BACKGROUND:Colorectal cancer (CRC), as one of the most common cancers globally, poses a significant challenge to public health due to its high incidence and mortality rates. This underscores the need for continuous exploration of new therapeutic targets and effective drugs. Sophocarpine (SC), a natural compound derived from traditional Chinese medicine, holds considerable therapeutic potential in the treatment of CRC, however, the relevant mechanisms remains unclear. PURPOSE:This study aims to explore the anti-tumor effects of SC against CRC by modulating gut microbiota, and uncover potential mechanisms linking SC's therapeutic effects to gut microbiota regulation by analyzing the impact of SC on microbiota composition and CRC progression. MATERIAL:This study explores the impact of SC on the gut microbiota in CRC by constructing subcutaneous xenograft tumors of CRC and integrating 16S rRNA sequencing and RNA transcriptomic sequencing. The fecal microbiota transplantation (FMT) mouse model was used to validate the biological function of SC in correcting gut microbiota dysbiosis to treat CRC. Subsequently, we conducted in vitro studies on the molecular mechanisms by which SC regulates the gut microbiota as an effective hallmark of CRC treatment, using lipopolysaccharide (LPS) to simulate an inflammatory gut microbiota environment and P38 MAPK knockdown cell line. RESULTS:SC significantly inhibited CRC cell proliferation with IC50 values of 2.547±0.256 μM for HCT116 and 2.851±0.332 μM for LoVo cells. In vivo experiments demonstrated that SC effectively suppressed tumor growth in xenograft models. 16S rRNA sequencing revealed that SC modulated gut microbiota composition, particularly affecting Bacteroides and Alistipes populations. SC significantly reduced the levels of inflammatory factors and inhibited the MAPK signaling pathway, as evidenced by decreased p-JNK, p-p38 MAPK, and p-NF-κB p65 expression. CONCLUSIONS:Current clinical practice still lacks effective therapeutic agents targeting CRC through gut microbiota modulation. This study presents the first evidence that SC, a natural compound, exhibits dual-action therapeutic efficacy against CRC progression by simultaneously modulating gut microbial composition and suppressing MAPK pathway-mediated inflammatory responses. These findings highlight SC's novel therapeutic potential as a promising microbiota-regulating candidate for CRC intervention, offering an innovative approach that bridges microbial ecology with cancer signaling pathways.

Background: JianPiTongLuo Recipe (JPTL Recipe) is a traditional Chinese medicine formula commonly used in the clinical treatment of colorectal cancer. Clinical studies have found that it can significantly improve the prognosis of patients with colorectal cancer. However, its mechanisms of action are not well understood, which has limited its further clinical application. Methods: We investigated the potential mechanisms of action of the JianPiTongLuo (JPTL) Recipe on colorectal cancer (CRC) using a multi-step approach. Initially, network pharmacology and bioinformatics analyses were conducted using databases such as TCMSP, HERB, BATMAN-TCM, and STRING to identify active components of JPTL Recipe and predict their therapeutic targets. Interaction networks and functional enrichment analyses were constructed to hypothesize relevant biological processes and pathways. In vitro studies involved treating human CRC cell lines HCT116, LoVo and SW480 with varying concentrations of JPTL Recipe extract, measuring cell viability with the CCK-8 assay, assessing apoptosis via flow cytometry, and analyzing signaling pathways through Western blotting. To corroborate these findings, in vivo experiments were performed on BALB/c nude mice implanted with HCT116 cells, divided into control, JPTL Recipe- treated, 5-fluorouracil (5-FU)-treated, and JPTL Recipe combined with 5-FU groups, with tumor growth and histological changes monitored. Mechanistic studies focused on the PI3K/AKT signaling pathway, examining the phosphorylation status of key pathway proteins using immunofluorescence and Western blot analyses to elucidate JPTL Recipe 's interaction with pathway activity. Results: We demonstrated that JPTL Recipe effectively inhibits colorectal cancer cell proliferation, anti-apoptotic ability, and exerts synergistic therapeutic effects with fluorouracil. Further analysis revealed that JPTL Recipe affects the activity of colorectal cancer cells by inhibiting the phosphorylation of the PI3K/AKT signaling pathway. Conclusion: In summary, we have discovered and confirmed that the traditional Chinese medicine compound JPTL Recipe can serve as a novel adjuvant therapy for colorectal cancer, offering a new treatment approach for the integration of traditional Chinese and Western medicine in the treatment of colorectal cancer.

