丹皮酚通过JAK-STAT信号通路对宫颈癌细胞增殖迁移及侵袭的作用机制

目的 分析丹皮酚通过Janus激酶(JAK)-信号传导和转录激活因子(STAT)信号通路对宫颈癌细胞(Hela细胞)增殖迁移及侵袭的作用机制。方法 采用不同浓度丹皮酚对Hela细胞进行处理,根据丹皮酚浓度不同分为0、7.5、15.0、22.5、30.0、60.0 mg/L组,分别在培养24、48、72 h时采用MTT法检测细胞增殖,流式细胞术检测细胞调亡,Transwells小室检测细胞迁移和侵袭情况,并比较各组细胞培养72 h后的JAK1、JAK2、STAT3水平及其mRNA相对表达水平。结果 使用不同浓度丹皮酚对Hela细胞处理24、48、72 h后,随处理时间的延长各组细胞吸光度(A)值、凋亡率均升高,细胞迁移个数、侵袭个数均增多,差异均有统计学意义(P <0.05);培养24、48、72 h时,7.5、15.0、22.5、30.0、60.0 mg/L组细胞A值、凋亡率均低于0 mg/L组,细胞迁移个数、侵袭个数均少于0 mg/L组,差异均有统计学意义(P <0.05),其中60 mg/L组细胞A值、凋亡率最低,细胞迁移个数、侵袭个数最少,7.5 mg/L组细胞A值、...     

京尼平苷调控Wnt/β-cantenin信号通路抑制胃癌转移的机制研究

目的 探讨京尼平苷（GEN）抑制人胃癌SGC-7901细胞转移的作用及其可能机制。方法 培养人胃癌SGC-7901细胞,使用GEN处理细胞,通过CCK8法检测GEN对SGC-7901细胞增殖的影响,运用Transwell实验检测GEN对SGC-7901细胞迁移和侵袭能力的作用,运用Westernblot和q-PCR检测GEN对SGC-7901细胞β-catenin、E-cadherin、Vimentin和Snail蛋白及mRNA表达的作用;运用Wnt通路激活剂（LiCl）和GEN联合处理SGC-7901细胞后,观察对SGC-7901细胞迁移和侵袭能力的影响,对β-catenin、E-cadherin、Vimentin和Snail蛋白及mRNA表达的影响。结果 Transwell实验结果显示,GEN能够抑制SGC-7901细胞的迁移和侵袭能力下降,差异有统计学意义（P<0.05）。Westernblot和q-PCR结果表明,GEN能够促进E-cadherin的表达,抑制β-catenin、Vimentin和Snail的表达,差异有统计学意义（P<0.05）。与GEN组比较,W...     

白鲜碱通过Wnt/β-catenin信号通路抑制前列腺癌骨转移PC-3细胞的作用

目的 探讨白鲜碱对人前列腺癌细胞上皮-间充质转化的抑制作用及其机制.方法 培养人前列腺癌PC-3细胞,用白鲜碱处理PC-3细胞,通过MTS检测白鲜碱的半抑制浓度IC50及对PC-3细胞增殖的时间依赖性.细胞侵袭能力的检测采用Transwell实验;E-cadherin、vimentin、β-catenin和Snail蛋...     

罗哌卡因对人甲状腺癌细胞线粒体呼吸作用的影响

目的探讨局麻药罗哌卡因对人甲状腺癌细胞线粒体呼吸作用的影响。方法将人甲状腺癌细胞系MDA-T120以4×104个/ml的密度接种于细胞培养板,随机分为四组:对照组不进行任何处理,0. 1 m M组在细胞培养板中加入罗哌卡因0. 1 m M,0. 5 m M组在细胞培养板中加入罗哌卡因0. 5 m M,1. 0 m M组在细胞培养板中加入罗哌卡因1. 0 m M组,罗哌卡因处理24 h。24 h后检测细胞增殖和细胞凋亡情况; JC-10染色检测细胞线粒体膜电位,Clark氧电极法检测细胞的耗氧量,分析线粒体呼吸复合物活性、ATP含量及氧化应激水平。结果与对照组相比,0. 1 m M、0. 5m M和1. 0 m M罗哌卡因均可降低甲状腺癌细胞增殖活性(P 0. 05),促进癌细胞凋亡(P 0. 05),降低基线耗氧量和最大耗氧量(P 0. 05),抑制线粒体呼吸复合物I和II的活性(P 0. 05),降低线粒体ATP的水平(P 0. 05),增加超氧化物及8-OHd G水平(P 0. 05),且呈剂量依赖性。但罗哌卡因对复合物Ⅳ和V活性及线粒体膜电位无显著影响。结论罗哌卡因呈剂量依赖性抑制人甲状腺癌细胞增殖,诱导其凋亡。其机制可能与罗哌卡因抑制癌细胞线粒体的呼吸作用,诱导能量耗损、氧化应激及氧化损伤有关。     

