Ovarian cancer (OC) remains a major threat to women’s health, with chemoresistance driven by the immunosuppressive tumor microenvironment. Formin-2 (FMN2), a cytoskeletal regulator, was investigated for its role in OC chemoresistance and macrophage polarization. Bioinformatics analysis identified high FMN2 expression in chemotherapy-resistant OC cell lines, validated experimentally. Stable FMN2 knockdown cell lines were generated via lentiviral transfection. Functional assays revealed that FMN2 overexpression conferred chemoresistance in vitro and in vivo and promoted M2 macrophage polarization via the CCL2/JAK2/STAT3 pathway. Co-culture with M2 macrophages enhanced cisplatin (DDP) resistance in OC cells, mediated by CXCL1 secretion, which activated the epithelial-mesenchymal transition (EMT) pathway. Clinically, FMN2 levels correlated with CCL2 and CD206 (M2 marker) in platinum-resistant patients, and high FMN2, CCL2, or CD206 expression predicted poorer overall and disease-free survival. This study identifies FMN2 as a key mediator of chemoresistance and immune evasion in OC, proposing FMN2-CCL2-CD206 signaling and macrophage-derived CXCL1 as therapeutic targets and prognostic markers for chemotherapy response.

T cell-based immunotherapies benefit only a minority of patients, primarily due to insufficient CD8+ T cell quantity and functional exhaustion. However, integrated strategies addressing both challenges remain scarce. Epigenetic dysregulation has recently been recognized as an important factor interfering with T cell responses in the tumor microenvironment. Herein, we develop an epigenetic nano-editor (P@cPG/sg) that simultaneously targets the epigenetic lysine-specific demethylase 1 (LSD1) in both tumor cells and T cells to reprogram the intratumoral T cell niche. The nano-editor consists of two guanidinium-based cationic carriers complexed with LSD1-targeting CRISPR/Cas9 plasmids, and can de-crosslink into tumor cell-targeting nanoparticles (PMG/sg) and T cell-targeting nanoparticles (PTG/sg). PMG/sg downregulates LSD1 in tumor cells, leading to the upregulation of chemokines that promote CD8+ T cell infiltration. Meanwhile, PTG/sg reduces LSD1 in T cells, lowering PD-1 expression, significantly enhancing T cell proliferation and rejuvenating exhausted cytotoxic CD8+ T cells in situ. Simultaneous LSD1 knockdown establishes a self-reinforcing cascade of anti-tumor immunity, achieving over 75 % tumor growth inhibition in both murine and humanized gastric cancer models. Thus, this nano-editor represents a standalone epigenetic immunotherapy that synchronously enhances intratumoral CD8+ T cell quantity and effector function, overcoming key limitations of current T cell-based immunotherapies.

目的 研究卵巢癌患者体内血清糖类抗原125（carbohydrate antigen 125，CA125）、人附睾蛋白4（Humanepididymisprotein4，HE4）、甲胎蛋白（alpha fetoprotein，AFP）、癌胚抗原（carcinoembryonic antigen，CEA）的表达水平及对临床分期及淋巴结转移的诊断效能。方法 选取2016年6月至2020年6月在郑州大学第三附属医院就诊的卵巢癌患者104例（卵巢癌组），卵巢良性疾病组患者50例（卵巢良性病变组），健康体检者50例（对照组）。采集各组患者血液标本，检测血清中CA125、HE4、AFP、CEA的表达水平，比较三组患者血清肿瘤标志物的水平，以及不同分期、有无淋巴结转移的卵巢癌患者血清肿瘤标志物水平的差异。以受试者工作特征曲线（ROC曲线）评价上述血清肿瘤标志物对临床分期及有无淋巴结转移的诊断效能。结果 卵巢癌组患者体内血清CA125和HE4表达水平高于良性病变组及对照组（P<0.001）；在卵巢癌组中，晚期患者（III-Ⅳ期）血清CA125和HE4的表达水平高于早期（I-Ⅱ期）患者（P<0.001）；淋巴结转移患者高于无淋巴结转移患者（P<0.001）。不同组织学类型患者CA125及HE4的表达水平有差异（P<0.001）。CA125和HE4联合检测的诊断灵敏度、特异度均高于单项检测。结论 CA125联合HE4检测对卵巢癌的分期及淋巴结转移具有较高的诊断效能。血清CA125、HE4表达水平能反映卵巢癌病变的程度，联合检测有助于判断卵巢癌的进展程度，可作为卵巢癌的诊断与病变评估的重要指标。