Background Er-Miao-San (EMS) is a classic prescription in traditional Chinese medicine (TCM) for the treatment of colorectal cancer (CRC) and has shown promising therapeutic effects in clinical practice. However, the specific components and molecular mechanisms of EMS remain unclear. Purpose The aim of this study was to analyze the effective components and molecular mechanisms of EMS in treating CRC through network pharmacology techniques and experimental validation. Methods The Traditional Chinese Medicine Systems Pharmacology database was used to screen the main active chemical components and targets of the EMS formula. The compound structures were verified using the PubChem database, which is an organic small-molecule bioactivity database. GeneCards and OMIM databases were utilized to predict target genes related to CRC. The Cytoscape 3.8 software was used to construct a “Drug-Active Ingredient-Target-Disease” intersection network. The STRING database was employed to analyze the core target protein–protein interaction network shared by EMS and CRC. The core targets were further subjected to Gene Ontology enrichment analysis and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analysis using the R language. Molecular docking between the core targets and the major active chemical components of EMS was performed using AutoDock software. The impact of the core targets on the prognosis of CRC patients was analyzed using the R language. Subsequently, we validated the potential mechanisms predicted by network pharmacology for the inhibition of CRC cell proliferation by the key proteins in the relevant pathways through CCK8 cell proliferation assays and Western blot experiments. Results Molecular docking results showed good docking affinity between the key active components, such as quercetin and baicalein, of EMS and the core targets. Kaplan–Meier survival analysis demonstrated a close correlation between the core targets and the survival prognosis of CRC patients. Cellular experiments showed that EMS significantly inhibited the proliferation of CRC cells and may promote apoptosis and autophagy of CRC cells by suppressing the expression of key proteins in the PI3K/AKT pathway. Conclusion The TCM formula EMS exerts anti-CRC effects through multiple pathways and targets, improving the prognosis and extending the survival period of CRC patients. This study provides preliminary insights into the effective components and molecular mechanisms of EMS in the treatment of CRC, which were preliminarily validated through molecular docking and experimental approaches.

Background:Colorectal cancer (CRC) is an insidious malignancy and the occurrence of chemotherapy resistance and toxicity seriously limits its clinical efficacy. Insect Compound Particle [Chong Yao Fu Fang (CYFF)] is a traditional Chinese medicine (TCM) compound based on the concepts of "invigorating spleen for strengthening vital qi" and "collateral disease theory". In long-term clinical application, it can reduce the toxicity of CRC chemotherapy and improve the anti-tumor effect. However, there is currently a lack of high-quality clinical evidence to prove the clinical efficacy and safety of CYFF in the treatment of CRC. Methods:We plan to include 262 patients with locally advanced stage III CRC who had undergone surgery and achieved R0 resection. These patients will be randomized into a CYFF group (treated with CYFF combined with chemotherapy) and a control group (treated with placebo plus chemotherapy) at a 1:1 ratio. The patients were routinely followed-up every 2 weeks within 2 months and every 4 weeks after 2 months after the treatment, every 3 months within 1 year, and every 6 months after 1 year. The primary endpoint is disease-free survival (DFS), defined as the time from random assignment to recurrence of primary CRC or death from any cause. The secondary endpoints include overall survival (OS) (defined as the time from randomization to death from any cause), safety [any adverse events (AEs)], and the Colorectal Cancer-Specific Quality of Life Questionnaire (QLQ-CR38) score. Conclusions:Compared with previous studies, our current study applies CYFF plus basic adjuvant chemotherapy, which is expected to achieve better efficacy and longer survival than standard chemotherapy, and reduce the toxic and side effects of chemotherapy, improve the safety of clinical treatment. In addition, our present study is the first clinical study to evaluate the safety and efficacy of CYFF in combination with chemotherapy in the treatment of stage III CRC after R0 resection. Trial Registration:This clinical trial has been registered in the Chinese Clinical Trial Registry (ChiCTR) (registration No. ChiCTR2000037568; August 28, 2020).