丁哌卡因和罗哌卡因应用于腰麻患者的临床效果观察

目的比较同浓度、同剂量和等比重的丁哌卡因和罗哌卡因对于腰麻患者的临床麻醉效果及不良反应的发生情况。方法择期在腰麻下行下腹部、会阴及下肢皮肤外科手术的患者80例,随机分为丁哌卡因组(B组,n=40)和罗哌卡因组(R组,n=40)。两组分别给以等比重的丁哌卡因或罗哌卡因各2.5³.0 ml(分别取0.75%的丁哌卡因或罗哌卡因1.5 ml,然后以相同容积的脑脊液稀释至3 ml)。比较两组麻醉后血流动力学的变化,感觉及运动神经阻滞效果、恢复情况,麻醉镇痛效果,术中、术后不良反应发生情况。结果 R组血流动力学变化更小(P<0.05),运动神经阻滞较轻且恢复更快(P<0.05),而感觉神经阻滞持续时间与B组相似。麻醉效果比较两组无统计学差异,术中、术后不良反应发生率R组低于B组(P<0.05)。结论下腹部、会阴及下肢皮肤外科手术患者应用等比重罗哌卡因腰麻,麻醉效果好,不良反应发生轻微,对患者各项生命体征的影响小于等比重丁哌卡因,是一种安全可靠的麻醉方法。     

SFRP5调控Wnt/β-Catenin信号通路对子痫前期滋养细胞迁移和侵袭的作用机制研究

目的 探讨分泌型卷曲相关蛋白5(SFRP5)在子痫前期(PE)患者中的表达水平及其对滋养细胞迁移和侵袭能力的影响。方法 收集2020年1月到2021年10月在长治医学院附属和济医院产科收治的15例PE患者(PE组)和15例健康孕妇(正常组)剖宫产手术中获得的胎盘组织和血液样本;采用酶联免疫吸附试验法和免疫组化法分别检测血清和胎盘组织中SFRP5表达水平;体外培养人滋养层细胞系HTR8/SVneo,分别用重组人SFRP5蛋白、Dickkopf相关蛋白1(Dkk-1)和氯化锂(LiCl)处理细胞;采用划痕实验和基底胶Transwell实验检测HTR8/SVneo滋养细胞迁移和侵袭能力;明胶酶谱法检测HTR8/SVneo滋养细胞基质金属蛋白酶(MMP)-2/9的活性;蛋白免疫印迹法检测HTR8/SVneo滋养细胞中糖原合成酶-3β(GSK3β)和β-catenin蛋白的表达。结果 与正常组[(9.03±1.75)ng/mL)]相比,PE组血清SFRP5水平[(48.07±3.81)ng/mL]显著升高,差异有统计学意义(t=36.063、P<0.001)。与对照组相比,SFRP5组HT...     

Wnt信号通路在足细胞中的作用和调节机制

Wnt信号通路在细胞的分化、增殖和凋亡等生理过程中以及在细胞癌变、肿瘤侵袭等病理过程中均发挥了重要的调控作用。最近研究显示,Wnt信号通路在肾脏疾病发展和上皮细胞特化中起重要作用,在损伤等不同的疾病条件下该通路被激活。基因修饰动物模型研究表明,在足细胞中Wnt信号通路持续激活通常与蛋白尿和肾小球硬化的进展有关。本文就Wnt信号在足细胞中的作用和调节机制作一综述。     

Paeoniflorin inhibits proliferation and invasion of breast cancer cells through suppressing Notch-1 signaling pathway

Paeoniflorin (PF), one of the major active ingredients of Chinese peony, was reported to possess anti-tumor effect. However, the role of PF in breast cancer remains to be clarified. Therefore, in this context, the present study investigated the effects of PF on breast cancer cell proliferation and invasion, as well as the underlying mechanism. Our results found that PF suppressed the proliferation and invasion of breast cancer cells. We further demonstrated that PF down-regulated the expression of Notch-1; in addition, overexpression of Notch-1 reversed PF-inhibited proliferation and invasion, and knockdown of Notch-1 enhanced PF-inhibited proliferation and invasion in breast cancer cells. In conclusion, the present study suggests that PF inhibits proliferation and invasion of breast cancer cells through suppressing Notch-1 signaling pathway. Therefore, PF may represent a chemopreventive and/or therapeutic agent in the prevention of breast cancer.     

Extracellular matrix protein ITGBL1 promotes ovarian cancer cell migration and adhesion through Wnt/PCP signaling and FAK/SRC pathway

Despite the advances in cancer treatment and the progresses in tumor biological, ovarian cancer remains a bad situation. In current study, we found a novel extracellular matrix protein, ITGBL1, which is highly expressed in ovarian cancer tissues by immunohistochemistry examination. The expression pattern of ITGBL1 in malignant tissues inspired us to investigate its role in ovarian cancer progression. Both loss- and gain-function assays revealed that ITGBL1 could promote ovarian cancer cell migration and adhesion. As it’s a secreted protein, we further used recombinant ITGBL1 protein treated cancer cells and found that ITGBL1 promotes cell migration and adhesion in a concentration dependent manner. Furthermore, we found that ITGBL1 not only influences the activity of Wnt/PCP signaling but also affects FAK/src pathway in vitro. Taken together, our results suggest that highly expressed ITGBL1 could promotes cancer cell migration and adhesion in ovarian cancer and as a secreted protein, ITGBL1 might be a novel biomarker for ovarian cancer diagnosis.     

