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siRNA of ADAM17 gene induces apoptosis, proliferation inhibition and enhances the effects of genistein on HepG2 cells ADAM17基因siRNA诱导HepG2细胞凋亡,抑制增殖,增强染料木素对HepG2细胞的作用
Pub Date : 2009-03-01 DOI: 10.1016/S1007-4376(09)60040-X
Yongcun Liu, Zuo-ren Wang, Yu Ji, Feng Li
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引用次数: 1
Recombinant adenovirus-mediated shRNA silencing of midkine gene in BxPC-3 cells 重组腺病毒介导的BxPC-3细胞midkine基因shRNA沉默
Pub Date : 2009-03-01 DOI: 10.1016/S1007-4376(09)60041-1
Mingyue Xiong, Kunzheng Wang
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引用次数: 2
Polymorphisms in XRCC5, XRCC6, XRCC7 genes are involved in DNA double-strand breaks(DSBs) repair associated with the risk of acute myeloid leukemia(AML) in Chinese population 在中国人群中,XRCC5、XRCC6、XRCC7基因多态性参与与急性髓性白血病(AML)风险相关的DNA双链断裂(DSBs)修复
Pub Date : 2009-03-01 DOI: 10.1016/S1007-4376(09)60034-4
Guoqiang Wang , Shuyu Wang , Qun Shen , Shiwei Yin , Chunping Li , Aiping Li , Jianyong Li , Jianwei Zhou , Qizhan Liu

Objective

To investigate the association between the X-ray repair cross complementing(XRCC) group 5, XRCC6 and XRCC7 polymorphisms and risk of acute myeloid leukemia(AML).

Methods

This hospital-based case-control study included 120 AML patients and 210 cancer-free controls in a Chinese population. Three polymorphisms of XRCC5, XRCC6 and XRCC7 were genotyped using the polymerase chain reaction(PCR) or polymerase chain reaction-restriction fragment length polymorphism(PCR-RFLP) method.

Results

We found that there was a significant decrease in risk of AML associated with the XRCC6 −61 CG/GG genotype(adjusted odd ratio (OR) = 0.55; 95% confident interval(CI) = 0.34-0.89) compared with the −61CC genotype. For the novel tandem repeat polymorphism (VNTR) in the XRCC5 promoter, we found when the XRCC5 six genotypes were dichotomized(i.e., 2R/2R, 2R/1R versus 2R/0R, 1R/1R, 1R/0R and 0R/0R), the latter group was associated with increased risk of AML(adjusted OR = 1.67; 95% CI = 1.00∼2.79) compared to 2R/2R+2R/1R genotype. However, the XRCC7 6721G > T polymorphism had no effect on risk of AML.

Conclusion

The XRCC6 −61C > G and XRCC5 2R/1R/0R polymorphisms, but not XRCC7 6721G > T polymorphism, could play an important role in the development of AML. Larger scale studies with more detailed data on environment exposure are needed to verify these findings.

目的探讨x线修复交叉互补(XRCC) 5组、XRCC6和XRCC7基因多态性与急性髓系白血病(AML)发病风险的关系。方法本以医院为基础的病例对照研究包括中国人群中120例AML患者和210例无癌对照。采用聚合酶链反应(PCR)或聚合酶链反应-限制性片段长度多态性(PCR- rflp)方法对XRCC5、XRCC6和XRCC7的3个多态性进行基因分型。结果我们发现,与XRCC6−61 CG/GG基因型相关的AML风险显著降低(调整奇比(OR) = 0.55;95%可信区间(CI) = 0.34-0.89)与−61CC基因型比较。对于XRCC5启动子中的新型串联重复多态性(VNTR),我们发现当XRCC5基因型被二分化时(即:, 2R/2R, 2R/1R相对于2R/0R, 1R/1R, 1R/0R和0R/0R),后者组与AML风险增加相关(调整OR = 1.67;95% CI = 1.00 ~ 2.79),与2R/2R+2R/1R基因型相比。然而,XRCC7 6721G >T多态性对AML风险无影响。结论:XRCC6−61C >G和XRCC5存在2R/1R/0R多态性,而XRCC7 6721G >不存在;T多态性可能在AML的发展中起重要作用。需要有更详细的环境暴露数据的更大规模的研究来验证这些发现。
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引用次数: 14
In vitro effects of sodium hyaluronate on the proliferation and the apoptosis in chondrocytes from patients with Kashin-Beck disease and osteoarthritis 透明质酸钠对大骨节病和骨关节炎患者软骨细胞增殖和凋亡的体外影响
Pub Date : 2009-03-01 DOI: 10.1016/S1007-4376(09)60036-8
Zongqiang Gao , Xiong Guo , Chen Duan , Weijuan Ma , Peng Xu , Ruiyu Liu , Qisheng Gu , Junchang Chen

Objective

To identify the in vitro effects of sodium hyaluronate(HA) on the proliferation and the apoptosis of chondrocytes from patients with Kashin-Beck disease(KBD) and osteoarthritis(OA).

