Cancer stem cells (CSCs) and tumor-associated macrophages (TAMs) are associated with the prognosis of colorectal cancer (CRC). Emerging studies indicate active crosstalk between CSCs and TAMs within the tumor microenvironment. However, the prognostic implications of integrating CSC- and TAM-associated markers for risk stratification remain incompletely defined in CRC. Expression levels of CD86, CD163, CD44 and CD133 were assessed by immunohistochemistry. Pearson s chi-square test was employed to analyze correlations between marker expression and clinicopathological parameters. The Kaplan-Meier method and log-rank test were used to determine survival differences and identify potential prognostic factors. Variables achieving statistical significance (P<0.05) in the univariate analysis were subsequently included in a multivariate Cox proportional hazards regression model to analyze independent predictors of overall survival. The results demonstrated that a combined expression profile of high CD86 with low CD163, CD44 and CD133 was significantly associated with prolonged survival. CD86 expression was negatively correlated with CD133 and CD44, while CD163 showed positive correlations with both markers. In addition, elevated CD163 and CD133 levels were positively correlated with poorer prognosis in patients with CRC. In conclusion, it was suggested that different TAM phenotypes in combination with CSC-related biomarkers serve as potential biomarkers for CRC onset and progression.

Astragalus polysaccharide, a bioactive substance with significant immunomodulatory functions, has not yet had its specific configuration–function relationship fully elucidated. In the present study, four Astragalus polysaccharide fractions with different polarities were successfully obtained through DE52 anion exchange column separation technology, and their pharmacological activities were screened. Homogeneous Astragalus polysaccharide was isolated and purified using DE52 polarity separation columns and gel column purification techniques. The types of glycosidic bonds in Astragalus polysaccharide were identified through monosaccharide composition analysis, infrared spectroscopy, molecular weight determination, and polysaccharide methylation analysis. The probable disaccharide repeating unit structure of AMPS-0.2A polysaccharide was determined to be α-(1,2)-l-Rha-α-(1,4)-d-GalA. Astragalus polysaccharide was found to induce the polarization of macrophages from the M2 phenotype to the M1 phenotype. This effect was primarily mediated through the regulation of the JNK/MAPK signaling pathway and the NLRP3/IL-1β signaling pathway, thereby promoting the polarization of M1 macrophages.

Agrocybe aegerita polysaccharides (AAP), known for their diverse pharmacological properties, have yet to be fully understood in terms of their structure evaluation, effects and mechanisms on tumor-associated macrophages in colorectal cancer. Agrocybe aegerita polysaccharides were extracted using hot water and subsequently purified. Their structure was elucidated through methylation and nuclear magnetic resonance analyses. The impact of AAP-0.2A on macrophage polarization was assessed using flow cytometry, immunofluorescence, and ELISA. Furthermore, transcriptomics, molecular docking and western blot were employed to investigate the specific mechanisms by which AAP-0.2A influence macrophage polarization. Conditioned media were applied to CT26 cells to evaluate the effects on the proliferation and apoptosis of colorectal cancer cells. These findings demonstrate that AAP-0.2A are neutral fuco-galactoglucans that increased M1 phenotype markers of CD86, CCR7, IFN-γ while decreased M2 phenotype markers of CD206, Arg1 and IL-10. They enhance M1 macrophage polarization by activating the NF-κB/NLRP3 and HIF1A/P53 pathways. Further studies have shown that AAP-0.2A inhibit the proliferation and induce apoptosis of colorectal cancer cells, counteracting the effects of IL-4-conditioned media. These results suggested that AAP-0.2A repolarized macrophages from M2 to M1 phenotype through activating NF-κB/NLRP3 and HIF-1α/p53 pathways to inhibit the proliferation and induce apoptosis of colorectal cancer cells.