Block of proliferation 1 promotes cell migration and invasion in human colorectal cancer cells via the JNK pathway

Metastasis is one of the most common causes of death in patients with colorectal cancer (CRC). Block of proliferation 1 (BOP1) regulates tumorigenesis, epithelial-to-mesenchymal transition, migration, metastasis, and drug resistance in several tumor types. However, the role of BOP1 in the regulation of colorectal cancer cell migration and invasion is still largely unclear. In this study, the results of immunohistochemistry showed that BOP1 was upregulated in our cohort of CRC patients. BOP1 knockdown inhibited the migration and invasion of CRC cells, confirmed by the downregulation of the mRNA levels of MMP-2 and MMP-9. The overexpression of BOP1 in CRC cells exerted the opposite effect. SP600125, an inhibitor of JNK signaling, partially abolished the BOP1 overexpression-mediated increase in the migratory and invasive ability of CRC cells. Our results indicated that BOP1 is an important regulator of CRC cell invasion and migration, predominantly through the JNK signaling pathway.     

The m6A methyltransferase METTL14 inhibits the proliferation,migration, and invasion of gastric cancer by regulating the PI3K/AKT/mTOR signaling pathway

Background N6‐methyladenosine (m6A) modification may participate in the regulation of occurrence and development of tumors. However, the m6A level and the potential regulatory mechanism of m6A in gastric cancer (GC) remain uncertain.MethodsRNA m6A quantification assay was conducted to detect the m6A level in GC tissues and cell lines. Methyltransferase‐like 14 (METTL14) expression in GC tissues was explored by bioinformatics and immunohistochemistry. Then, the function of METTL14 in GC cells was examined by CCK‐8, colony formation assay, wound healing assay, and Transwell assay. Besides, Western blotting was conducted to probe the PI3K/AKT/mTOR pathway and the epithelial‐mesenchymal transformation (EMT) pathway‐related gene expression.ResultsThe m6A modification level was decreased in GC and METTL14 was a key regulator resulting in m6A disorder in GC. METTL14 was downregulated in GC by analyzing both clinical samples and bioinformatics. METTL14 overexpression suppressed GC cell proliferation and aggression by deactivating the PI3K/AKT/mTOR pathway and the EMT pathway, respectively.ConclusionsOur findings indicate that METTL14 partakes in the biological process of GC as a tumor suppressor and may be an emerging biomarker in GC.     

姜黄素抑制Hedgehog信号诱导胃癌细胞凋亡

目的探讨姜黄素对胃癌细胞MKN45的作用及可能机制。方法不同浓度的姜黄素作用胃癌细胞MKN45后,采用MTT法检测细胞增殖,流式细胞仪检测细胞凋亡,Westernblot技术检测索尼克刺猬信号(Shh)、脑胶质瘤相关癌基因1(GLI1)的表达水平。结果不同浓度的姜黄素与胃癌细胞MKN45共培养后,随着姜黄素浓度的逐渐增加,MKN45细胞的增殖抑制也逐渐增加,经统计学分析发现,姜黄素5μmol/ml组与对照组比较,姜黄素10μmol/ml组与对照组比较,姜黄素20μmol/ml组与10μmol/ml组、5μmol/ml组、对照组比较,差异均有统计学意义(t分别=16.24、14.57、21.16、25.00、38.20,P均<0.05)。胃癌细胞MKN45经姜黄素处理后,姜黄素20μmol/ml组的细胞凋亡率与10μmol/ml组、5μmol/ml组、对照组比较,差异均有统计学意义(t分别=57.05、59.93、61.98,P均<0.05)。经姜黄素处理的MKN45细胞,Shh和GLI1表达均明显降低,与对照组比较,差异均有统计学意义(t分别=3.76、3.55,P均<0.05)。结论姜黄素能通过抑制Hedgehog信号通路,抑制胃癌细胞的增殖,诱导其凋亡。     

lncRNA HOTAIR通过miR-126/ADAMTS-4轴抑制口腔鳞状细胞癌细胞增殖与侵袭的机制研究

目的 检测长链非编码RNA HOTAIR(lncRNA HOTAIR)对口腔鳞状细胞癌增殖与侵袭的影响并探讨潜在的作用机制.方法 收集该院临床确诊的口腔鳞状细胞癌患者组织标本和癌旁正常组织标本,并培养TSCCA、Tca8113和HOK细胞,实时荧光定量PCR(RT-qPCR)检测lncRNA HOTAIR、miR-12...