Methods

Samples of articular cartilages from KBD and OA patients, as well as healthy volunteers(6 subjects in each of the 3 groups) were dissected, digested with collagenase and the cells cultured in monolayers. Chondrocytes from each sample were assigned to an untreated group and two HA-treated groups: H0(no HA), H100(HA, 0.1 g/L) and H500(HA, 0.5 g/L). The first passage chondrocytes were used to observe proliferation using the MTT assay, and apoptosis by flow cytometry through Annexin V/PI staining.

Results

HA promoted proliferation of chondrocytes in all the three groups, and in KBD and OA groups, for cells cultured for 4 and 6 days, H500 significantly promoted the cell proliferation. The apoptotic rates of both KBD and OA group chondrocytes were in the order H500 < HA100 < H0.

Conclusion

Sodium hyaluronate administration has a dose-dependent in vitro effect to promote proliferation and inhibit apoptosis of chondrocytes from patients with KBD and OA.

目的探讨透明质酸钠(HA)对大骨节病(KBD)和骨关节炎(OA)患者软骨细胞增殖和凋亡的体外影响。方法解剖骨性关节炎和骨性关节炎患者及健康志愿者(3组各6例)的关节软骨,用胶原酶消化,培养成单层细胞。将每个样本的软骨细胞分为未处理组和两个HA处理组:H0(无HA)、H100(HA, 0.1 g/L)和H500(HA, 0.5 g/L)。用MTT法观察第一代软骨细胞增殖,Annexin V/PI染色用流式细胞术观察细胞凋亡。结果三组均能促进软骨细胞增殖,而在KBD组和OA组,H500对培养4和6 d的细胞增殖有显著促进作用。KBD组和OA组软骨细胞凋亡率依次为H500 <HA100 & lt;H0。结论透明质酸钠对大骨节关节炎患者软骨细胞增殖和抑制凋亡具有剂量依赖性。
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引用次数: 2
The effect of methylseleninic acid on paclitaxel efficacy in A2780 ovarian cancer cells 甲基亚硒酸对紫杉醇对A2780卵巢癌细胞疗效的影响
Pub Date : 2009-03-01 DOI: 10.1016/S1007-4376(09)60037-X
Qiaoli Zhang , Rami G. Azrak

Objective

The role of methylseleninic acid (MSeA), a selenium compound, has been documented in cancer chemoprevention. However, the therapeutic effect of MSeA in combination with paclitaxel, a chemotherapeutic agent used to treat ovarian cancer, is unknown. In this study, we investigated the effect of combination treatment of MSeA and paclitaxel against ovarian cancer cells.

Methods

Ovarian cancer cells(A2780) were treated with different concentrations of MSeA, paclitaxel alone or in combination. The individual and combined concentrations of drugs that achieved certain cells growth/death were determined using a sulforhodamine B(SRB) assay. Drug effects on cell viability were further confirmed using floating cell count and trypan blue exclusion assay. The mean values, standard deviation were calculated and compared between treatment groups using unpaired t test.

Results

The concentration of paclitaxel alone that inhibited 50% of cell growth(IC50) was 0.5 μmol/L. This concentration increased to 1.2 μmol/L when paclitaxel was given in sequential combination with MSeA. The number of dead cells after the combination treatment did not show a significance increase when compared with drug alone.

Conclusion

Pretreatment with MSeA did not enhance the paclitaxel effect against A2780 ovarian cancer cells.

