Duodenitis refers to inflammation that occurs in the duodenum. Helicobacter pylori (Hp) is a known risk factor for duodenitis. This paper attempted to analyze the correlation between Hp virulence genotypes and the initiation and development of duodenal bulbar inflammation (DBI) to lay the foundation for the management of duodenitis induced by Hp infection. Total RNA was extracted from duodenal samples of 156 Hp-positive patients [70 with DBI and 86 with duodenal bulbar ulcer (DBU)] and 80 Hp-free DBI patients, followed by RT-qPCR detection of COX-2 mRNA expression and the presence of virulence factors. The cagA positive (62.2%), vacAs1 (21.79%), vacAm2 (23.72%), vacAs1m2 (19.87%) and iceA1 (55.80%) genotypes were dominant in 156 Hp-positive samples. Statistical difference was observed in vacAs and vacA mixtures between DBI and DBU patients. Gastric metaplasia had an association with vacA allelotypes, and its occurrence had strong correlations with vacAs1 and vacAs1m2 genotypes. The vacAs1 and vacAs1m2 genotypes were correlated with gastric metaplasia occurrence (all p<0.05). There were significant correlations between vacAs and vacA mixtures with cagA genotypes, and between iceA genotypes with vacA mixtures (all p<0.05). COX-2 was strongly expressed in Hp-infected duodenal mucosa and showed correlations with vacA genotype. COX-2 was differentially expressed in vacAs1- and vacAs2-positive patients. COX-2 was more highly upregulated in vacAs1m1- and vacAs1m2-positive patients than vacAs2m2-positive patients. Overall, Hp virulence genotype vacA was correlated with DBI and DBU initiation and development.

目的 探讨结肠肿瘤组织中长链非编码RNA(long NON-Coding RNA,lncRNA)NONHSAT017458的表达情况及潜在临床意义.方法 运用高通量测序技术,建立基因与lncRNAs差异表达谱.通过基因本体(GO)注释分析及京都基因和基因组百科全书(KEGG)通路富集分析,对差异表达的lncRNA NONHASAT017458进行功能注释.采用定量反转录聚合酶链反应法(qRT-PCR)对10例结肠癌及腺瘤患者结肠肿瘤及瘤旁正常组织检测lncRNA NONHSAT017458的表达,分析其表达量与患者临床病理特征的关系.结果 筛选出表达差异明显的ln-cRNA NONHSAT017458,通过qRT-PCR方法在结肠癌中验证结果一致.与正常癌旁组织相比,结肠癌组织中lncRNA NONHSAT017458呈现表达升高,差异有统计学意义(P＜0.05).但与正常肿瘤旁组织相比,结肠腺瘤组织中lncRNA NONHSAT017458,差异无统计学意义(P＞0.05).lncRNA NONHSAT017458的表达与结肠癌患者年龄、性别、肿瘤大小、TNM分期无明显相关性(均P＞0.05).结论 lncRNA NONHSAT017458在结肠癌肿瘤组织中表达上调,其可能作为临床中新型的潜在的诊断和治疗靶点.

