Runx2 regulates peripheral nerve regeneration to promote Schwann cell migration and re-myelination

Runx2 is a major regulator of osteoblast differentiation and function;however,the role of Runx2 in peripheral nerve repair is unclea r.Here,we analyzed Runx2expression following injury and found that it was specifically up-regulated in Schwann cells.Furthermore,using Schwann cell-specific Runx2 knocko ut mice,we studied peripheral nerve development and regeneration and found that multiple steps in the regeneration process following sciatic nerve injury were Runx2-dependent.Changes observed in Runx2 knoc kout mice include increased prolife ration of Schwann cells,impaired Schwann cell migration and axonal regrowth,reduced re-myelination of axo ns,and a block in macrophage clearance in the late stage of regeneration.Taken together,our findings indicate that Runx2 is a key regulator of Schwann cell plasticity,and therefore peripheral nerve repair.Thus,our study shows that Runx2 plays a major role in Schwann cell migration,re-myelination,and peripheral nerve functional recovery following injury.

MAD2L2 overexpression attenuates the effects of TNF-α-induced migration and invasion capabilities in colorectal cancer cells

Background:Colorectal cancer is a major global health concern,exacerbated by tumor necrosis factor-alpha(TNF-α)and its role in inflammation,with the effects of Mitotic Arrest Deficient 2 Like 2(MAD2L2)in this context still unclear.Methods:The colorectal carcinoma cell lines HCT116 and SW620 were exposed to TNF-αfor a period of 24 h to instigate an inflammatory response.Subsequent assessments were conducted to measure the expression of inflammatory cytokines,the activity within the p38 mitogen-activated protein kinase(p38 MAPK)and Phosphoinositide 3-Kinase/AKT Serine/Threonine Kinase pathway(PI3K/AKT)signaling cascades.Transcriptome sequencing and subsequent integrative analysis with the Cancer Genome Atlas(TCGA)program database revealed a significant downregulation of the key factor MAD2L2.Enhancement of MAD2L2 expression was facilitated via lentiviral vector-mediated transfection.The influence of this overexpression on TNF-α-prompted inflammation,intracellular signaling pathways,and the migratory and invasive behaviors of the colorectal cancer cells was then scrutinized.Results:TNF-αtreatment significantly increased the expression of Interleukin-1 beta(IL-1β)and Interleukin-6(IL-6),activated the MAPK p38 and PI3K/AKT signaling pathways,and enhanced cell migration and invasion.A decrease in MAD2L2 expression was observed following TNF-αtreatment.However,overexpression of MAD2L2 reversed the effects of TNF-α,reducing IL-1βand IL-6 levels,attenuating PI3K/AKT pathway activation,and inhibiting cell migration and invasion.Conclusions:Overexpression of MAD2L2 attenuates the pro-inflammatory effects of TNF-α,suggesting that MAD2L2 plays a protective role against TNF-α-induced migration and invasion of colorectal carcinoma cells.Therefore,MAD2L2 holds potential as a therapeutic target in the treatment of colorectal cancer.

Absent in melanoma 2 attenuates proliferation and migration and promotes apoptosis of human colorectal cancer cells by activating P38MAPK signaling pathway

Colorectal cancer(CRC)stands among the top prevalent cancers worldwide and holds a prominent position as a major contributor to cancer-related mortality globally.Absent in melanoma 2(AIM2),a constituent of the interferoninducible hematopoietic interferon-inducible nuclear antigens with 200 amino acid repeats protein family,contributes to both cancer progression and inflammasome activation.Despite this understanding,the precise biological functions and molecular mechanisms governed by AIM2 in CRC remain elusive.Consequently,this study endeavors to assess AIM2’s expression levels,explore its potential antitumor effects,elucidate associated cancer-related processes,and decipher the underlying signaling pathways in CRC.Our findings showed a reduced AIM2 expression in most CRC cell lines.Elevation of AIM2 levels suppressed CRC cell proliferation and migration,altered cell cycle by inhibiting G1/S transition,and induced cell apoptosis.Further research uncovered the participation of P38 mitogen-activated protein kinase(P38MAPK)in AIM2-mediated modulation of CRC cell apoptosis and proliferation.Altogether,our achievements distinctly underscored AIM2’s antitumor role in CRC.AIM2 overexpression inhibited proliferation and migration and induced apoptosis of CRC cells via activating P38MAPK signaling pathway,indicating AIM2 as a prospective and novel therapeutic target for CRC.

