HMGB1 promotes the proliferation and invasion of oral squamous cell carcinoma via activating epithelial-mesenchymal transformation

This study aimed to investigate the role of high mobility group box-1 (HMGB1) expression in oral squamouscell carcinoma; HMGB1 promoted the proliferation and invasion of oral squamous cell carcinoma via activatingepithelial-mesenchymal transformation (EMT). In this study, RNA transfection was used to silence the expression ofHMGB1 in oral squamous cell carcinoma cells. CCK-8, cell clone formation and trans-well assays were used to detectthe proliferation and invasion of cells before and after HMGB1 silencing. qRT-PCR and Western blot were used todetect changes in EMT marker protein expression before and after transfection. HMGB1 was significantly higher inOSCC tissues than in adjacent tissues, and of the cell lines examined, HMGB1 was highest in SCC-9 cells. Additionally,HMGB1 silencing decreased SCC-9 cell proliferation and viability. Down-regulation of HMBG1 expression inhibitednot only the proliferation but also the invasion of SCC-9 cells. The expression of N-cadherin, Snail, and Slug, but notE-cadherin, were promoted after silencing HMGB1. The expression of HMGB1 in OSCC tissue and cell lines washigher, and HMGB1 silencing decreased SCC-9 cell proliferation and invasion, suggesting that HMGB1 has positiveeffects on OSCC development. Down-regulation of HMBG1 expression regulates EMT markers, suggesting thatHMBG1 promotes OSCC cell proliferation and invasion is likely to be associated with EMT activation.     

Secretome-microRNA and anti-proliferative APRO family proteins as cancer prevention and stem cell research strategies

Stemness of cancer cells contains limitless self-renewal proliferation. For the purpose of proliferation, secretome might exert its effects via the paracrine signaling. Specific microRNAs enclosed in the secretome of cancer stem cells could regulate the expression of anti-proliferative APRO family proteins. The biological functions of APRO family proteins seems to be quite intricate, however, which might be a key modulator of microRNAs, then could regulate the proliferation of cancer cells. In addition to affecting proliferation/differentiation during cellular development, APRO family proteins might also play an imperious role on keeping homeostasis in healthy stem cells under a physiological condition. Therefore, relationship between the microRNAs and the APRO family proteins has attracted much attention in the field of cancer research and regenerative medicine. Here, we have described the molecular mechanism behind this interplay that have a potential role in the future promising tools with targeting APRO family proteins for the medical applications.     

Effect of minor actinides doping on plutonium produced in large-scale FBR blanket

The present study focuses on the effect of minor actinides (MAs) addition into the FBR blanket as ways of increasing fraction of even-mass-number plutonium isotopes, especially ²³⁸Pu, aiming at enhancing the proliferation resistance of plutonium produced in the blanket. The MA loading potential to enhance the proliferation resistance of plutonium is investigated, with considering actual design constraints on the fuel decay heat from the fuel handling and fabrication points of view, as MAs considerably generate decay heat. It reveals that depending on doping quantity of MAs, it is possible to denature produced plutonium by MA transmutation. MA addition in the blanket gives a significant increment in ²³⁸Pu fraction of generated plutonium but less effect on other even-mass-number plutonium isotopes. However, it is important that MA compositions should be adequately controlled to satisfy both the proliferation resistance requirements and the decay heat constraints for fuel handling.     

天然类胡萝卜素抑制细胞恶性转化机理的初步研究

实验对天然类胡萝卡素抑制细胞恶性转化的机理进行研究。结果表明：斑蝥黄素、β－胡眩素和番茄红素均能显著升调细胞间隙连接通讯功能。抑制细胞生长，并使细胞周期时相左移、Ｍ期百分比下降、ＭＩ降低；细胞转化及类胡萝卜素处理过程中不伴随间隙连接蛋白基因Ｃｘ４３染色体ＤＮＡ的丢失或突变，提示：类胡萝卡素抑制细胞增殖，升调细胞间隙连接通讯功能及其参入间隙连接蛋白基因Ｃｘ４３的表达与调控可能是其抑制细胞恶性转化的重     