目的研究硒化合物甲基亚硒酸(MSeA)在癌症化学预防中的作用。然而,MSeA联合紫杉醇(一种用于治疗卵巢癌的化疗药物)的治疗效果尚不清楚。本研究探讨了MSeA与紫杉醇联合治疗卵巢癌细胞的作用。方法用不同浓度的MSeA、紫杉醇单独或联合治疗卵巢肿瘤细胞A2780。使用硫代丹B(SRB)试验确定了实现某些细胞生长/死亡的药物的单个和组合浓度。通过浮动细胞计数和台盼蓝排斥试验进一步证实药物对细胞活力的影响。采用非配对t检验计算各组间的平均值和标准差。结果紫杉醇单药浓度为0.5 μmol/L,对细胞生长有50%的抑制作用。紫杉醇与MSeA序贯给药时,该浓度升高至1.2 μmol/L。与单独用药相比,联合用药后死细胞数未见明显增加。结论MSeA预处理不能增强紫杉醇对A2780卵巢癌细胞的作用。
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引用次数: 4
Effect of the gap junction blocker 1-heptanol on chondrogenic differentiation of mouse bone marrow mesenchymal stem cells in vitro 间隙连接阻滞剂1-庚醇对小鼠骨髓间充质干细胞成软骨分化的影响
Pub Date : 2009-03-01 DOI: 10.1016/S1007-4376(09)60038-1
Liu Ou-yang, Yukun Zhang, Shuhua Yang, Shunan Ye, Weihua Xu

Objective

To investigate the effect of the gap junction blocker 1-heptanol on the in vitro chondrogenic differentiation of mouse bone marrow mesenchymal stem cells(MSCs) following induction by GDF-5.

Methods

MSCs were isolated from mouse bone marrow and cultured in vitro. After 3 passages cells were induced to undergo chondrogenic differentiation with recombinant human GDF-5(100 ng/ml), with or without 1-heptanol(2.5μ mol/L). The effect of 1-heptanol on MSCs proliferation was investigated using the MTT assay. Type, collagen mRNA and protein were examined by RT-PCR and immunocytochemistry respectively, and the sulfate glycosaminoglycan was assessed by Alcian blue dye staining. Connexin43(Cx43) protein was examined by western blotting.

Results

GDF-5 induced proliferation and chondrogenic differentiation of MSCs. While 1-heptanol treatment had no effect on this proliferation, it inhibited the expression of both type, collagen mRNA and protein. The Alcian blue staining revealed that 1-heptanol also inhibited the deposition of the typical cartilage extracellular matrix promoted by recombinant GDF-5. Western blotting demonstrated that 1-heptanol had no effect on the expression of Cx43.

Conclusion

These results suggest that mouse bone marrow MSCs can be differentiated into a chondrogenic phenotype by GDF-5 administration in vitro. While the gap junction blocker, 1-heptanol, did not reduce gap junction Cx43, these intercellular communication pathways clearly played an important functional role in GDF-5-induced cartilage differentiation.

目的探讨间隙连接阻断剂1-庚醇对GDF-5诱导小鼠骨髓间充质干细胞体外成软骨分化的影响。方法从小鼠骨髓中分离smscs并进行体外培养。3代后,用重组人GDF-5(100 ng/ml)、1-庚醇(2.5μ mol/L)和不加1-庚醇(2.5μ mol/L)诱导细胞成软骨分化。采用MTT法研究1-庚醇对MSCs增殖的影响。采用RT-PCR和免疫细胞化学分别检测胶原蛋白类型、mRNA和蛋白含量,阿利新蓝染色检测硫酸糖胺聚糖含量。western blotting检测Connexin43(Cx43)蛋白。结果gdf -5可诱导MSCs增殖和成软骨分化。虽然1-庚醇处理对这种增殖没有影响,但它抑制了类型、胶原mRNA和蛋白质的表达。阿利新蓝染色显示,1-庚醇也抑制了重组GDF-5促进的典型软骨细胞外基质的沉积。Western blotting结果显示,1-庚醇对Cx43的表达无影响。结论GDF-5可诱导小鼠骨髓间充质干细胞向软骨细胞表型分化。虽然间隙连接阻滞剂1-庚醇不能减少间隙连接Cx43,但这些细胞间通讯途径显然在gdf -5诱导的软骨分化中发挥了重要的功能作用。
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引用次数: 1
Impairments of spatial learning and memory in rat offspring with fetal growth restriction 胎儿生长受限大鼠子代空间学习记忆障碍
Pub Date : 2009-01-01 DOI: 10.1016/S1007-4376(09)60027-7
Pu Huang , Wenli Gou , Mali Jiang , Rui Zhang , Yunping Sun

Objective

Throughout the world, fetal growth restriction(FGR) is one of the most severe complications occurring during pregnancy. It is subsequently associated with neurologic abnormalities in chldren. Our aim was to investigate the spatial learning and memory ability of rat offspring born with FGR.

Methods

A rat model of FGR was constructed using the method of passive smoking. Spatial learning and memory were studied in rat offspring born with FGR by assessing the animals' performance using the Morris water maze task.