<p>Supplementary Figure1-10, Table1-2 Figure S1. The relations of REGγ with Hippo-YAP signal pathway in colon cancer. A. The protein levels of Lats2 and p-Lats1 were unchanged in HCT116 and HT29 human colon cancer cells with REGγ knockdown. The expression of REGγ, Lats2 and p-Lats1 were measured by Western Blot. B. REGγ knockdown did not change the levels of p-YAP (S397) in HCT116 and HT29 human colon cancer cells. Figure S2. REGγ promotes degradation of Lats1. A. Silencing REGγ slowed down degradation of endogenous Lats1. REGγ sh-N or sh-R HCT116 cells were treated with cycloheximide (100μg/ml) for indicated time followed by Western Blotting. Quantitated results were plotted to indicate dynamic changes (Analysis of Variance, n=3, *p<0.05, **p<0.01, ***p<0.001). B. Ectopic expression of wild-type (WT), but not inactive mutant N151Y REGγ promoted the degradation of endogenous Lats1 in HEK293 cells. Figure S3. REGγ promotes YAP signaling via degradation of Lats1. A Silencing Lats1 restored the expressions of YAP target genes in HCT116 sh-R cells similar to those in HCT116 cells by RT-PCR analysis. Data are presented as the means {plus minus} SEM (Analysis of Variance, n=3, **p<0.01, ***p<0.001). B. RNAi efficiently depleted Lats1 in HCT116 cells for experiments in A. HCT116 cells were harvested 72h after transient transfection of a control (Ctrl) or Lats1 small interfering RNA (siRNA) followed by Western blot analysis. C. Overexpression of Lats1 in HCT116 sh-N cells changed the expression of YAP target genes similar to the levels in HCT116 sh-R cells by RT-PCR analysis. Data are presented as the means {plus minus} SEM (Analysis of Variance, n=3, *p<0.05, **p<0.01, ***p<0.001). D. Western blot analysis validated successful expression of exogenous Lats1 in experiments shown in C. E Figure S4. REGγ promotes proliferation of human colon cancer cells. A. REGγ deletion and YAP silencing inhibited cell proliferation of HCT116 human colon cancer cells to a similar extent. After 72 h of transfection with a control- siRNA or YAP-siRNA, cell viability was measured on days 1, 2, 3, 4 and 5 by using MTT assays. Western Blot analysis showing marked silencing of YAP expression in HCT116 cells after 72h transfection with control (Ctrl) or YAP small interfering RNA (siRNA) oligos. B. Silencing REGγ or YAP alone or in combination inhibited cell proliferation of HT29 human colon cancer cells. Cell viability was measured on days 1, 2, 3, 4 and 5 by MTT assays following RNAi for 72h. Western blot analysis demonstrated the knockdown efficiency. C Figure S5. Constitutive YAP fully reversed the retardation of tumor growth induced by REGγ depletion. A. Xenograft tumors were generated by injecting HCT116 sh-N, HCT116 sh-N+YAP (S127A), HCT116 sh-R and HCT116 sh-R+YAP (S127A) cells into dorsal flanking sites of nude mice. B Tumors were dissected and volumes were measured. Values were presented as the means {plus minus} SEM (two-tailed Analysis of Variance, n=3, *p < 0.05, **p < 0.01). C. The xenografts were harvested 30 days post-injection and analyzed by Western blotting with antibodies against YAP or REGγ. Data in this