Simulation Study on the Migration Range of CO_(2) in the Offshore Saline Aquifer

The geological storage of carbon dioxide(CO_(2)) is a crucial technology for mitigating climate change. Offshore deep saline aquifers have elicited increased attention due to their remarkable potential for storing CO_(2). During long-term storage, CO_(2) migration in a deep saline aquifer needs special attention to prevent it from reaching risk points and leading to security issues. In this paper, a mechanism model is established according to the geological characteristics of saline aquifers in an offshore sedimentary basin in China. The CO_(2) migration over 100 years is simulated considering geological changes such as permeability, dip angle, thickness, and salinity. The effects of injection conditions on the CO_(2) migration range are also investigated. Results reveal that the migration range of CO_(2) in the injection period exceeds 70%, even if the postinjection period's duration is five times longer than that of the injection period. As the values of the above geological parameters increase, the migration range of CO_(2) increases, and permeability has a particularly substantial influence. Moreover, the influences of injection rate and well type are considerable. At high injection rates, CO_(2) has a greater likelihood of displacing brine in a piston-like scheme. CO_(2) injected by long horizontal wells migrates farther compared with that injected by vertical wells. In general, the plane migration range is within 3 000 m, although variations in the reservoir and injection parameters of the studied offshore saline aquifers are considered. This paper can offer references for the site selection and injection well deployment of CO_(2) saline aquifer storage. According to the studied offshore aquifers, a distance of at least 3 000 m from potential leakage points, such as spill points, active faults, and old abandoned wells, must be maintained.

功能化氮杂环卡宾聚合树脂对Cu^(2+)的吸附研究

该研究制备了功能化氮杂环卡宾聚合树脂(PNO),旨在去除废水中Cu^(2+);基于静态和动态吸附实验,研究了PNO对废水中Cu^(2+)的吸附效果。结果表明:PNO对Cu^(2+)的最佳吸附条件为吸附剂投加量100 mg、吸附时间30 min、pH值4.0~5.9、温度298 K、转速150 r/min,最大吸附量为51.55 mg/g。PNO对Cu^(2+)的吸附过程符合Langmuir、Freundlich等温吸附模型和准二级动力学模型。动态吸附量随柱高增加、流速降低和进水Cu^(2+)浓度增加而增大。使用Thomas和Bohart-Adams模型拟合,相关系数R^(2)均大于0.92,预测值与实验值相符。经过5次静态吸附-解吸和3次动态循环再生后,PNO对Cu^(2+)的去除率仍达到第一次循环的96%以上,去除效果和再生性能良好。PNO对含铜废水高效处理具有广泛的应用前景。