Results

At 1- and 2-months of age, both female and male offspring rats showed impairment of performance, while at 4 months of age, only female rats showed impaired performance. The FGR offspring spent a longer time swimming and used inefficient strategies(P < 0.05, respectively). However, there were no significant maze performance FGR effects in the 4 month old male rats. In all groups of FGR offspring, irrespective of age or sex, the time spent in the platform quadrant by the rat was significantly less than that in the control group(P < 0.05).

Conclusion

The Morris water maze performance decreased in rat offspring born with FGR. It is suggested that FGR can cause impairments of spatial learning and memory in young animals.

目的胎儿生长受限(FGR)是妊娠期最严重的并发症之一。它随后与儿童神经系统异常有关。我们的目的是研究FGR大鼠后代的空间学习和记忆能力。方法采用被动吸烟法建立FGR大鼠模型。通过Morris水迷宫任务,研究FGR小鼠的空间学习和记忆能力。结果雌性和雄性子代大鼠在1月龄和2月龄时均表现出功能障碍,而在4月龄时,只有雌性大鼠表现出功能障碍。FGR后代花更长的时间游泳,并使用低效的策略(P <分别为0.05)。而在4月龄雄性大鼠中,FGR对迷宫表现无明显影响。在所有FGR后代中,无论年龄或性别,大鼠在平台象限的时间均显著少于对照组(P <0.05)。结论FGR后大鼠水迷宫表现下降。提示FGR可引起幼龄动物空间学习记忆功能的损伤。
{"title":"Impairments of spatial learning and memory in rat offspring with fetal growth restriction","authors":"Pu Huang ,&nbsp;Wenli Gou ,&nbsp;Mali Jiang ,&nbsp;Rui Zhang ,&nbsp;Yunping Sun","doi":"10.1016/S1007-4376(09)60027-7","DOIUrl":"10.1016/S1007-4376(09)60027-7","url":null,"abstract":"<div><h3>Objective</h3><p>Throughout the world, fetal growth restriction(FGR) is one of the most severe complications occurring during pregnancy. It is subsequently associated with neurologic abnormalities in chldren. Our aim was to investigate the spatial learning and memory ability of rat offspring born with FGR.</p></div><div><h3>Methods</h3><p>A rat model of FGR was constructed using the method of passive smoking. Spatial learning and memory were studied in rat offspring born with FGR by assessing the animals' performance using the Morris water maze task.</p></div><div><h3>Results</h3><p>At 1- and 2-months of age, both female and male offspring rats showed impairment of performance, while at 4 months of age, only female rats showed impaired performance. The FGR offspring spent a longer time swimming and used inefficient strategies(<em>P</em> &lt; 0.05, respectively). However, there were no significant maze performance FGR effects in the 4 month old male rats. In all groups of FGR offspring, irrespective of age or sex, the time spent in the platform quadrant by the rat was significantly less than that in the control group(<em>P</em> &lt; 0.05).</p></div><div><h3>Conclusion</h3><p>The Morris water maze performance decreased in rat offspring born with FGR. It is suggested that FGR can cause impairments of spatial learning and memory in young animals.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60027-7","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90904416","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Induction of interleukin-8 production by angiotensin II in rat vascular smooth muscle cells 血管紧张素II诱导大鼠血管平滑肌细胞产生白细胞介素-8
Pub Date : 2009-01-01 DOI: 10.1016/S1007-4376(09)60026-5
Zhi Wang, Lili Zhang, Baogui Sun, Qiuyan Dai

Objective

Interleukin-8(IL-8) represents the prototypical chemokine that is made by a wide variety of cell types. Previously studies have suggested that angiotensin II(Ang II) is involved in atherogenesis through induction of proinflammatory cytokines such as interleukin-6 or monocyte chemoattractant protein-1(MCP-1) in vascular smooth muscle cells(VSMCs), while the role of Ang II on IL-8 expression in VSMCs is poorly studied.

Methods

In this study, VSMCs were isolated from the thoracic aorta of Sprague-Dawley rats. The expression of smooth muscle α-actin was confirmed by an immunohistochemical method. Semi-quantitative RT-PCR and enzyme-linked immunosorbent assay (ELISA) analyses were conducted to detect IL-8 expression.

Results

In the present study we found that Ang II significantly increased the expression of IL-8 both at the mRNA and protein levels in rat VSMCs in a dose- and time-dependent manner.