figure are representatives of three independent repeats. Figure S6. P65 strengths YAP transcription and its signal pathway A. Quantitative PCR analysis of YAP expression in HT29 cells treated with TNFα (20 ng/ml) or IL-6 (20 ng/ml). Data are presented as the means {plus minus} SEM (Analysis of Variance, n=3, ***p<0.001). B. HCT116 cells were treated with or without TNFα (20 ng/ml) for 3 hours and processed for ChIP assay using anti-YAP antibodies. Immunoprecipitated chromatin was analyzed by RT-PCR using the specific primers for Cyr61 promoter. C. and D. TNFα or IL-6 treatment enhanced the expression of YAP downstream positive regulatory genes (Cyr61, AREG) and decreased the expression of negative regulatory gene (Trail, DDT4) in HCT116 and HT29 cells. Cells were treated were treated with TNFα (20 ng/ml) or IL-6 (20 ng/ml) with or without Verteporfin (VP) for 3 hours and were analyzed by real-time PCR. Figure S7. YAP enhances p65 transcription and its signal pathway A. Quantitative PCR analysis of p65 expression in HT29 cells treated with/without Verteporfin (VP) or transfected with S127A mutant YAP (S127A-YAP) compared with the empty vector. Data are presented as the means {plus minus} SEM (Analysis of Variance, n=3, **p<0.01). B. YAP activation increased the transcriptional activity of NF-κB in HT29 human colon cancer cells. NF-κB luciferase reporter activities were measured in sh-N, sh-N+YAP (S127A), sh-R and sh-R+YAP (S127A) cells. Data represent the means {plus minus} SEM (Analysis of Variance, n=3, ***P<0.001). C. and D. Figure S8. Clinical implication of REGγ in human colon cancer. A. A significant correlation among REGγ, YAP1 and RELA mRNA expression in 53 patients with ulcerative colitis. Pearson correlation coefficient was 0.737, 0.917 and 0.734, respectively. P<0.0001. B. The correlation of survival rate with p-p65 overexpression in 172 CRC patients. p=0.379. C. Diagrams summarizing the percentage of positive staining for each marker examined. Results were evaluated in a double-blinded fashion. D. High expression of REGγ was not related with patient age, patient gender, tumor size, tumor grade and tumor metastasis (p>0.05) Figure S9. A Model of crosstalk among REGγ, Hippo-Yap, and NF-κB. In human colon cancer cells, overexpression of REGγ promotes the degradation of Lats1, thus activating YAP signaling. YAP activation empowers a reciprocal positive regulation with NF-κB, leading to aberrant cell proliferation and development of inflammationassociated colon cancer. In contrast, cells with REGγ depletion are resistant to Lats1 inactivation, inhibiting YAP activation and its crosstalk to NF-κB to prevent tumor formation Figure S10. P53 was not affected by REGγ deficiency in human colon cancer cells. A. Western Blot analysis for REGγ and p53 in HCT116 sh-N and sh-R human colon cancer cells. β-actin served as a loading control. B. Western Blot analysis of p53 from mouse normal colon and tumor tissues of REGγ+/+ and REGγ-/- mice showed no marked changes. All experiments were repeated three times. Table 1. Sequences of primers used for Q-PCR Table 2. Sequences of primers used for ChIP</p>