磁性三乙烯四胺/单宁树脂对Cu^(2+)、Pb^(2+)的吸附性能研究

利用曼尼希反应将三乙烯四胺(TETA)固化到单宁(TA)基体表面,热溶剂法制得磁性单宁基树脂(MTETA-TA)。通过红外光谱、扫描电镜、比表面积及孔隙度分析仪、振动样品磁强计对M-TETA-TA进行表征,表明M-TETA-TA具有疏水性强、比表面积大的优势,Fe_(3)O_(4)的成功引入有效解决吸附剂回收难的问题。对含Cu^(^(2+))、Pb^(2+)废水溶液进行了静态吸附实验,探讨了其对金属的吸附性能。在pH为5的酸性条件下,吸附效果较好;Cu^(^(2+))和Pb^(2+)吸附动力学均符合准二级反应动力学模型,主要为化学吸附;Cu^(^(2+))的吸附等温线符合Langmuir模型,属单层吸附,理论吸附最大值为173.33 mg·g^(-1);Pb^(2+)的吸附等温线符合Sips模型,属多层吸附,理论吸附最大值为217.14 mg·g^(-1)。推测M-TETA-TA对Pb^(2+)的吸附除了螯合、氧化还原等化学反应,还存在静电和离子交换作用,氨基和酚羟基为主要参与官能团。循环再生5次后,仍有较高的吸附性能和磁性强度。

Role of Tissue Factor Pathway Inhibitor-2 in Ovarian Tumor Migration and Invasion

Objective: To elucidate the relation between human tissue factor pathwayinhibitor-2 (TFPI-2) expression and ovarian tumor migration and invasion. Methods: Human TFPI-2expression vector pBos-Cite-neo/TFPI-2 was transfected into ovarian tumor cells line A2780- Afterthe transfected cells were selected by G418, transfected and nontransfected cells were screened forTFPI-2 mRNA and protein by reverse transcription-polymerase chain reaction and Western blotanalysis, respectively. The number of transfected or nontransfected cells passing through membraneof Boyden chamber was counted as the basis assessing tumor cells migratory and invasive behaviors.Results: Expression of mRNA and protein of TFPI-2 was detectable in transfected cells. In invasionassay, the number of TFPI-2-expressing cells to traverse a Matrigel-coated membrane was obviouslydecreased compared with that of nonexpressing cells (59.3±6.5 vs 109.7±5.5, P 【 0.01); While inmigration assay, no significant difference through a noncoated membrane was observed amongtransfected and nontransfected cells (114.7±8.6 vs 127.3±7.1, P 】 0.05). Conclusion: Expression ofTFPI-2 may strongly inhibit the invasive ability of ovarian tumor cells in vitro, but has no effecton the migratory ability which provides an experimental basis for genotherapy of human ovariantumor.

ZIF-8/PEO杂化泡沫对TC和Cu^(2+)吸附研究

以提高金属有机骨架ZIF-8水处理中可回收性为目标,利用聚氧化乙烯PEO作为致孔剂,采用冰模板-冷冻干燥法制备金属有机骨架杂化泡沫ZIF-8/PEO,利用XRD、SEM、TG-DSC和N2吸附-脱附等表征手段,分析ZIF-8/PEO杂化泡沫的理化性能,研究ZIF-8/PEO对四环素TC和铜离子Cu^(2+)吸附性能及吸附机理。试验结果表明:ZIF-8/PEO形成了更加规则的网状结构且具有良好的机械强度和吸附性能。在吸附时间12 h,pH 7,吸附剂投加量40 mg,TC和Cu^(2+)初始浓度均为30 mg/L的最佳条件下,ZIF-8/PEO对TC和Cu^(2+)的吸附容量为107.55 mg/g和107.81 mg/g;等温吸附过程符合Langmuir模型,动力学过程符合拟二级动力学模型,ZIF-8/PEO吸附TC,Cu^(2+)属于自发、放热、趋于有序的过程。在循环吸附7次后,ZIF-8/PEO吸附剂对TC和Cu^(2+)的去除率仍在70%以上。