目的 检测含血小板反应蛋白 19 型基序的解聚素样金属蛋白酶(a disintegrin and metalloproteinase with thrombospondin motif 19,ADAMTS19)在子宫内膜癌(endometrial cancer,EC)中的表达情况,并探讨ADAMTS19 对子宫内膜癌Ishikawa细胞生物学功能及其意义.方法 免疫组化(IHC)和实时荧光定量聚合酶链反应(qRT-PCR)检测子宫内膜癌组织和癌旁组织中ADAMTS19 蛋白表达水平及mRNA相对表达水平;分析ADAMTS19 表达水平与子宫内膜癌患者临床特征的相关性;体外使用si-RNA沉默Ishikawa细胞中ADAMTS19 的表达,qRT-PCR检测其沉默效率,研究细胞增殖、迁移及侵袭能力,蛋白印迹法检测p-STAT3 蛋白的表达水平.结果 IHC和qRT-PCR结果表明:与癌旁组织相比,子宫内膜癌组织中ADAMTS19 表达明显降低(IHC:P＜0.001;qRT-PCR:P＜0.001);ADAMTS19 的低表达与淋巴结转移(P =0.022)、FIGO分期较晚(Ⅲ+Ⅳ期,P=0.025)及肿瘤组织分化程度(P=0.004)密切相关;体外细胞实验表明,与阴性对照组相比,沉默ADAMTS19 组Ishikawa 细胞的增殖、迁移和侵袭能力明显增强,差异具有统计学意义(增殖:P＜0.001,迁移:P＜0.05,侵袭:P＜0.001).沉默ADAMTS19 组中p-STAT3 蛋白的表达水平明显增强(P＜0.05).结论ADAMTS19 在子宫内膜癌组织中呈低表达,且与子宫内膜恶性临床特征密切相关,可能是通过促进磷酸化STAT3 的表达促进肿瘤细胞增殖、迁移和侵袭能力.ADAMTS19 有望成为子宫内膜癌潜在的分子靶标.

目的:研究MG53 蛋白对创伤性脑损伤(TBI)小鼠小胶质细胞极化和神经炎症的调控作用.方法:改良式自由落体法建立中度TBI小鼠模型,随机分为TBI组和MG53 组,每组3 只;免疫荧光检测脑组织中CD3、胶质纤维酸性蛋白(GFAP)、CD86、CD206 和巢蛋白(Nestin)的表达;ELISA法检测血清IL-1β、TNF-α、IL-4 和IL-10 水平;qRT-PCR检测脑组织中CD86、诱导型一氧化氮合酶(iNOS)、CD206、精氨酸酶 1(ARG1)、Nestin、双皮质醇(DCX)、脑源性神经营养因子(BDNF)、神经生长因子(NGF)mRNA的表达;Western blot检测脑组织中核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)、Cleaved-Caspase-1 和IL-1β蛋白的表达.结果:与TBI组相比,MG53 组小鼠脑组织中CD3、GFAP的表达减少,血清中促炎因子IL-1β和TNF-α水平降低,而抗炎因子IL-4 和IL-10 水平升高(P<0.05).此外,与TBI组相比,MG53 组小鼠脑组织中CD86 和iNOS mRNA表达降低,而CD206、Nestin、DCX、BDNF和NGF mRNA表达增加(P<0.05).与TBI组相比,MG53 组小鼠NLRP3、Cleaved-Caspase-1 和IL-1β蛋白表达降低(P<0.05).结论:MG53 蛋白可能通过抑制NLRP3/Caspase-1/IL-1β信号通路,抑制小胶质细胞极化和神经炎症,进而对TBI小鼠发挥神经保护作用.