目的 探究健脾通络方对结直肠癌细胞侵袭、迁移的影响及机制.方法 构建敲减MALAT1基因的HCT116细胞模型.采用细胞划痕实验和Transwell实验检测细胞侵袭、迁移能力.采用蛋白质印迹法检测经健脾通络方干预后的MALAT1正常/敲减表达的HCT116细胞中Wnt3a、β-catenin蛋白水平.采用实时荧光定量PCR法检测MALAT1的表达水平.构建裸鼠肺转移模型,采用小动物活体成像技术监测肿瘤转移情况,并检测转移灶中Wnt3a、β-catenin和MALAT1的表达水平.结果 经健脾通络方干预后,HCT116细胞中MALAT1、Wnt3a和β-catenin的表达水平均降低,HCT116细胞迁移能力下降.在裸鼠肺转移模型中,经健脾通络方干预后裸鼠的转移灶减少,转移灶中Wnt3a、β-catenin和MALAT1的表达水平均降低.结论 健脾通络方通过下调HCT116细胞中MALAT1的表达,使Wnt/β-catenin信号通路中Wnt3a、β-catenin的蛋白表达水平降低,从而抑制结直肠癌细胞的增殖、侵袭和迁移能力.

消化系统肿瘤是中国常见的恶性肿瘤,由于目前治疗方法存在局限性,研究方向从单纯研究肿瘤细胞内部机制延伸至研究肿瘤微环境中的外泌体与免疫细胞之间的作用和关系.消化系统肿瘤微环境中的外泌体可以通过传递信号抑制免疫细胞的杀伤能力,促进肿瘤的发生、发展.肿瘤细胞通过释放外泌体传递信息,诱导巨噬细胞极化,抑制免疫细胞活性,促进肿瘤转移及免疫逃逸.该文综述了消化系统肿瘤源性外泌体在肿瘤微环境中对免疫细胞作用的研究进展.

Objective Bufalin, the main active anti-tumor monomer of toad venom, is crucial in cancer treatment. However, intrinsic issues, such as poor solubility and systematic toxicity, have considerably mitigated its anticancer functions and caused unwanted side effects. It is essential to develop innovative targeting systems to precisely and efficiently deliver anticancer drugs to achieve satisfying therapeutic efficiency. Methods This work established a novel and more efficient system for simultaneously detecting and killing colorectal cancer cells. The proposed method designed two allosteric probes, a report probe and a recognize probe. The method exhibited high sensitivity towards cell detection via the recognizing probe identifying target cancer cells and the report probe’s signal report. Combining bufalin and fluorouracil endowed better tumor cell inhibition. Results We observed significantly enhanced fluorescence dots surrounding the HCT-116 cell membranes. No fluorescence increments in the other three cells were identified, indicating that the established liposome complex could specifically bind with target cells. In addition, the best ratio of bufalin to fluorouracil was 0.15 and 0.5, respectively. This improved the anti-tumor effects and achieved more than 60% tumor cell inhibition. Conclusion This method will provide new opportunities for intracellular biomolecule detection and targeted cancer cell therapy.

目的 分析比较左右半结肠癌及直肠癌根治术后患者的生存预后差异及影响因素.方法 选取2004年1月—2016年12月于上海中医药大学附属市中医医院、上海市普陀区中心医院和复旦大学附属肿瘤医院肿瘤科收治的Ⅰ～Ⅲ期结直肠癌根治术后病例1028例,分为右半结肠癌组243例、左半结肠癌组339例和直肠癌组446例,对比3组无疾病生存期(DFS)、总生存期(OS)、复发转移率的差异及其影响生存预后因素.结果 右半结肠癌组、左半结肠癌组和直肠癌组的中位DFS分别为9.13、16.43和52.17个月,3组比较差异有统计学意义(χ2/P=167.362/0.000),中位OS分别为22.93、28.98和60.83个月,3组比较差异有统计学意义(χ2/P=122.748/0.000).复发转移率比较,右半结肠癌组>左半结肠癌组>直肠癌组(χ2/P=172.251/0.000).化疗和中药治疗是OS的保护因素,肿瘤部位是影响OS的危险因素,右半结肠癌影响总生存期的风险是直肠癌的2.004倍(95％CI 1.582～2.540),左半结肠癌影响OS的风险是直肠癌的1.379倍(95％CI 1.082～1.758).中药治疗是DFS的保护因素,肿瘤部位为右半结肠是影响DFS的危险因素[OR(95％CI)=0.794(0.655～0.961),1.365(1.098～1.698)].结论 直肠癌的生存预后明显优于结肠癌,相比左半结肠癌,右半结肠癌患者的生存期更短,复发转移率更高.中药治疗不仅能延长生存期,还能降低结直肠癌术后患者复发转移的风险.