Background Connexin 43 (Cx43) and Cx43-gap-junction-intercellular-communications (Cx43-GJs) play an important role in metastasis. While dioscin exhibits remarkable anticancer activities in various cancers, its effect on Cx43/Cx43-GJs in gastric cancer (GC) remains poorly understood. Purpose This study aimed to elucidate the anti-metastatic efficacy and underlying mechanism of the plant-derived compound dioscin against gastric cancer cells. Methods We integrated network pharmacology, molecular docking, and dynamics simulations to identify targets. Using in vitro models (overexpression, G21R mutant, siRNA knockdown) and in vivo xenograft models, we assessed dioscin’s effects on proliferation, invasion, migration, epithelial-mesenchymal transition (EMT), and signaling pathways via Western blot, immunofluorescence, wound healing, transwell, and co-immunoprecipitation assays. Results Bioinformatic analysis highlighted the VEGFA/PI3K/AKT/mTOR pathway as central to GC malignancy. Dioscin suppressed this axis in a time- and concentration-dependent manner by upregulating Cx43 and enhancing gap junction function. Loss-of-function (siRNA/G21R) and rescue experiments confirmed that functional Cx43 is essential for the efficacy of dioscin. The G21R mutant revealed the critical role of Cx43’s scaffolding function in signaling regulation. Dioscin, via a Cx43-mediated "dual-barrier" mechanism-strengthening epithelial adhesion and triggering migration inhibition-effectively suppressed EMT and cell motility. Conclusion This study elucidates a novel mechanism by which dioscin inhibits GC via Cx43-mediated suppression of VEGFA/PI3K/AKT/mTOR signaling and establishes Cx43 as a key nexus linking natural compounds to oncogenic pathways. The non-channel scaffolding function of Cx43 offers a new theoretical framework and therapeutic strategy for GC intervention.

Neuroblastoma is the most common extracranial solid tumour in children, and genetic susceptibility plays a crucial role in its development. The impact of tRNA Dimethyltransferase 1 (TRDMT1), a primary methyltransferase catalysing 5-methylcytosine (m5C) RNA modification, on neuroblastoma susceptibility remains unexplored. We conducted a case-control study involving 402 neuroblastoma patients and 473 controls from Jiangsu, China. TRDMT1 polymorphisms (rs7074891 T>C, rs10904887 T>C and rs2273734 C>T) were genotyped via the TaqMan assay. Logistic regression was used to assess odds ratios (ORs) and 95% confidence intervals (CIs), while stratification analysis and expression quantitative trait locus (eQTL) analysis were used to examine subgroup-specific effects and regulatory impacts. Additionally, clinical correlation analysis and survival analysis were performed on neuroblastoma datasets used to evaluate. The rs7074891 TC/CC genotype reduced neuroblastoma risk (adjusted OR = 0.75, 95% CI = 0.57-0.98, p = 0.036), especially in children aged ≤ 18 months and those with mediastinal-origin tumours. Conversely, the rs10904887 CC (adjusted OR = 1.73, 95% CI = 1.27-2.38, p = 0.0006) and rs2273734 TT genotypes (adjusted OR = 1.80, 95% CI = 1.09-2.97, p = 0.023) were associated with increased risk, with distinct subgroup-specific effects. Combined 1-3 risk genotypes further confirmed increased susceptibility (adjusted OR = 1.81, 95% CI = 1.38-2.37, p < 0.0001), particularly in males and older children. eQTL analysis revealed that the rs7074891 C and rs10904887 C alleles increased TRDMT1 expression, whereas the rs2273734 T allele decreased it. Elevated TRDMT1 expression was correlated with poor prognosis and high-risk clinical features. TRDMT1 polymorphisms are significantly associated with neuroblastoma susceptibility, providing insights into their genetic and epigenetic mechanisms and potential as biomarkers and therapeutic targets.