The nano-drug delivery system activated by the tumour microenvironment (TME) can effectively treat tumours with low toxicity. Based on a high level of reductive GSH in TME and the different coordination properties of Fe ions, this project intended to prepare a GSH-activated cascade catalytic nanoreactor for breast cancer treatment using Fe3+/Fe2+ as the molecular switch. In this study, the glucose oxidase (GOx) loaded iron alginate nano hydrogel (FeAlg/GOx) was prepared by the simple one-step titration method. Results showed that FeAlg/GOx could remain stable during in vivo circulation to avoid hypoglycaemia. When it reached the targeted tumour site, reductive GSH can reduce Fe3+ to Fe2+. Thereafter, FeAlg/GOx nanogel was broken and GOx was released to consume the essential nutrient glucose (Glu) to achieve tumour starvation therapy. Next, the substrate H2O2 generated by the reaction between GOx and Glu can be catalysed by Fe2+ to produce highly cytotoxic center dot OH in situ, which could further kill tumour cells. The in vivo pharmacodynamics results demonstrated that compared with the control group (V/V0 = 8.36 +/- 1.73), FeAlg/GOx group showed the most significant anti-tumour effect with V/V0 of 3.08 +/- 1.06. In conclusion, this "inactivated" FeAlg/GOx nanogel can be converted into "activated" therapeutic substances in situ to achieve starvation-chemodynamic combined treatment for breast cancer.

BACKGROUND:Long non-coding RNA (LncRNA) controls cell proliferation and plays a significant role in the initiation and progression of esophageal squamous cell carcinoma (ESCC). N6-methyladenosine (m6A) modification now is recognized as a master driver of RNA function to maintain homeostasis in cancer cells. However, how m6A regulates LncRNA function and its role in tumorigenesis of ESCC remain unclear.METHODS:Multiple ESCC datasets were used to analyze gene expression in tumor tissues and normal tissues. Kaplan-Meier method and the ROC curve were conducted to evaluate the prognostic value and diagnostic value of LINC00022 in ESCC, respectively. Both gain-of-function and loss-of-function experiments were employed to investigate the effects of LINC00022 on ESCC growth in vitro and in vivo. Bioinformatics analysis, colorimetric m6A assay, RIP, MeRIP and co-IP was performed to explore the epigenetic mechanism of LINC00022 up-regulation in ESCC.RESULTS:Here we report that m6A demethylation of LncRNA LINC00022 by fat mass and obesity-associated protein (FTO) promotes tumor growth of ESCC in vivo. Clinically, we revealed that LINC00022 was up-regulated in primary ESCC samples and was predictive of poor clinical outcome for ESCC patients. Mechanistically, LINC00022 directly binds to p21 protein and promotes its ubiquitination-mediated degradation, thereby facilitating cell-cycle progression and proliferation. Further, the elevated FTO in ESCC decreased m6A methylation of LINC00022 transcript, leading to the inhibition of LINC00022 decay via the m6A reader YTHDF2. Over-expression of FTO was shown to drive LINC00022-dependent cell proliferation and tumor growth of ESCC.CONCLUSIONS:Thus, this study demonstrated m6A-mediated epigenetic modification of LncRNA contributes to the tumorigenesis in ESCC and LINC00022, specific target of m6A, serves as a potential biomarker for this malignancy.