Fe^(2+)、Cu^(2+)诱导工艺对柞木表板颜色变化规律的影响

木材中的木质素、抽提物等物质具有能与金属盐溶液产生颜色反应的特性。利用这一特性以硫酸亚铁、硫酸铜溶液作为诱导剂,通过正交试验得到色差最大时的工艺参数,探究金属Fe^(2+)、Cu^(2+)的诱导剂质量分数、诱导时间、干燥时间、干燥温度对实木复合地板柞木表板颜色变化的影响。结果表明:Fe^(2+)、Cu^(2+)的诱导剂质量分数对柞木表板色彩色调的影响极为显著(F值分别为20.4453、8.8442);柞木表板的明度色品指数(L^(*))、红绿轴色品指数(a^(*))、黄蓝轴色品指数(b^(*))均随着Fe^(2+)、Cu^(2+)的诱导剂质量分数、诱导时间、干燥时间的增加而逐渐减少,总色差(ΔE^(*))逐渐增大,最大为31.53、9.90,表板色调逐渐偏暗、偏绿、偏蓝;随着干燥温度的增加,Fe^(2+)、Cu^(2+)诱导时的柞木表板总色差都逐渐减小。

不同质量浓度Cu^(2+)和Ag^(+)对大麦成熟胚组培特性的影响

【目的】探究不同质量浓度Cu^(2+)和Ag^(+)对大麦成熟胚组培特性的影响。【方法】以Bowman、北青7号和光头大麦的成熟胚为材料,研究不同质量浓度Cu^(2+)和Ag^(+)对大麦成熟胚愈伤诱导率、长根率、长芽率、褐化率、绿化率、再分化率和愈伤湿质量的影响。【结果】Bowman、北青7号和光头大麦成熟胚的7种组培特性间存在不同程度差异。与对照相比,0.75 mg/L Cu^(2+)可减少10.43%的成熟胚长根、7.48%的成熟胚长芽、8.24%的愈伤组织褐化、20.74 mg的愈伤湿质量;4.00 mg/L Ag^(+)可提高6.47%的愈伤组织诱导率,可减少9.08%的成熟胚长根、7.96%的成熟胚长芽和9.67%的愈伤褐化;0.75 mg/L Cu^(2+)和4.00 mg/L Ag^(+)对愈伤细胞转绿、愈伤增殖和再分化均无抑制。【结论】适宜质量浓度的Cu^(2+)和Ag^(+)可有效抑制大麦成熟胚长根、长芽和愈伤组织褐化,Ag+还可有效提高愈伤诱导率;在基于MS培养基的大麦成熟胚愈伤组织诱导和再分化培养中,Cu^(2+)和Ag^(+)的适宜质量浓度分别为0.75和4.00 mg/L。研究结果可为构建大麦成熟胚的愈伤诱导及其再分化技术体系提供理论支持。

钠化污泥生物炭复合凹凸棒石对水体中Cu^(2+)的吸附效果研究

含铜废水严重威胁人体健康和环境安全,利用废弃污泥和凹凸棒石制备了钠化污泥生物炭复合凹凸棒石材料,并将其用于含Cu^(2+)废水的处理。利用SEM、XRD及FT-IR对材料的结构和表面性质进行了分析表征,复合材料表面的含氧官能团的络合或C=C键的Π电子作用是吸附重金属的主要机制。研究了复合材料对Cu^(2+)的吸附效果和机理,结果表明,污泥/凹凸棒石质量比2∶1,pH=5,添加量为1.5 g/L,Cu^(2+)初始浓度4 mg/L条件下,材料对Cu^(2+)有最大的吸附容量为3.339 mg/g。吸附过程更好地拟合了准二级动力学模型和Langmuir吸附等温式,表明材料对Cu^(2+)的吸附是单分子层化学吸附。利用响应面分析法预测,pH值为5.04,吸附剂添加量1.16 g/L,Cu^(2+)初始浓度3.60 mg/L是最佳吸附条件。钠化污泥生物炭复合凹凸棒石在实际含铜废水处理中是一种极具潜力的吸附剂。