BACKGROUND:N6-methyladenosine (m6A) RNA methylation regulators have been implicated in the carcinogenesis and progress of a variety of cancers. Until now, the effects of them on intrahepatic cholangiocarcinoma (ICC) have been poorly understood.METHODS:We used the GEO databases to systematically evaluate the expression profiles of 36 m6A RNA methylation regulators in ICC patients and produced a signature to assess its prognostic values. In vitro experiments were implemented to confirm the expression level.RESULTS:Compared to normal intrahepatic bile duct tissues, more than half of these 36 genes showed different levels of expression in ICC tissues. Two groups emerged from the consensus cluster analysis of these 36 genes. The two cluster of patients had significantly different clinical outcomes. In addition, we created a m6A-related prognostic signature that performed exceptionally well in the prognostic categorization of ICC patients, based on the ROC curves, Kaplan-Meier curves, and univariate and multivariate Cox regression analyses. Further research showed that there was a significant association between the m6A-related signature and the manifestations of tumor immune microenvironment in ICC. The expression level and biological effect of METTL16, one of the two m6A RNA methylation regulators incorporated in the signature, were confirmed and explored by using in vitro experiments.CONCLUSIONS:This analysis revealed the predictive roles of m6A RNA methylation regulators in ICC.

Aim: This study aimed to investigate the biological functions of miRNAs in hepatobiliary tumors as the focus of targeted therapy research. Background: Hepatobiliary tumors are among the leading causes of cancer-related deaths worldwide. Many microRNAs (miRNAs) play an important regulatory role in tumor progression. Our study aims to explore some biologically functional miRNAs from different datasets of hepatobiliary tumors for disease diagnosis or treatment. Objective: In this study, we tried to filter out differentially expressed miRNAs in different tumor datasets from the GEO database. Methods: In this study, we first perform analyses in different GEO data sets. After taking the intersection, the initial scope is limited to several differential RNAs. Then, combined with the existing research results from Kaplan-Meier survival analysis and literature, the candidate molecule was finally identified to be studied. Furthermore, the biological characteristics analysis of the candidate molecule was performed on the basis of Cancermirnome online tool, including expression levels in tumors, KEGG and GO analysis, ROC analysis, and target gene prediction. Furthermore, the effect of the candidate molecule on the biological functions of liver cancer was verified by in vitro assay. Results: The preliminary analysis of bioinformatics shows that 16 differentially expressed miRNAs may play an important role in HCC or ICC. Ultimately, we identified miRNA-99a-5p as the only molecule to study. The results showed that miRNA-99a-5p is abnormally expressed in many tumors, and in liver cancer, its level of expression in tumor tissue is significantly lower than that in normal tissue. Then, the KEGG and GO analysis found that it functions in multiple pathways. At the same time, the ROC analysis found that it showed great potential for prognostic prediction in HCC and we also predicted that RUNDC3B is the most likely target to which it binds. Finally, the experimental results of overexpression and knockdown confirmed that miRNA-99a-5p could inhibit cell proliferation in HCC, which also suggested that it may be an important tumor suppressor in HCC. Conclusion: MiRNA-99a-5p was negatively correlated with HCC progression and could act as a novel therapeutic target for HCC.

GNAO1, the alpha O1 subunit of G protein, was reported to be significantly downregulated in hepatocellular carcinoma (HCC), as well as being implicated in a variety of intracellular biological events; findings suggest that it may act as a tumor suppressor. Our goal was to further explore the expression of GNAO1 in HCC patients and its potential clinical significance. Oncomine and Kaplan-Meier plotter databases were used to assess the mRNA expression of GNAO1 in HCC tissues and patient survival time. Subsequently, immunohistochemistry (IHC) was used to measure GNAO1 protein level in tissue from 79 cases of HCC and paired adjacent tissues. The Kaplan-Meier survival analysis, Cox regression model, and prognostic nomogram were used to evaluate the prognostic role of GNAO1 in HCC. Results demonstrated that mRNA and protein expressions of GNAO1 were both lower in HCC tissues than in adjacent tissues (all p < 0.01). HCC patients with high expression of GNAO1 had better relapse-free survival (RFS) than those with low GNAO1 expression (all p < 0.05). A high expression of GNAO1, meanwhile, functioned as a good predictor of late relapse for HCC (p < 0.05). The nomogram consisting of GNAO1 expression and the tumor-node-metastasis (TNM) model presented good ability in predicting the 3-year relapse for HCC (C-index = 0.614). In conclusion, GNAO1 was a reliable biomarker of relapse prediction for HCC.

AbstractPurpose: Colorectal cancer is one of the most commonly diagnosed cancers closely associated with inflammation and hyperactive growth. We previously demonstrated a regulatory circuit between the proteasome activator REGγ and NF-kappaB (NF-κB) during colon inflammation, known to be important in the development of colitis-associated cancer as well as sporadic colorectal cancer. How the inflammatory microenvironment affects the Hippo pathway during colorectal cancer development is largely unknown.Experimental Design: Here, we used REGγ-deficient colon cancer cell lines, REGγ knockout mice, and human colorectal cancer samples to identify the novel molecular mechanism by which REGγ functions as an oncoprotein in the development of colorectal cancer.Results: REGγ can directly interact with Lats1 and promote its degradation, which facilitates Yes-associated protein (YAP) activation in colon cancer cells. REGγ deficiency significantly attenuated colon cancer growth, associated with decreased YAP activity. Suppression of tumor growth due to REGγ depletion was overcome by constitutively active YAP. Surprisingly, reciprocal activation of the YAP and NF-κB pathways was observed in human colon cancer cells. REGγ overexpression was found in over 60% of 172 colorectal cancer specimens, highly correlating with the elevation of YAP and p65. Postoperative follow-up revealed a significantly lower survival rate in patients with concomitantly high expression of REGγ, YAP, and p-p65.Conclusions: REGγ could be a master regulator during colorectal cancer development to promote YAP signaling and reinforce cross-talks between inflammation and growth pathways, and REGγ might be a new marker for prognosis of colorectal cancer patients. Clin Cancer Res; 24(8); 2015–25. ©2018 AACR.