背景:海藻酸盐可以改善创面敷料的亲水性质、创造湿润的创面微环境、清除创面渗出物.目前,海藻酸盐生物高分子材料己被应用于多种创面敷料的设计和开发,以提高创面愈合的效率.目的:总结海藻酸盐基水凝胶/敷料在皮肤创面愈合中的研究及进展.方法:应用计算机检索2000至2020年PubMed、Science Direct和CNKI等数据库中的相关文章,英文检索词为“Alginate hydrogel,Wound healing, Wound dressing, Mesenchymal stem cell, Growth factor, Nanoparticles, Diabetic wound, Antibiotics, Bioactive peptide, three-dimensional printing”,中文检索词为“海藻酸盐、创面修复”.根据纳入与排除标准最终保留60篇文献进行综述.结果 与结论:①海藻酸盐与其他有机或无机材料发生交联可提高复合材料的机械性能和生物降解性,创造湿润温和的创面微环境;②海藻酸盐基水凝胶/敷料可以作为传递平台负载种子细胞、生长因子或其他生物活性物质,加快创面愈合的速度;③如何使海藻酸盐材料具有较多的细胞识别位点,如何改善复合支架材料的力学性能,如何控制海藻酸盐生物材料的微观结构及如何控制药物或细胞的动态释放、持续释放和顺序释放等问题,仍需研究者们进一步探索.

Background: PR-M refers to a novel truncated progesterone receptor located on the outer membrane of mitochondria, capable of facilitating the proliferation of leiomyoma cells and breast cancer cells, as well as inhibiting apoptosis as impacted by progesterone or progesterone agonists. However, its role in ovarian tumors has not yet been elucidated. Objective: To study the expression of PR-M in different ovarian tumor tissues and normal tissues, and the effect exerted by progesterone on the proliferation and migration of SKOV-3 cells that achieve high PR-M expression. Methods: Real- time PCR and Western blot were employed for determining PR-M levels in cell lines, non-cancer tissues and ovarian cancer tissues. By immunohistochemistry, PR-M protein expression in benign tumor, borderline tumor and epithelial carcinoma was detected, and the clinicopathological characteristics between PR-M and cancer were analyzed. Furthermore, CCK-8 and scratch test were performed to explore the proliferation and migration of SKOV-3 cells exhibiting high PR-M expression. Results: PR-M increased significantly in cancer tissues and ovarian cancer cell lines, in comparison to normal cells and non-cancer tissues. The abnormal expression showed a significant correlation with intraperitoneal metastasis, lymph node metastasis, clinically related stage and CA125 level, suggesting that high PR-M expression may affect the progression of ovarian tumors. During the cell experiment, PR-M achieved the maximum expression in SKOV-3 cells (PR-A / B(-)). As impacted by progesterone, SKOV-3 cells (PR-A / B(-)) achieved the enhanced proliferation and migration. Besides, the enhancing effect was dose and time-dependent. Conclusion: PR-M is critical to develop ovarian cancer. Progesterone may facilitate the proliferation and migration of ovarian cancer cells exhibiting high PR-M expression.

目的:探讨MS-275联合顺铂(DDP)对食管鳞状细胞癌(鳞癌)EC9706细胞氧化损伤和细胞凋亡的影响.方法:采用CCK-8法检测0.5、1.0、2.0、4.0和8.0μmol/L MS-275和0.25、0.50、1.00、2.00和4.00μmol/L DDP作用24、48、72 h对EC9706细胞存活率的影响.EC9706细胞分为空白对照组(不作处理)、MS-275组、DDP组和联合(MS-275+DDP)组,MS-275和DDP分别采用2.0和1.00μmol/L的浓度作用48 h,CCK-8法检测细胞的存活率,流式细胞仪检测细胞凋亡和细胞内活性氧(ROS)水平,相应试剂盒检测丙二醛(MDA)含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-PX)活力,JC-1染色检测线粒体膜电位,Western blot检测Bax、Bcl-2和Trx蛋白的表达.结果:2.0μmol/L MS-275和1.00μmol/L DDP均能降低EC9706细胞存活率,升高凋亡率(P均<0.001),增加细胞内ROS水平和MDA含量(P均<0.001),降低线粒体膜电位以及SOD、GSH-PX活力(P均<0.001),同时降低Bcl-2和Trx蛋白表达,增加Bax蛋白表达(P均<0.001);两药联合具有一定的协同效应(P均<0.001).结论:MS-275联合DDP可诱导EC9706细胞的氧化损伤和凋亡.