UiO-66-NH_(2)的改性及其吸附Cu^(2+)性能

通过溶剂热法合成了锆基金属有机框架材料中的UiO-66-NH_(2),用多巴胺(DA)对其进行后合成改性,制备了UiO-66-NH_(2)/PDA复合材料,用于去除重金属Cu^(2+)。探究了pH、初始ρ(Cu^(2+))、接触时间和温度对吸附过程的影响,结果表明,Cu^(2+)的吸附动力学和等温线数据分别符合准二级和Langmuir模型,吸附过程为自发吸热反应;初始ρ(Cu^(2+))=50 mg/L,pH=5.5,t<30 min,Cu^(2+)去除率为93%。

用于吸附养殖尾水中Cu^(2+)的温度敏感型淀粉基水凝胶制备及性能分析

为了快速移除水产养殖尾水中的铜离子(Cu^(2+)),合成了一种新型温度敏感多糖基水凝胶,以具有结构和性能优势的2-羟基-3-异丙氧基丙基淀粉醚(HIPS)和羧甲基淀粉钠(CMS)为原料,以乙二醇二缩水甘油醚(EDGE)和CaCl 2为交联剂,通过形成共价键和离子键的混合交联方式制备具有温度敏感性能的HIPS/CMS复合凝胶,利用傅里叶转换红外光谱(FT-IR)、扫描电镜(SEM)对复合凝胶的结构和内部形貌进行表征,研究复合凝胶的温度敏感性能,并探究了复合凝胶对水产养殖尾水中Cu^(2+)的吸附效果。结果表明:HIPS/CMS复合凝胶具有优异的温度敏感性能,当温度高于其体积相转变温度(VPTT,34.1℃)时,复合凝胶体积明显收缩,溶胀率从62.1倍下降至33.6倍;HIPS/CMS复合凝胶对水产养殖尾水中Cu^(2+)具有良好的吸附性能,最大吸附量可达25.2 mg/g;复合凝胶对Cu^(2+)吸附过程符合Langmuir吸附模型,属于单分子层化学吸附;利用该复合凝胶的温度敏感性能,可实现HIPS/CMS复合凝胶的回收再利用,并且经5次吸附-解吸循环后吸附量仍可达15.1 mg/g。研究表明,本研究制备的HIPS/CMS复合凝胶对养殖尾水中的Cu^(2+)的去除效果较好且绿色环保,可以重复使用。

Cu^(2+)污染原状黄土的物化及结构特性

为制定环境保护和土壤污染防治和修复策略,以及为污染场地工程建设提供理论支撑,该文研究了Cu^(2+)对原状黄土物化特性及结构特性的影响。通过制备不同掺量的Cu^(2+)污染黄土试样,进行了粒径分布、CaCO_(3)含量和pH值的测定。利用扫描电镜和激光粒度仪获得试样的SEM图像和粉粒各粒径含量,并借助分形理论深入分析了Cu^(2+)对原状黄土微观结构的影响机理。对Cu^(2+)污染的原状黄土试样进行了压缩试验,并对试样的综合结构势进行了分析。结果表明,随着Cu^(2+)掺量的增大,黏粒含量表现为先增后减,再增再减的趋势,粉粒含量则表现为先减后增,再减再增,砂粒含量保持不变;CaCO_(3)的含量呈线性减小;pH值先迅速减小,后保持不变;污染黄土试样的综合结构势先增大后减小,之后再增大再减小。总体而言,重金属Cu^(2+)的掺入,导致土壤pH值降低,主要胶结物质碳酸钙被溶解,而又因黏粒之间的静电引力和范德华力,黏粒聚集体的形态和成分发生变化,从而影响了土体的密实度和结构强度。