Conclusion

These findings suggested that Ang II may participate in atherosclerosis through induction of inflammatory mediator in VSMCs.

目的白细胞介素-8(IL-8)是一种由多种细胞类型合成的典型趋化因子。先前的研究表明,血管紧张素II(Ang II)通过诱导血管平滑肌细胞(VSMCs)中的促炎细胞因子如白细胞介素-6或单核细胞趋化蛋白-1(MCP-1)参与动脉粥样硬化的形成,而Ang II对血管平滑肌细胞中IL-8表达的作用研究较少。方法从sd大鼠胸主动脉中分离VSMCs。免疫组化法证实平滑肌α-肌动蛋白的表达。采用半定量RT-PCR和酶联免疫吸附法(ELISA)检测IL-8的表达。结果在本研究中,我们发现Ang II显著提高了大鼠VSMCs中IL-8 mRNA和蛋白水平的表达,并呈剂量依赖性和时间依赖性。结论Angⅱ可能通过诱导VSMCs炎症介质参与动脉粥样硬化。
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引用次数: 1
Relationship between obstructive sleep apnea hypopnea syndrome and cardiovascular disorders in adult snorers 成人打鼾者阻塞性睡眠呼吸暂停低通气综合征与心血管疾病的关系
Pub Date : 2009-01-01 DOI: 10.1016/S1007-4376(09)60028-9
Rui Wu , Xilong Zhang , Ling Hu , Enzhi Jia

Objective

To investigate the relationship between sleep apnea hypopnea syndrome(OSAHS) and some cardiovascular disorders in adult habitual snorers as well as the effectiveness of nasal continuous positive airway pressure(NCPAP) on those with OSAHS.

Methods

With the use of polysomnography, 262 adult habitual snorers were examined and divided into the OSAHS group and the Non-OSAHS group (control). Using ambulatory electrocardiogram and blood pressure measurement, daily nocturnal rhythm of blood pressure, hypertension, heart rate variability, some arrythmias and angina pectoris of coronary heart disease were monitored and compared between the two groups, before and after 14 days of treatment with NCPAP in the OSAHS group.

Results

This study indicated a higher incidence (39.6%) of OSAHS in adult snorers and demonstrated that there was a significantly higher incidence of hypertension, disappearance of the daily nocturnal rhythm of blood pressure, poor effectiveness of nitrate on angina pectoris of coronary heart disease, decreased heart rate variability during sleep, increased arrythmias and lower SpO2 levels in the OSAHS group than in the Non-OSAHS group. After NCPAP treatment during sleep, snoring control, significantly higher SpO2 and lower apnea hypopnea indices were achieved in the OSAHS group; heart rate variability and daily nocturnal rhythm of blood pressure returned to normal levels.

Conclusion

The results of this research suggested that there was a close relationship between the development of OSAHS and some cardiovascular disorders. Furthermore, NCPAP treatment was effective not only on OSAHS but also on coexisting cardiovascular disorders.

目的探讨成人习惯性打鼾患者睡眠呼吸暂停低通气综合征(OSAHS)与心血管疾病的关系及鼻持续气道正压通气(NCPAP)对OSAHS患者的治疗效果。方法采用多导睡眠描记仪对262例成人习惯性打鼾者进行检查,并将其分为OSAHS组和非OSAHS组(对照组)。采用动态心电图和血压测量,监测两组患者在NCPAP治疗前后的每日夜间血压节律、高血压、心率变异性、部分冠心病心律失常和心绞痛情况,并进行比较。结果成人打鼾者OSAHS发病率(39.6%)较高,且OSAHS组高血压发生率明显高于非OSAHS组,每日夜间血压节律消失,硝酸盐治疗冠心病心绞痛效果差,睡眠心率变异性降低,心律失常增加,SpO2水平降低。睡眠期间NCPAP治疗后,OSAHS组SpO2明显升高,呼吸暂停低通气指数明显降低;心率变异性和每日夜间血压节律恢复正常水平。结论OSAHS的发生与部分心血管疾病有密切关系。此外,NCPAP治疗不仅对OSAHS有效,而且对合并的心血管疾病也有效。
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引用次数: 3
Effect of Rapamycin on TGF-β1-induced epithelial-mesenchymal transition in LoVo colonic adenocarcinoma cells 雷帕霉素对TGF-β1诱导的LoVo结肠腺癌细胞上皮-间质转化的影响
Pub Date : 2009-01-01 DOI: 10.1016/S1007-4376(09)60020-4
Renhu Sun, Jiang Li, Jing Cui, Qing Lv, Xinghua Liu, Guobin Wang

Objective

To investigate the effect of Rapamycin on epithelial-mesenchymal transition(EMT) of LoVo colonic adenocarcinoma cells in vitro.