目的:探讨重组人MG53蛋白对人脐带间充质干细胞(hUC-MSCs)氧化损伤的保护作用及分子机制.方法:实验分为对照组(CON组,不处理)、LPS组(加入200 mg/L LPS)、MG53组(加入30 mg/L重组人MG53蛋白)和MG53+LPS组(同时加入重组人MG53蛋白和LPS),48 h后,采用CCK-8法检测细胞活力,AO-EB染色检测细胞凋亡,JC-1染色评价线粒体膜电位变化,DCFH-DA荧光探针法检测细胞内活性氧(ROS)水平,酶标法检测丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性和过氧化氢酶(CAT)活性,Western blot法检测磷酸化Akt和GSK-3β蛋白的表达.结果:与LPS组相比,MG53+LPS组细胞存活率升高,凋亡率和线粒体膜电位降低,细胞内ROS和MDA含量降低,SOD和CAT活性升高,同时磷酸化Akt和磷酸化GSK-3β的表达升高(P<0.05).结论:重组人MG53蛋白可能通过激活Akt/GSK-3β信号通路,保护hUC-MSCs免受LPS诱导的氧化损伤.

目的:探讨p97抑制剂NMS-873对食管鳞状细胞癌Eca109细胞增殖、凋亡、迁移的影响.方法:用不同浓度的NMS-873分别处理Eca109细胞24、48、72 h,采用CCK-8法检测细胞增殖;在此基础上选用1、2、3μmol/L NMS-873分别作用于Eca109细胞48 h,采用AnnexinV-FITC/PI双染法检测细胞凋亡,Transwell迁移实验检测细胞迁移能力的变化,EdU荧光法检测细胞增殖.结果:NMS-873可呈时间和剂量依赖性抑制Eca109细胞增殖;1、2、3μmol/L的NMS-873分别作用于Eca109细胞48 h后,与阴性对照组相比,随着NMS-873浓度的增加,NMS-873组Eca109细胞凋亡率提高,迁移细胞数减少,增殖率降低(P<0.05).结论:NMS-873能有效抑制Eca109细胞增殖,促进细胞凋亡,并降低细胞迁移能力.

目的:研究MG53蛋白联合人脐带间充质干细胞(hUC-MSCs)移植对阿尔茨海默病(AD)小鼠行为和情绪失调的改善作用.方法:将3月龄AD小鼠随机分为APP+组、MG53组、hUC-MSCs组和联合组,每组8只.APP+组小鼠尾静脉注射0.1 mL生理盐水,hUC-MSCs组同法注射0.1 mL细胞密度为1×107个/mL的hUC-MSCs悬液,MG53组按3 mg/kg注射0.1 mL rhMG53,联合组小鼠尾静脉注射含hUC-MSCs和rhMG53的混合液,1次/d,连续3 d.治疗3 d后,DHE染色法检测小鼠(n=3)脑内ROS含量;治疗后第26～28天,采用旷场实验、新事物识别实验和新奇抑制喂养实验(n=4)评价小鼠的记忆、认知能力和抑郁情绪;治疗后第29天,进行脑组织尼氏染色(n=4),硫磺素S染色法检测Aβ斑块面积(n=4),Western blot法检测Nrf2通路相关蛋白Nrf2、NQO1和Keap-1的表达(n=1).结果:MG53和hUC-MSCs移植单独应用均可增加AD小鼠脑内尼氏小体数量,降低ROS含量,减小Aβ斑块面积,改善小鼠的学习记忆能力和焦虑情绪(P均<0.05).二者联用有协同增效的作用(P均<0.05).MG53和hUC-MSCs移植可以促进AD小鼠脑组织中Nrf2、NQO1蛋白的表达,降低Keap-1蛋白的表达.结论:MG53蛋白联合hUC-MSCs移植可以激活Nrf2通路,在一定程度上改善AD小鼠的行为能力.