两种磁性生物炭耦合Diaphorobacter sp.DFA4去除2,4-DFA和Cu^(2+)的特性

以橘子皮为原料,氯化铁、镍锰铁氧体为磁性介质,制备了氯化铁和镍锰铁氧体改性生物炭(分别记为FBC和MBC),重点考察FBC和MBC介导Diaphorobacter sp.DFA4耦合体系去除2,4-二氟苯胺(2,4-DFA)和Cu^(2+)的特性。结果表明:在0.5~2.0 g/L FBC/MBC的介导作用下,Diaphorobacter sp.DFA4对2,4-DFA和Cu^(2+)的去除效果明显提升。当2,4-DFA初始质量浓度为100~900 mg/L时,相比纯菌Diaphorobacter sp.DFA4培养体系,FBC和MBC介导耦合体系对2,4-DFA的降解强化倍数分别为2.24~4.04倍和1.96~4.71倍,Cu^(2+)去除率则分别由59.70%~69.95%提升至88.57%~93.20%和82.12%~88.20%。当pH为6.0~8.0时,较纯菌Diaphorobacter sp.DFA4培养体系,MBC、FBC介导耦合体系对2,4-DFA的去除率分别提高了15.35%~36.32%和22.43%~37.42%,对Cu^(2+)的去除率则分别提高了37.63%~42.34%和43.61%~47.83%;当盐度由0提高至4%时,两个耦合体系对2,4-DFA的去除率基本保持在85%及以上,而纯菌Diaphorobacter sp.DFA4培养体系对2,4-DFA的去除率则由77.98%降至55.19%。机理分析发现,耦合体系可诱导分泌更多的腐殖酸,且在偏碱条件下,FBC更有利于促使腐殖酸的分泌。

Ca2+/calmodulin-dependent protein kinase II regulates colon cancer proliferation and migration via ERK1/2 and p38 pathways

AIM To investigate the role of calmodulin-dependent protein kinase Ⅱ(Ca MKⅡ) in colon cancer growth,migration and invasion.METHODS Ca MKⅡ expression in colon cancer and paracancerous tissues was evaluated via immunochemistry. Transcriptional and posttranscriptional levels of Ca MKⅡin tissue samples and MMP2,MMP9 and TIMP-1 expression in the human colon cancer cell line HCT116 were assessed by q RTPCR and western blot. Cell proliferation was detected with the MTT assay. Cancer cell migration and invasion were investigated with the Transwell culture system and woundhealing assay.RESULTS We first demonstrated that CaMK Ⅱ was ove rexpressed in human colon cancers and was associated with cancer differentiation. In the human colon cancer cell line HCT116,the Ca MKII-specific inhibitor KN93,but not its inactive analogue KN92,decreased cancer cell proliferation. Furthermore,KN93 also significantly prohibited HCT116 cell migration and invasion. The specific inhibition of ERK1/2 or p38 decreased the proliferation and migration of colon cancer cells.CONCLUSION Our findings highlight Ca MKⅡ as a potential critical mediator in human colon tumor development and metastasis.

Thymoquinone suppresses migration of Lo Vo human colon cancer cells by reducing prostaglandin E2 induced COX-2 activation

AIM To identify potential anti-cancer constituents in natural extracts that inhibit cancer cell growth and migration. METHODS Our experiments used high dose thymoquinone (TQ) as an inhibitor to arrest LoVo (a human colon adenocarcinoma cell line) cancer cell growth, which was detected by cell proliferation assay and immunoblotting assay. Low dose TQ did not significantly reduce LoVo cancer cell growth. Cyclooxygenase 2 (COX-2) is an enzyme that is involved in the conversion of arachidonic acid into prostaglandin E2 (PGE2) in humans. PGE2 can promote COX-2 protein expression and tumor cell proliferation and was used as a control. RESULTS Our results showed that 20 mu mol/L TQ significantly reduced human LoVo colon cancer cell proliferation. TQ treatment reduced the levels of p-PI3K, p-Akt, p-GSK3 beta, and beta-catenin and thereby inhibited the downstream COX-2 expression. Results also showed that the reduction in COX-2 expression resulted in a reduction in PGE2 levels and the suppression of EP2 and EP4 activation. Further analysis showed that TG treatment inhibited the nuclear translocation of beta-catenin in LoVo cancer cells. The levels of the cofactors LEF-1 and TCF-4 were also decreased in the nucleus following TQ treatment in a dose-dependent manner. Treatment with low dose TQ inhibited the COX-2 expression at the transcriptional level and the regulation of COX-2 expression efficiently reduced LoVo cell migration. The results were further verified in vivo by confirming the effects of TQ and/or PGE2 using tumor xenografts in nude mice. CONCLUSION TQ inhibits LoVo cancer cell growth and migration, and this result highlights the therapeutic advantage of using TQ in combination therapy against colorectal cancer.

