21蛋白水平明显增强(P0.010),细胞增殖能力明显减弱,细胞凋亡率从1.4%升至6.14%(t=-7.960,P=0.001)。结论 ERβ1可以通过上调p21基因抑制乳腺癌MDA-MB-231细胞的增殖。     

维甲酸诱导基因G慢病毒表达载体的构建及对肺癌细胞A549的影响

背景与目的：维甲酸诱导基因G(retinoic acid-induced gene G,RIG-G)是从急性早幼粒细胞性白血病细胞系NB4细胞中克隆出的肿瘤抑制基因。我们通过调控基因(Tet-on)系统构建受强力霉素(doxycycline,DOX)诱导RIG-G基因表达的A549细胞系,并观察其对A549细胞增殖的作用。方法：采用实时定量PCR(quantitative real-time PCR,qRT-PCR)技术扩增RIG-G基因片段,利用LR重组系统构建pLenti6/TO/V5-GIM-RIG-G慢病毒载体,对该慢病毒载体和Tet-on慢病毒载体包装和病毒滴度测定后,感染A549细胞;采用有限稀释法筛选稳定株;使用细胞免疫荧光和蛋白［质］印迹法(Western blot)鉴定RIG-G基因受DOX调控表达的效果;CCK-8试验检测细胞增殖能力。结果：成功构建pLenti6/TO/V5-GIM-RIG-G慢病毒载体,包装后测得其活性滴度为1.0×10⁸ TU/mL;慢病毒经Tet-on包装后物理滴度为4×10⁹ VP/mL;RIG-G蛋白成功地在慢病毒感染后的A549稳定株中合成和表达,并且受DOX的诱导调控。RIG-G蛋白表达成功后,A549细胞的增殖与对照组相比显著降低(1.168±0.107 vs 2.099±0.162,P<0.05)。结论：本研究成功建立了RIG-G基因可调控表达的A549稳定株;RIG-G蛋白对A549的增殖有抑制作用。     

ZONAB和E-cadherin在膀胱癌细胞系中的表达及RNA干扰ZONAB表达对癌细胞侵袭力的影响

目的:探讨慢病毒介导ZONAB基因的RNA干扰对膀胱癌侵袭力的影响.方法:用Realtime PCR法分别检测人类尿路上皮永生细胞系sv-huc-1和膀胱尿路上皮癌细胞系UM-UC-3、T24、5637中ZONAB和E-cadherin的mRNA表达水平,用Western blot法分别检测各细胞系中ZONAB蛋白表达水平,设计、合成干扰靶点,构建纯化重组慢病毒,感染人膀胱癌UM-UC-3细胞,根据ZONAB基因的抑制率,筛选最有效的ZONAB基因RNAi靶序列组,验证ZONAB基因的沉默效果,用Transwell侵袭试验检测UM-UC-3细胞体外侵袭力的改变.结果:Realtime PCR法和Western blot法测得UM-UC-3、T24、5637中ZONAB的表达水平高于sv-huc-1,均具有显著性差异(P<0.05);而Realtime PCR法测得UM-UC-3、T24、5637中 E-cadherin的mRNA表达水平低于sv-huc-1(P<0.05).成功构建ZONAB基因RNA干扰慢病毒载体并获得相应的慢病毒,与对照组相比RNA干扰组UM-UC-3细胞ZONAB基因mRNA水平的抑制率为71.4%(P<0.05),蛋白水平抑制率为76.8%,其穿过人工基底膜的平均细胞数为13.1±2.8/HP,明显少于阴性对照组和空白对照组(P<0.05).结论:ZONAB在膀胱癌细胞系中表达上调,慢病毒介导ZONAB基因的RNA干扰能够抑制UM-UC-3细胞侵袭.