目的:探讨重组人MG53蛋白(rhMG53)作为干细胞低温保护剂的特殊组分对小鼠骨髓间充质干细胞(BMSCs)冷冻保存后生物学特性的影响.方法:常规培养BMSCs,分为对照组(DMEM/F12培养基、FBS、DMSO的体积比为5:4:1并添加30 mg/L BSA)和rhMG53组(DMEM/F12培养基、FBS、DMSO的体积比为5:4:1并添加30 mg/L rhMG53)冻存.冻存1 a后,复苏细胞,qRT-PCR检测两组细胞冻存复苏后干性相关基因Nanog、OCT4和SOX2 mRNA的表达;CCK-8法检测细胞增殖;台盼蓝染色检测细胞存活能力;茜素红S染色和油红O染色分别检测两组干细胞的成骨和成脂分化;免疫荧光检测两组细胞成神经分化相关因子DCX和NSE的表达.结果:与对照组相比,rhMG53组BMSCs的Nanog、OCT4和SOX2 mRNA表达无明显变化(P>0.05),但细胞增殖能力增强,存活率升高,成骨、成脂和成神经分化效率增加(P均<0.05).结论:rhMG53作为保护剂的特殊组分对冷冻保存的BMSCs有较好的保护效果.

外泌体是细胞通过出芽方式向外分泌的一种囊泡状小体,内含丰富的mRNA、miRNA及蛋白质等,能够与靶细胞融合并将其内含物注入靶细胞中,可在肿瘤的发生、发展过程中发挥至关重要的作用.干细胞来源的外泌体具有免疫原性低、稳定性高、运输效率高等特点.作为肿瘤微环境的传播者,干细胞来源的外泌体能运载各种基因类或抗癌类药物,可调控受体细胞存活、增殖和凋亡等生物学过程.间充质干细胞(MSCs)是目前应用前景最广泛的一类干细胞,MSCs源性外泌体既可通过抑制免疫细胞引发抗肿瘤反应,也可诱导免疫抑制或调节细胞群介导的免疫抑制.MSCs源性外泌体高表达的miR-143-3p、miR-10b-5p、miR-486-5p、miR-22-3p、miR-21-5p可作为致癌基因或肿瘤抑制因子在肿瘤的发生、发展过程中发挥重要作用.

目的:观察MS-275对食管鳞癌KYSE-70细胞存活、细胞周期、凋亡以及迁移的影响,并分析其对PI3K/Akt/mTOR信号通路相关蛋白p-Akt1和p-mTOR的影响.方法:采用qRT-PCR和Western blot检测KYSE-70细胞和正常食管上皮Het-1A细胞中HDAC1 mRNA及蛋白的表达;CCK-8法检测不同浓度(0.25、0.50、1.00、2.00、4.00、8.00μmol/L)MS-275对KYSE-70细胞存活的影响;以0.00、0.25、0.50、1.00和2.00μmol/L MS-275处理KYSE-70细胞,48 h后流式细胞仪检测细胞周期,Annexin V/PI染色检测细胞凋亡,划痕实验检测细胞迁移情况,Western blot检测细胞中Cyclin D1、Cleaved caspase-3、E-cadherin、p-Akt1和p-mTOR蛋白的表达情况.结果:与Het-1A细胞相比,KYSE-70细胞中HDAC1 mRNA和蛋白表达显著增加(P<0.05);MS-275对KYSE-70细胞存活的影响具有时间和剂量依赖性(P<0.05);随着MS-275处理浓度的增加,KYSE-70 G0/G1期细胞增加、S期细胞降低,细胞凋亡率提高,划痕愈合率降低(P<0.05).MS-275可提高Cleaved caspase-3和E-cadherin蛋白的表达,降低Cyclin D1、p-Akt1和p-mTOR蛋白的表达(P<0.05).结论:MS-275可降低KYSE-70细胞存活率,有效抑制细胞迁移,阻滞细胞于G0/G1期,促进细胞凋亡,其作用可能与PI3K/Akt/mTOR信号通路的抑制有关.