目的 探索优化基于目标管理理论的国家自然科学基金项目申报组织管理模式,进一步提高医院科研管理的质量效益.方法 以近3年(2017-2019年)上海市某三级甲等中医医院国家自然科学基金项目(NSFC)申报组织管理实践为研究样本,梳理分析存在的问题,依照目标制定、目标分解、目标执行、绩效考核、信息反馈五个步骤重构管理模式,制定优化医院NSFC项目组织管理的措施,并通过2019年度NSFC申报工作进行初步验证.结果 近3年申报数由前两年的年均50～60项,增加到2019年度的100项,增幅超过80％.立项数由前两年年均4～6项,增加到近两年的年均9.5项,增长率达50％以上,服务满意度(含服务到位、比较到位)达98.5％.结论 运用基于目标管理理论的国家自然科学基金申报管理模式,可有效促进管理规范化水平,明显提升管理质量效益.

目的 探究散结抑癌方联合贝伐珠单抗对BALB/c裸鼠结肠癌肺转移的影响,以及对血管内皮生长因子(VEGF)蛋白表达的影响.方法 采用经尾静脉注射对数生长期的人源结肠癌HCT116荧光细胞的方法,构建BALB/c裸鼠肺转移模型.将造模成功的20只裸鼠随机分为4组,每组5只.中药组,散结抑癌方灌胃;西药组,贝伐珠单抗腹腔注射;联合组,散结抑癌方灌胃+贝伐珠单抗腹腔注射;对照组,生理盐水灌胃.每周进行1次活体荧光成像观察肿瘤生长情况,记录小鼠体质量.干预4周后取小鼠肺组织,H-E染色观察小鼠结肠癌肺转移情况,免疫组织化学法检测VEGF蛋白表达情况.结果 与干预前比较,对照组在干预后体质量下降最多.干预后,中药组体质量略高于对照组(P>0.05),联合组体质量略高于西药组(P>0.05),联合组和西药组体质量均明显高于对照组(P<0.05).小动物成像定量分析结果显示,干预后中药组、西药组和联合组生物发光光子数均少于对照组(P均<0.05).H-E染色结果指出,对照组转移灶面积最大,转移处最多,联合组转移灶面积最小,转移处最少.免疫组织化学检测结果显示,对照组VEGF蛋白平均阳性细胞率为48.57％,高于中药组(39.91％)、西药组(35.82％)和联合组(29.03％),差异均有统计学意义(P均<0.01).结论 散结抑癌方可以抑制结肠癌肺转移,作用途径可能与VEGF蛋白表达相关.