FABP7基因真核表达载体的构建及其对人乳腺癌细胞MCF-7增殖的影响

目的构建脑脂肪酸结合蛋白(BLBP/B-FABP,FABP7)基因的真核表达载体,并检测其对人乳腺癌细胞MCF-7增殖的影响。方法采用逆转录方法从星型细胞瘤组织中扩增FABP7基因,双酶切后插入线性化的pcDNA3.1载体真核启动子下游,构建重组真核表达载体,转染人乳腺癌细胞MCF-7后,采用半定量RT-PCR检测FABP7基因mRNA的表达,MTT法检测细胞的增殖活性、流式细胞术检测细胞的周期变化情况,并对细胞进行计数。结果FABP7基因重组真核表达质粒经双酶切及测序鉴定证明构建正确,转染MCF-7细胞后48、72和96h,pcDNA3.1-FABP7组的细胞数和细胞的A490值均比pcDNA3.1空质粒组明显降低,G1期细胞百分含量均明显升高。结论已成功构建了FABP7基因的真核表达载体,该载体可抑制人乳腺癌细胞MCF-7的增殖。     

姜黄素对HeLa细胞增殖和凋亡的影响

目的探讨姜黄素对HeLa细胞增殖和凋亡的影响及其机制。方法分别用10、20、40μmol/L姜黄素处理HeLa细胞24h后,MTT法检测细胞的增殖,光镜观察细胞形态,TUNEL技术检测细胞的凋亡,免疫细胞化学法检测Cytochrome C和Caspase-9蛋白的表达,Western blot法检测XIAP蛋白的表达。结果姜黄素对HeLa细胞的增殖有抑制作用,并呈剂量依赖性;部分细胞呈现典型的凋亡形态学改变;姜黄素作用后,Cytochrome C和Caspase-9蛋白的表达显著增强,XIAP蛋白的表达显著下降,且均呈剂量依赖性。结论姜黄素能抑制HeLa细胞增殖并诱导其凋亡,Cytochrome C和Caspase-9的表达上调及XIAP的表达下调可能参与凋亡过程。     

核桃楸皮提取物对胃癌细胞增殖的影响

目的观察核桃楸皮乙酸乙酯提取物(HYT)对小鼠前胃癌细胞MFC及人正常胃黏膜上皮细胞GES-1增殖的影响。方法从核桃楸皮中提取HYT,以不同浓度作用于MFC和GES-1细胞,MTT法检测HYT对MFC及GES-1细胞增殖的影响;流式细胞术检测MFC细胞周期变化及细胞凋亡情况。结果与阴性对照组比较,HYT可明显抑制MFC细胞增殖,促进细胞凋亡,对GES-1细胞无明显杀伤作用;HYT使MFC细胞阻滞于G0-G1和G2-M期。结论HYT可通过影响胃癌细胞周期,促进细胞凋亡,抑制其增殖。     

MMP-2反义寡核苷酸对人胃癌SGC7901细胞增殖和侵袭能力的影响

目的研究基质金属蛋白酶-2(MMP-2)反义寡核苷酸(ASODN)对人胃癌SGC7901细胞增殖及侵袭能力的影响。方法将不同浓度的硫代磷酸化修饰的MMP-2ASODN转染入人中低分化胃腺癌SGC7901细胞株,RT-PCR法检测细胞MMP-2基因mRNA的转录水平;Transwell试验检测细胞体外迁移和侵袭能力变化;MTT法检测细胞的增殖活性。结果转染MMP-2ASODN后,SGC7901细胞中MMP-2基因mRNA的转录水平显著降低,细胞的体外迁移和侵袭能力受到抑制,且抑制作用随ASODN浓度的增加而增强;而细胞的增殖活性无明显变化。结论MMP-2ASODN可抑制胃腺癌SGC7901细胞MMP-2基因mRNA的转录水平及细胞的体外迁移和侵袭能力,但与胃癌细胞的增殖活性无明显相关性。     

柯萨奇病毒A组16型G20分离株在不同培养条件下的增殖动力学

目的探讨柯萨奇病毒A组16型(Coxsackievirus A16,CA16)G20分离株在不同培养条件下的增殖动力学。方法常规培养Vero和人二倍体KMB-17细胞,待细胞长至单层,接种G20株病毒,进行病毒蚀斑试验,以0.1 MOI的感染复数分别感染此两种细胞,置不同温度和pH维持液中进行培养,每2 h收样1次至第24 h,以48 h收样作为对照样,微量滴定法检测病毒滴度,并绘制增殖动力学曲线。结果 G20株病毒在Vero及KMB-17细胞中传代适应后,均可导致细胞病变。G20株病毒在此两种细胞中培养,pH 6.0、pH 6.5时,不同培养温度下,病毒基本不增殖;pH 7.5与pH 7.0的病毒增殖基本一致,增殖速度随温度呈现37℃>35℃>33℃的趋势;在33℃～37℃、pH 7.0～8.0时,病毒均有不同程度的增殖;在41℃、各pH条件下,病毒增殖均明显受到限制。结论病毒在此两种细胞中,37℃,pH 7.5培养条件下,增殖速度及滴度均较理想。