Effects of ginsenoside Rh2 on growth and migration of pancreatic cancer cells

AIM:To investigate the effects of ginsenoside Rh2 on the human pancreatic cancer cell line Bxpc-3.METHODS:The human pancreatic cancer cell line Bxpc-3 was cultured in vitro and treated with or without ginsenoside Rh2.Growth rates for Bxpc-3 cells were assessed by methyl thiazolyl tetrazolium(MTT) and colony formation assays.Cell cycle changes were analyzed by flow cytometry.Apoptosis was measured by flow cytometry and Hoechst 33258 fluorescence staining.A scratch assay and a Matrigel invasion assay were used to detect cell migration and invasion.Expression of Bax,Bcl-2,survivin,cyclin D1,matrix metalloproteinase(MMP)-2,MMP-9,cleaved caspase-3,caspase-8,and caspase-9 mRNA were determined by reverse transcriptase-polymerase chain reaction(RT-PCR).Bax,Bcl-2,survivin,cyclin D1,cleaved caspase-3,caspase-8 and caspase-9 protein levels were examined by western blotting.Expression of MMP-2 and MMP-9 proteins in culture supernatants were determined by enzymelinked immunosorbent assay(ELISA).RESULTS:Rh2 significantly inhibited Bxpc-3 cell proliferation in a dose-and time-dependent manner,as evaluated by the MTT(P < 0.05) and colony formation assays(P < 0.05).Compared to the control group,Rh2 significantly increased the percentage of Bxpc-3 cells in the G 0 /G 1 phase from 43.32% ± 2.17% to 71.32% ± 1.16%,which was accompanied by a decrease in S phase(from 50.86% ± 1.29% to 28.48% ± 1.18%) and G 2 /M phase(from 5.81% ± 1.19% to 0.20% ± 0.05%) in a dose-dependent manner(P < 0.05),suggesting that Rh2 arrested cell cycle progression at the G 0 /G 1 phase,as measured by flow cytometry.Compared to the control group,cells treated with Rh2 showed significantly higher apoptosis ratios in a dosedependent manner(percentage of early apoptotic cells:from 5.29% ± 2.28% to 38.90% ± 3.42%(F = 56.20,P < 0.05);percentage of late apoptotic cells:from 4.58% ± 1.42% to 36.32% ± 2.73%(F = 86.70,P < 0.05).Rh2 inhibited Bxpc-3 cell migration and invasion,as detected by scratch wound healing assay and Matrigel invasion assay [percentages of scratch wound healing for 12 h,24 h and 48 h(control vs experimental group):37.3% ± 4.8%vs 18.30% ± 1.65%,58.7% ± 3.5% vs 38.00% ± 4.09% and 93.83% ± 4.65% vs 65.50% ± 4.09%,respectively;t = 6.489,t = 6.656 and t = 7.926,respectively,P < 0.05;the number of cells invading at various concentrations(0 μmol/L,35 μmol/L,45 μmol/L and 55 μmol/L):81.10 ± 9.55,46.40 ± 6.95,24.70 ± 6.88 and 8.70 ± 3.34,respectively(F = 502.713,P < 0.05)].RT-PCR,western blotting or ELISA showed that mRNA and protein expression of Bax,cleaved caspase-3 and caspase-9 were upregulated(P < 0.05),while mRNA and protein expression of Bcl-2,survivin,cyclin D1,MMP-2 and MMP-9 were downregulated(P < 0.05).CONCLUSION:Ginsenoside Rh2 inhibits proliferation,migration and invasion and induces apoptosis of the human pancreatic cancer cell line Bxpc-3.