目的 探讨骨桥蛋白在大鼠重度创伤性脑损伤后肠黏膜中表达水平的变化.方法 选取雄性SD大鼠24只,随机分入假手术组(n=6)和重度创伤性脑损伤组(n=18);再按照术后1、3、5 d时间点,将重度创伤性脑损伤组分为伤后1 d组、伤后3d组、伤后5d组3个亚组,每组6只大鼠.光学显微镜下观察各组肠黏膜组织形态变化;荧光异硫氰酸盐葡聚糖法检测肠通透性;酶联免疫吸附试验检测肠组织和血浆中骨桥蛋白、肿瘤坏死因子-α、白细胞介素-6的表达水平.结果 重度创伤性脑损伤组大鼠的肠黏膜病理学评分和通透性,肠组织和血浆中骨桥蛋白、肿瘤坏死因子-α、白细胞介素-6的表达水平均明显高于假手术组,且随着伤后时间的延长而上升,各组间比较,差异均有统计学意义(P<0.05).血浆骨桥蛋白表达与肠黏膜病理学评分、肠黏膜通透性、肿瘤坏死因子-α及白细胞介素-6的表达水平具有相关性(P<0.05).结论 骨桥蛋白在大鼠重度创伤性脑损伤后肠黏膜屏障损伤的病理过程中发挥重要作用,是评价肠道通透性的一个新的潜在指标.

结直肠癌(colorectal cancer,CRC)是消化道常见恶性肿瘤之一,发生率及死亡率高.早期不易发现,当就诊时多数已属于晚期,治疗效果较差,预防CRC的发生尤为重要.近几年关于CRC预防的研究也在不断深入,结合最新国内外文献,本文将主要对CRC一级预防的研究进展做一总结.

Helicobacter pylori (H.pylori) infection is the most common chronic infection in the world and H.pylori is a class Ⅰ carcinogen of gastric cancer.H.pylori infection can contribute to the development of gastritis,peptic ulcer,gastric mucosa associated lymphoid tissue lymphoma,and other diseases;however,obesity,gastroesophageal reflux disease and allergic diseases in children can benefit from H.pylori infection.During the process of H.pylori eradication treatment,antibiotic resistance and intestinal flora disturbance may occur.H.pylori eradication treatment has become a hot topic again in recent years.This article focuses on the updated views and major controversies about eradication of H.pylori,with an aim to help clinicians make rational decisions in H.pylori eradication.