Objective To analyze the active compounds, potential targets, and diseases of JianPi Fu Recipe (JPFR) based on network pharmacology and bioinformatics and verify the potential biological function and mechanism of JPFR in vitro and in vivo. Methods Network pharmacology databases including TCMSP, TCM-PTD, TCMID, and DrugBank were used to screen the active compounds and potential drug targets of JPFR. Cytoscape 3.7 software was applied to construct the interaction network between active compounds and potential targets. The DAVID online database analysis was performed to investigate the potential effective diseases and involved signaling pathways according to the results of the GO function and KEGG pathways enrichment analysis. To ensure standardization and maintain interbatch reliability of JPFR, High Performance Liquid Chromatography (HPLC) was used to establish a “chemical fingerprint.” For biological function validation, the effect of JPFR on the proliferation and migration of CRC cells in vitro was investigated by CCK-8 and transwell and wound healing assay, and the effect of JPFR on the growth and metastasis of CRC cells in vivo was detected by building a lung metastasis model in nude mice and in vivo imaging. For the potential mechanism validation, the expressions of MALAT1, PTBP-2, and β-catenin in CRC cells and transplanted CRC tumors were detected by real-time PCR, western blot, and immunohistochemical staining analysis. Results According to the rules of oral bioavailability (OB) > 30% and drug-likeness (DL) > 0.18, 244 effective compounds in JPFR were screened out, as well as the corresponding 132 potential drug targets. By the analysis of DAVID database, all these key targets were associated closely with the cancer diseases such as prostate cancer, colorectal cancer, bladder cancer, small cell lung cancer, pancreatic cancer, and hepatocellular carcinoma. In addition, multiple signaling pathways were closely related to JPFR, including p53, Wnt, PI3K-Akt, IL-17, HIF-1, p38-MAPK, NF-κB, PD-L1 expression and PD-1 checkpoint pathway, VEGF, JAK-STAT, and Hippo. The systematical analysis showed that various active compounds of JPFR were closely connected with Wnt/β-catenin, EGFR, HIF-1, TGFβ/Smads, and IL6-STAT3 signaling pathway, including kaempferol, isorhamnetin, calycosin, quercetin, medicarpin, phaseol, spinasterol, hederagenin, beta-sitosterol, wighteone, luteolin, and isotrifoliol. For in vitro experiments, the migration and growth of human CRC cells were inhibited by the JPFR extract in a dose-dependent way, and the expression of MALAT1, PTBP-2, β-catenin, MMP7, c-Myc, and Cyclin D1 in CRC cells were downregulated by the JPFR extract in a dose-dependent way. For in vivo metastasis experiments, the numbers of lung metastasis were found to be decreased by the JPFR extract in a dose-dependent manner, and the expressions of metastasis-associated genes including MALAT1, PTBP-2, β-catenin, and MMP7 in the lung metastases were downregulated dose dependently by the JPFR extract. For the orthotopic transplanted tumor experiments, the JPFR extract could inhibit the growth of orthotopic transplanted tumors and downregulate the expression of c-Myc and Cyclin D1 in a dose-dependent manner. Moreover, the JPFR extract could prolong the survival time of tumor-bearing mice in a dose-dependent manner. Conclusions Through effective network pharmacology analysis, we found that JPFR contains many effective compounds which may directly target cancer-associated signaling pathways. The in vitro and in vivo experiments further confirmed that JPFR could inhibit the growth and metastasis of CRC cells by regulating β-catenin signaling-associated genes or proteins.

新型冠状病毒肺炎(Novel coronavirus pneumonia,简称COVID-19)是指由新型冠状病毒(简称2019-nCoV)引起的以发热、咳嗽、头痛、乏力、呼吸困难等症状为主要临床表现的病毒型肺炎.我国最早的COVID-19患者被发现于武汉,患者从感染到发病通常在14天内,该病毒具有较强的传染性.截止至2020年2月23日,COVID-19患者累计77049例,导致不少于2445位患者死亡.与SARS相比,COVID-19进展快,危重患者多存在肺损伤、肝功能异常、急性呼吸窘迫综合征,最终发展至多器官衰竭、休克.危重COVID-19患者的病理变化机制目前仍未阐释清楚,有学者从COVID-19引起的炎症瀑布揭示COVID-19患者肝功能异常.COVID-19病理发展变化最终需要详实的解剖和病理研究证实.COVID-19给我国造成的危害不亚于2003年我国爆发的SARS.在当前COVID-19防治工作中,仍未形成全球公认最佳疗效的治疗指南,现代医学与传统医学救治措施均有报道.本文将COVID-19的最新中西医防治方法和措施予以汇总,为COVID-19防治工作提供支持.