Methods

Cultured LoVo colonic adenocarcinoma cells were divided into three groups: negative control group, EMT-inducing group(TGF-β 1) and EMT-interfering group(TGF-β 1 plus Rapamycin). E-cadherin expression in LoVo cells was detected by Western Blot, while the expression of vimentin was evaluated through immunocytochemistry. The Snail mRNA in LoVo cells was examined by RT-PCR.

Results

TGF-β 1 induced LoVo cell switching from polygonal to spindle-shaped. TGF-β 1 enhanced the expression of vimentin, but lowered the level of E-cadherin. In contrast, Rapamycin impaired the transition induced by TGF-β 1. Rapamycin dramatically abrogated TGF-β 1-induced vimentin expression and restored E-cadherin expression in LoVo cells. Rapamycin significantly repressed the up-regulation of Snail mRNA expression induced by TGF-β 1.

Conclusion

Rapamycin dramatically abrogated TGF-β 1 induced Snail mRNA expression in LoVo cells, hence inhibiting EMT of these cells in vitro.

目的探讨雷帕霉素对结肠癌细胞上皮-间质转化(EMT)的影响。方法将培养的LoVo结肠腺癌细胞分为阴性对照组、emt诱导组(TGF-β 1)和emt干扰组(TGF-β 1 +雷帕霉素)。Western Blot检测LoVo细胞中E-cadherin的表达,免疫细胞化学检测vimentin的表达。RT-PCR检测LoVo细胞中Snail mRNA的表达。结果stgf -β 1诱导LoVo细胞由多角形向纺锤形转变。TGF-β 1提高了vimentin的表达,降低了E-cadherin的表达。相反,雷帕霉素对TGF-β 1诱导的细胞转移有抑制作用。雷帕霉素显著消除TGF-β 1诱导的vimentin表达,恢复E-cadherin在LoVo细胞中的表达。雷帕霉素可显著抑制TGF-β 1诱导的Snail mRNA表达上调。结论雷帕霉素可明显抑制TGF-β 1诱导的LoVo细胞Snail mRNA的表达,从而抑制LoVo细胞的EMT。
{"title":"Effect of Rapamycin on TGF-β1-induced epithelial-mesenchymal transition in LoVo colonic adenocarcinoma cells","authors":"Renhu Sun,&nbsp;Jiang Li,&nbsp;Jing Cui,&nbsp;Qing Lv,&nbsp;Xinghua Liu,&nbsp;Guobin Wang","doi":"10.1016/S1007-4376(09)60020-4","DOIUrl":"10.1016/S1007-4376(09)60020-4","url":null,"abstract":"<div><h3>Objective</h3><p>To investigate the effect of Rapamycin on epithelial-mesenchymal transition(EMT) of LoVo colonic adenocarcinoma cells <em>in vitro</em>.</p></div><div><h3>Methods</h3><p>Cultured LoVo colonic adenocarcinoma cells were divided into three groups: negative control group, EMT-inducing group(TGF-β <sub>1</sub>) and EMT-interfering group(TGF-β <sub>1</sub> plus Rapamycin). E-cadherin expression in LoVo cells was detected by Western Blot, while the expression of vimentin was evaluated through immunocytochemistry. The Snail mRNA in LoVo cells was examined by RT-PCR.</p></div><div><h3>Results</h3><p>TGF-β <sub>1</sub> induced LoVo cell switching from polygonal to spindle-shaped. TGF-β <sub>1</sub> enhanced the expression of vimentin, but lowered the level of E-cadherin. In contrast, Rapamycin impaired the transition induced by TGF-β <sub>1</sub>. Rapamycin dramatically abrogated TGF-β <sub>1</sub>-induced vimentin expression and restored E-cadherin expression in LoVo cells. Rapamycin significantly repressed the up-regulation of Snail mRNA expression induced by TGF-β <sub>1</sub>.</p></div><div><h3>Conclusion</h3><p>Rapamycin dramatically abrogated TGF-β <sub>1</sub> induced Snail mRNA expression in LoVo cells, hence inhibiting EMT of these cells <em>in vitro</em>.</p></div>","PeriodicalId":100807,"journal":{"name":"Journal of Nanjing Medical University","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2009-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/S1007-4376(09)60020-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"72983098","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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Journal of Nanjing Medical University
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