Objective To survey the awareness and knowledge of Helicobacter pylori (Hp) infection among medical staff in Shanghai.Methods A questionnaire survey was conducted among 316 medical staff in Shanghai,including 74 gastroenterologists (GI),158 general practitioners (GP),and 68 gastroenterology nurses(GN),from October 2014 to September 2015.The questionnaire was designed according to the Fourth Helicobacter Pylori Infection Treatment Consensus Report of China (the Consensus).There were 4 parts and 29 questions in the questionnaire,including the knowledge and performance of the Consensus (8 questions),the indications of Hp eradication (8 questions),detection methods of Hp infection (7 questions)and the therapy of Hp eradication (6 questions).Results Total 300 valid questionnaires were received with a response rate of 94.9％ (300/316).The awareness rate of the Consensus in GI,GP and GN groups was 81.1％ (60/74),57.6％ (91/158) and 26.4％ (18/68),respectively (χ2 =43.67,P=0.001).GI had higher awareness rate than GP and GN in indications of Hp eradications (for peptic ulcer,mucosa-associated lymphoid malignancies,post-resection patients of early gastric cancer,and family history of gastric cancer,the χ2 values were 16.68,35.60,33.46 and 39.22,respectively;all P ＜0.05).In part of Hp infection detection methods,the responses of GI,GP and GN groups in C14 or C13 urea breathing test were 97.3％ (72/74),47.5％ (75/158) and 82.1％ (55/68),respectively (χ2 =72.38,P =0.001);in gastric mucosa tissue rapid urease test were 70.3％ (52/74),13.9％ (22/158) and 25.4％ (17/68),respectively (χ2 =78.22,P =0.001);in serological test were 58.1％ (43/74),20.9％ (33/158)and 44.8％ (30/68),respectively (χ2 =40.30,P =0.001);in gastric mucosa tissue section staining were 56.8％ (42/74),13.3％ (21/158) and 22.4％ (15/68),respectively (χ2 =50.35,P =0.00).In part of Hp eradication therapy the responses of GI,GP and GN groups in recommended bismuth quadruple therapy were 71.6％ (53/74),47.5％ (75/158) and 40.3％ (25/62),respectively (χ2 =15.93,P =0.001);in triple therapy were 27.0％ (20/74),51.6％ (81/158) and 42.0％ (26/62),respectively (χ2 =12.42,P =0.002);in 10 or 14 d for treatment duration were 78.4％ (58/74),78.5％ (124/158)and 67.6％ (46/68),respectively (χ2 =3.36,P =0.186).Conclusion Gastroenterologists are more likely to adhere with the Consensus than general practitioners and gastroenterological nurses in the management of Hp infection.The survey suggests that more attention should be paid for popularization and implementation of Hp infection guidelines and consensus among Shanghai medical staff,especially for GP and nurses.

Increasing incidence of inflammatory bowel disorders demands a better understanding of the molecular mechanisms underlying its multifactorial aetiology. Here we demonstrate that mice deficient for REGg, a proteasome activator, show significantly attenuated intestinal inflammation and colitis-associated cancer in dextran sodium sulfate model. Bone marrow transplantation experiments suggest that REGg’s function in non-haematopoietic cells primarily contributes to the phenotype. Elevated expression of REGg exacerbates local inflammation and promotes a reciprocal regulatory loop with NFkB involving ubiquitinindependent degradation of IkBe. Additional deletion of IkBe restored colitis phenotypes and inflammatory gene expression in REGg-deficient mice. In sum, this study identifies REGg-mediated control of IkBe as a molecular mechanism that contributes to NFkB activation and promotes bowel inflammation and associated tumour formation in response to chronic injury. DOI: 10.1038/ncomms10761 OPEN

缺血性结肠炎（ischemic colitis,IC）是急性下消化道出血的常见病因,近年来的检出率和患病率逐年上升.多见于老年人,大多数IC病例为一过性和自限性,仅有少数病例为重症,容易被误诊或漏诊.为提高对该病的认识,本文着重对IC诊断与治疗的研究进展作一综述.

目的观察骨桥蛋白（osteopontin,OPN）对大鼠小肠隐窝上皮细胞（intestinal epithelial cells-6,IEC-6）分化、增殖、迁移等生物学性状的影响。方法分别采用相差显微镜、细胞贴壁率检测、噻唑蓝比色法、划痕实验、Western blot和ELISA法,观察不同浓度OPN对IEC-6细胞增殖、分化和迁移能力的影响,并从鸟氨酸脱羧酶（ornithine decarboxylase,ODC）表达变化和炎性反应角度,探讨其可能的作用机制。结果经不同浓度的OPN处理后,IEC-6细胞形态、贴壁率和增殖率均未见明显变化。OPN能促进IEC-6细胞的移行功能,且OPN浓度越高细胞迁移速度越快。与低浓度或高浓度OPN相比,适当浓度的OPN能促进IEC-6细胞内ODC1蛋白表达（0.1μg/mL和1.0μg/mL OPN）和细胞内炎性反应（0.05μg/mL OPN）。结论 OPN能促进IEC-6细胞的移行功能,从而促进损伤黏膜早期修复,其机制可能与特定浓度的OPN能促进细胞内ODC1蛋白的表达和损伤IEC-6细胞的炎性反应有关。