MicroRNAs (miRNAs) detection with high specificity and sensitivity received abundant attention because miRNAs have been reported to play a vital role in pathological development of many diseases and regarded as potential biomarkers for the diagnosis and prognosis of diseases. We reported here a highly specific method for molecular exosomal miRNAs detection in constant temperature by integrating the advantages of CRISPR/Cas system and rolling circular amplification (RCA) techniques. Especially, the proposed strategy was demonstrated to obtain a high sensitivity attributed to the dual-specific recognition from miRNA-padlock initiated RCA and CRISPR-Cas12a-triggered specific cleavage. Eventually, the proposed strategy showed a sensitivity of 34.7 fM which was robust enough for exosomal miRNA detection and obtained a high consistency with reverse transcription quantitative polymerase chain reaction (RT-qPCR), revealing the potential of developing a universal molecular detection platform for the screening, diagnosing, and prognosis prediction of multiple diseases.

随着我国经济的不断发展和人民健康意识的不断提高,医院的发展面临着严峻的挑战.医院要想在激烈的竞争中立于不败之地,就必须提升医疗的服务质量,而优质的服务质量需要先进理念和技术的支撑.学科是医院的组成单位,而重点学科是具有优势和特色的学科,要通过不断细化和延伸来巩固终点学科的优势.总之医院及学科只要不断创新,不断积累,强化自身优势,才能为社会提供优质的医疗服务,提高医院及学科的核心竞争力.

"络病学说"作为重要的中医基础病机之一,近年来被广泛应用于肿瘤类疾病的临床诊疗中,其对于肿瘤的发生发展以及转移等机制研究与治疗均有理论指导意义."络病"在形态与功能上与现代医学中的肿瘤微血管、微循环概念相似;瘀阻络脉与肿瘤患者血液高凝状态类似,故运用"通络法"抗肿瘤具有充足的理论依据.虫类药是动物药的别称,作为通络药的代表,善于搜刮剔络,在肿瘤的防治中起到了活血化瘀通络、攻毒散结通络、搜风解毒通络以及补益培本通络等作用.通过梳理"络病学说"的起源、发展与成熟阶段的主要思想内涵,整理并总结现代肿瘤治疗中"络病学说"的相关研究与应用,并分析虫类药在通络法中的具体应用,以期为开展中医络病防治肿瘤的临床应用提供理论依据.

消化系统肿瘤的发生是由多种因素引起的抑癌基因或促癌基因发生突变所导致的.NF2基因是一种抑癌因子,其编码Merlin蛋白功能的缺失是造成消化系统肿瘤发生、发展的重要因素.NF2/Merlin通过Hippo/Yap、Wnt/β-catenin、转化生长因子-β(TGF-β)等多条信号通路发挥抗肿瘤作用.该文综述了NF2基因及其表达产物Merlin蛋白在消化系统肿瘤发生、发展过程中的抑制作用,旨在为探究NF2/Merlin的抑癌机制及肿瘤防治方法提供新思路.

目的 系统评价中医药辅助卡培他滨片维持治疗结直肠癌的临床疗效.方法 检索Pubmed、Embase、Cochrane Library、中国知识资源总库(CNKI)、中国学术期刊数据库(万方数据)、中文科技期刊数据库(维普网)及中国重要会议论文全文数据库中医药辅助卡培他滨片维持治疗结直肠癌随机对照试验(RCT),检索时间范围为建库至2018年11月.采用Cochrane偏倚风险评估工具对纳入研究进行质量评价,应用RevMan5.3进行Meta分析.结果 共纳入13项RCT,涉及患者964例.Meta分析结果显示:与对照组比较,试验组明显提高卡氏评分(RR=0.35,95％CI[0.26,0.49],P<0.00001),改善手足综合征(RR=0.55,95％CI[0.38,0.79],P=0.001),减少白细胞降低(RR=0.66,95％CI[0.49,0.89],P=0.006),减轻恶心呕吐(RR=0.51,95％CI[0.36,0.72],P=0.0002),减轻腹泻(RR=0.49,95％CI[0.35,0.68],P<0.0001),增加CD3+、NK细胞计数(RR=5.62,95％CI[3.08,8.16],P<0.05;RR=7.18,95％CI[5.31,9.06],P<0.05).试验组对瘤体有效率与对照组比较差异无统计学意义(RR=0.78,95％CI[0.57,1.05],P=0.10).结论 中医药辅助卡培他滨片维持治疗晚期结直肠癌患者疗效优于单纯化疗,可改善患者生活质量,减轻化疗毒副作用,提高机体免疫力,但尚需更多大样本高质量的RCT验证.