Annexin A2 silencing inhibits invasion, migration, and tumorigenic potential of hepatoma cells

AIM: To investigate the effects of Annexin A2 (ANXA2) silencing on invasion, migration, and tumorigenic potential of hepatoma cells. METHODS: Human hepatoma cell lines [HepG2, SMMC-7721, SMMC-7402, and MHCC97-H, a novel human hepatocellular carcinoma (HCC) cell line with high metastasis potential] and a normal hepatocyte cell line(LO2) were used in this study. The protein and mRNA expression levels of ANXA2 were analysed by western blotting and real-time polymerase chain reaction, re-spectively. The intracellular distribution profile of ANXA2 expression was determined by immunofluorescence and immunohistochemistry. Short hairpin RNA target-ing ANXA2 was designed and stably transfected into MHCC97-H cells. Cells were cultured for in vitro analy-ses or subcutaneously injected as xenografts in mice for in vivo analyses. Effects of ANXA2 silencing on cell growth were assessed by cell counting kit-8 (CCK-8) as-say (in vitro ) and tumour-growth assay (in vivo ), on cell cycling was assessed by flow cytometry and propidium iodide staining (in vitro ), and on invasion and migration potential were assessed by transwell assay and wound-healing assay, respectively (both in vitro ). RESULTS: The MHCC97-H cells, which are known to have high metastasis potential, showed the highest lev-el of ANXA2 expression among the four HCC cell types examined; compared to the LO2 cells, the MHCC97-H expression level was 8-times higher. The ANXA2 expres-sion was effectively inhibited (about 80%) by ANXA2-specific small hairpin RNA (shRNA). ANXA2 expression in the MHCC97-H cells was mainly localized to the cel-lular membrane and cytoplasm, and some localization was detected in the nucleus. Moreover, the proliferation of MHCC97-H cells was obviously suppressed by shR-NA-mediated ANXA2 silencing in vitro , and the tumour growth inhibition rate was 38.24% in vivo . The per-centage of MHCC97-H cells in S phase dramatically de-creased (to 27.76%) under ANXA2-silenced conditions. Furthermore, ANXA2-silenced MHCC97-H cells showed lower invasiveness (percentage of invading cells de-creased to 52.16%) and suppressed migratory capacity (migration distance decreased to 63.49%). It is also worth noting that shRNA-mediated silencing of ANXA2 in the MHCC97-H cells led to abnormal apoptosis. CONCLUSION: shRNA-mediated silencing of ANXA2suppresses the invasion, migration, and tumorigenic potential of hepatoma cells, and may represent a useful target of future molecular therapies.

TPX2 promotes migration and invasion of human breast cancer cells

Objective:To investigate the expression of targeting protein for Xenopus kinesin-like protein 2(TPX2) in breast cancer tissue and to explore its role in proliferation,migration and invasion of breast cancer cells.Methods:The mRNA and protein expressions of TPX2 in breast cancer tissue and cell lines were assessed by quantitative RT-PCR and Western blot.The effect of TPX2 with RNA interference on proliferation,invasion and migration of breast cancer cells was observed by MTT and Transwell assays.Results:Both mRNA and protein expressions of TPX2 were upregulated in breast cancer tissues compared to tumor-adjacent tissue.TPX2 expression was also upregulated in breast cancer cell lines,and the TPX2 interfered by small interfering RNA could inhibit the proliferation,invasion and migration of breast cancer cells by inhibiting matrix metalloproteinase-2 and matrix metalloproteinase-9.Conclusions:Significantly upregulated TPX2 expression is observed in breast cancer tissue and cells,and contributes to promote the proliferation,migration and invasion of breast cancer cells.