Increasing incidence of inflammatory bowel disorders demands a better understanding of the molecular mechanisms underlying its multifactorial aetiology. Here we demonstrate that mice deficient for REGγ, a proteasome activator, show significantly attenuated intestinal inflammation and colitis-associated cancer in dextran sodium sulfate model. Bone marrow transplantation experiments suggest that REGγ's function in non-haematopoietic cells primarily contributes to the phenotype. Elevated expression of REGγ exacerbates local inflammation and promotes a reciprocal regulatory loop with NFκB involving ubiquitin-independent degradation of IκBɛ. Additional deletion of IκBɛ restored colitis phenotypes and inflammatory gene expression in REGγ-deficient mice. In sum, this study identifies REGγ-mediated control of IκBɛ as a molecular mechanism that contributes to NFκB activation and promotes bowel inflammation and associated tumour formation in response to chronic injury.

Increasing incidence of inflammatory bowel disorders demands a better understanding of the molecular mechanisms underlying its multifactorial aetiology. Here we demonstrate that mice deficient for REG gamma, a proteasome activator, show significantly attenuated intestinal inflammation and colitis-associated cancer in dextran sodium sulfate model. Bone marrow transplantation experiments suggest that REG gamma's function in non-haematopoietic cells primarily contributes to the phenotype. Elevated expression of REG gamma exacerbates local inflammation and promotes a reciprocal regulatory loop with NF kappa B involving ubiquitin-independent degradation of I kappa B epsilon. Additional deletion of I kappa B epsilon restored colitis phenotypes and inflammatory gene expression in REG gamma-deficient mice. In sum, this study identifies REG gamma-mediated control of I kappa B epsilon as a molecular mechanism that contributes to NF kappa B activation and promotes bowel inflammation and associated tumour formation in response to chronic injury.

目的:探究正常直肠组织和直肠癌组织中JAK-STAT信号通路重要成员以及通路下游重要蛋白的表达变化情况及其临床意义,并通过体外实验观察STAT3对直肠癌细胞侵袭、转移以及增殖的影响.方法:收集2013年5月1日至2014年5月1日在本院行手术切除并经病理证实为直肠癌患者的癌组织和非直肠癌(痔疮、肛瘘肛裂、结肠炎、肠息肉等)患者正常直肠组织各50份,采用Western blotting法检测组织中STAT3、p-STAT3及JAK-STAT信号通路下游Cyclin D1、Bcl2的表达,分析STAT3蛋白表达与直肠癌临床病理特征关系.以慢病毒介导的STAT3-shRNA转染直肠癌细胞Colo320,采用MTT法和Transwell侵袭和迁移实验检测sh-RNA干扰STAT3表达对直肠癌Colo32细胞增殖、侵袭和转移的影响.结果:与正常组织相比,直肠癌组织中STAT3蛋白的表达显著升高(P＜0.01),p-STAT3、Cyclin D1和Bcl2蛋白的表达也明显高于正常直肠组织(P ＜0.05);STAT3蛋白表达水平与直肠癌分化程度、淋巴转移有关(P＜0.05),而与肿瘤大小无关(P＞0.05).慢病毒介导的shRNA转染Colo320细胞可有效抑制其STAT3和p-STAT3表达,沉默STAT3后Colo320细胞的增殖和侵袭转移能力显著下降(P＜0.05).结论:STAT3能通过影响JAK-STAT信号通路下游重要蛋白的表达,促进直肠癌的增殖、侵袭和转移,研究结果为直肠癌的防治提供潜在的新靶点.