Merlin ((Moesin-ezrin-radixin-like protein, also known as schwannomin) is a tumor suppressor protein which is encoded by the neurofibromatosis type 2 gene, NF2. Loss of function mutations or deletions in NF2 which normally restrains tumor growth, leads to the formation of multiple tumors including schwannoma, meningioma and ependymoma. We tested whether NF2/Merlin is expressed and exerts similar control on proliferation of colorectal cancer cells and modulates the rate of their apoptosis. Expression of NF2/Merlin was reduced in colorectal cancer cells as compared with adjacent non-cancerous cells. Overexpression of NF2 inhibited colony formation by tumor cells and inhibited proliferation of cancer cells both in vitro and in vivo. The rate of apoptosis was also increased in colorectal cancer cells by overexpression of NF2. These findings show that NF2/Merlin is also reduced in tumors that do not arise in the context of neurofibromatosis and that induction of its expression might be used to control tumor growth.

大肠癌在中国是常见恶性肿瘤,赫捷等对2013年中国恶性肿瘤发病和死亡状况分析显示,大肠癌发病率位列恶性肿瘤第四位;2013 年中国有超过16 . 5万例大肠癌患者死亡,病死率位列第五位,并且大肠癌发病有逐年上升趋势[1]. 尽管"大肠癌"并未出现在传统医学经典著作中,其临床症状与中医学中"锁肛痔""癥瘕""肠覃""积聚"等病症有极高相似度[2] ,故在中医学上大肠癌被归类于上述病症范畴. 目前中医学对大肠癌的证型分类尚未取得统一,然而国内专家学者对大肠癌病机特点的认识渐趋一致,即本虚标实和虚实夹杂;脾虚和肾虚是虚之本,气、湿、痰、瘀、毒为实之标[3-5]. 健脾解毒方和健脾补肾方、健脾除湿方等代表方剂从脾和肾论治大肠癌防治的临床和基础研究较为常见,而从肺论治大肠癌的研究和应用较少. 中医整体观是对人体各器官和组织在生理上密切联系,病理变化相互影响的高度概括,也是指导"同病异治"的思想基础. 大肠主津,传导糟粕,以通为用,其功能正常运转,一方面需要肺气宣发肃降,使气机畅达,大肠才能传导糟粕有力;另一方面肺通调水道,布散津液,使大肠茹润而不燥结. "肺与大肠相表里",是指肺和大肠生理上密切联系,病理上相互影响,大肠相关病变受肺功能的影响,即可以通过治肺以治大肠癌,或以治肺之药治大肠病变. 若肺失肃降,则气机不畅,水津输布失常,大肠传导失司,易使致湿、瘀、毒积聚,继而发为肠癌.

目的 鉴定人结直肠癌LoVo/HCT116细胞上清外泌体中Wnt3a和Wnt5a蛋白的表达情况,探讨外泌体对人结直肠癌迁移的调节作用.方法 培养人结直肠癌LoVo/HCT116细胞,提取上述两种细胞的上清液抽提外泌体,运用透射电镜、纳米颗粒跟踪分析仪(NTA)、蛋白印迹法(Western blot)对外泌体进行鉴定.结果 透射电镜下观察到外泌体具有膜结构,NTA检测提示粒径大小主要分布在94 nm左右,可检测到外泌体膜标志蛋白HSP70、CD63、CD9以及Wnt3a、Wnt5a表达.人结直肠癌LoVo/HCT116细胞外泌体能被人结直肠癌细胞摄取,并对人结直肠癌细胞迁移有促进作用.结论 人结直肠癌LoVo/HCT116细胞能抽提得到外泌体,外泌体表达膜标志蛋白HSP70、CD63、CD9以及Wnt3a、Wnt5a蛋白.外泌体能被结直肠癌细胞吸收,而吸收了外泌体的人结直肠癌细胞其迁移能力增强.