BACKGROUND: Umbilical cord mesenchymal stem cells (UC-MSCs) are a group of cells that have self-renewal, highly proliferative and multidrug differentiation potential. The properties of UC-MSCs and their tumor tropism make them an ideal tool for glioma cell therapy. These cells can act by paracrine or as a delivery system for genes and drugs. It has been demonstrated that UC-MSCs can inhibit the growth of glioma and improve the survival after transplantation into the brain. OBJECTIVE: To summarize the molecular mechanisms and safety of UC-MSCs in the treatment of glioma and to provide a useful reference for further research. METHODS: We searched the PubMed and CNKI databases from 2000 to 2017 with the English terms of "glioma; umbilical cord mesenchymal stem cells" and the Chinese terms of "glioma; umbilical cord mesenchymal stem cells; safety; molecular mechanism". Based on the inclusion and exclusion criteria, 55 articles were finally reserved for review. RESULTS AND CONCLUSION: UC-MSCs have obvious effect on treating glioma. These cells can treat glioma through homing mechanism and paracrine mechanism as gene carrier and co-culture. Moreover, UC-MSCs have certain safety in the treatment of glioma.

Objective: To investigate the effect of tumor-associated macrophages on the stemness of esophageal cancer cells and the potential mechanism of antiproliferative effects of aspirin (ASA). Methods: The effects of aspirin on the stemness characteristics of KYSE-450 cells and KYSE-450 cells co-cultured with M2 macrophages (KYSE-450+ M2) were performed using spheroid formation assay. After treatment with aspirin, the expression of different chemokines, the core pluripotency gene Nanog and the stem cell marker CD90 in different cell groups were determined by real-time quantitative PCR, flow cytometry and Western blot. Results: The number of spheres formed in the ASA and KYSE-450+ M2 cell groups were 7.00±1.23 and 34.33±2.33, respectively, showing statistically significant difference compared with that of control group (14.50±2.33, all P<0.05). The number of spheres in KYSE-450+ M2+ ASA cell group were 20.67±2.33, which was significantly lower than that of KYSE-450+ M2 group (P<0.05). The expression levels of Nanog gene in control and ASA groups were 1.00 and 0.50±0.10, respectively, and the difference was statistically significant (P<0.05). Moreover, the expression of Nanog gene in cells of KYSE-450+ M2 group and M2+ KYSE-450+ ASA group was 1.74±0.13 and 1.43±0.05, showing statistically significant difference (P<0.05). When chemokine CCL2 was knocked down, the levels of Nanog gene in M2+ shCCL2-KYSE450+ ASA group and M2+ shCCL2-KYSE450 group were decreased to 1.22±0.11 and 1.17±0.08, respectively, and there was no statistically significant difference between them (P=0.69). Flow cytometry analyses showed that the expression levels of CD90 in control and ASA cells were (2.93±0.52)% and (1.30±0.17)%, respectively, and the difference was statistically significant (P<0.05). Moreover, the expression levels of CD90 in M2+ shCCL2-KYSE450 cells and M2+ shCCL2-KYSE450+ ASA cells were (4.07±0.12)% and (4.73±0.38)%, respectively, showing no statistically significant difference (P=0.17). Conclusions: Tumor-associated macrophages enhances the stemness of esophageal cancer cells, whereas aspirin attenuates the stemness by suppressing the expression of CCL2. Aspirin plays an anti-tumor effect in esophageal cancer cells.

创伤性颅脑损伤(traumatic brain injury,TBI)是发生在中枢神经系统的一种常见疾病.近年来人脐带间充质干细胞(human umbilical cord mesenchymal stem cells,hUC-MSCs)移植为其治疗提供了新思路.间充质干细胞(mesenchymal stem cells,MSCs)能优先归巢到受损组织,分泌多种因子从而发挥营养、保护、清理、激活和桥接作用.但是,目前干细胞移植治疗TBI的研究大部分还处于实验动物模型阶段,其在临床上的安全性和有效性仍缺乏有效证据,还需要在大宗和长期的临床试验中进行评价和验证.笔者对hUC-MSCs移植治疗TBI的研究进展情况作一综述,为其开展更为广泛的研究提供有益参考.