Objective Cancer stem cells (CSC) can recruit tumor-associated macrophages (TAMs) into the tumor microenvironment and accelerate their polarization into tumor-accelerating macrophages. And TAMs maintain CSC stemness and construct niches that are poor for CSC patients survival.Thus we study that different phenotypes of TAMs and biomarkers of cancer stem cells (CSC) were measured as prognostic and predictive biomarkers in colorectal cancer (CRC). Materials and Methods Expression of CD86, CD163, CD44 and CD133 were detected by immunohistochemistry (IHC). Pearson chi-square test was used to analyze the correlation between CD86, CD163, CD44, CD133 and clinicopathological parameters. Survival difference and prognosis factors were established by Kaplan-Meier method with the log-rank test. Then the factors with p < 0.05 in univariate analysis were analyzed for overall survival by Cox proportional hazard regression model. Results The results showed that high expression of CD86 and low expression of CD163 as well as CD44 and CD133 were remarkably associated with longer survival. Then,the protein level of CD86 exhibited a negative correlation with the levels of CD133 and CD44, while CD163 showed a positive associated with CD133 and CD44. Furthermore, the high expression of CD163 and CD133 in combination were positively correlated with poor prognosis in patients with CRC. Conclusion These results suggested that different phenotypes of TAMs and biomarkers of CSCs can be used as potential biomarkers for the development and progression of CRC.

Efficient milk production in mammals confers evolutionary advantages by facilitating the transmission of energy from mother to offspring. However, the regulatory mechanism responsible for the gradual establishment of milk production efficiency in mammals, from marsupials to eutherians, remains elusive. Here, we find that mammary gland of the marsupial sugar glider contained milk components during adolescence, and that mammary gland development is less dynamically cyclic compared to that in placental mammals. Furthermore, fused in sarcoma (FUS) is found to be partially responsible for this establishment of low efficiency. In mouse model, FUS inhibit mammary epithelial cell differentiation through the cyclin-dependent kinase inhibitor p57Kip2, leading to lactation failure and pup starvation. Clinically, FUS levels are negatively correlated with milk production in lactating women. Overall, our results shed light on FUS as a negative regulator of milk production, providing a potential mechanism for the establishment of milk production from marsupial to eutherian mammals. Efficient milk production in mammals confers advantages by facilitating the transmission of energy from mother to offspring. However, the factors for establishing the efficiency in mammals are unknown. Here, the authors identify FUS as a regulator of efficient milk production in mammals.

Objective:To investigate the effect of two “half pocket” suture embedding method in strengthening duodenal stump during radical gastrectomy of gastric cancer.Methods:The clinical data of 194 patients with gastric cancer who underwent radical gastrectomy from December 2018 to March 2021 were retrospectively analyzed. According to different methods of strengthening duodenal stump during the operation，two “half-bag” suture embedding method were used in the observation group（110 cases），and sarcomuscular suture embedding method was used in the control group（84 cases）. SPSS 25.0 software was used for statistical analysis，and the perioperative indicators（xˉ±s）of the two groups were compared by independent sample t test，and postoperative complications（%）were compared by χ2 test. P < 0.05 was considered to be statistically significant.Results:None of the patients died. The incidence of duodenal stump leakage in the observation group was significantly lower than that in the control group（0% vs. 3.6%， P = 0.046）. The ratio of duodenal stump length ≤0.5 cm in observation group was significantly higher than that in control group（27.3% vs. 13.1%，P = 0.016）. Duodenal embedding time in the observation group was significantly shorter than that in the control group［（2.5 ± 0.8）vs.（4.7 ± 0.9）min，P < 0.001］.Conclusion:The occurrence of duodenal stump leakage can be significantly reduced by using two “half pocket” suture embedding method to strengthen duodenal stump during radical gastrectomy. The embedding time of the method is short，the operation is simple，and the embedding difficulty caused by the short duodenal stump can be solved. Therefore，this method is worth popularizing and applying in gastric cancer surgery.

Background: Hepatocellular carcinoma (HCC), one of the world's most prevalent malignancies, accounts for 90% of primary liver cancer cases. Recent studies have shown an increased expression of denticles E3 ubiquitin protein ligase homolog (DTL) in several different tumor types, but its function and regulatory mechanisms remain unclear. Aims: This study aimed to investigate the expressions of the Cullin4 (CUL4) complex in HCC and elucidate the roles of DTL in HCC cells. Methods: The relative expression of the CUL4 complex and its clinical significance were analyzed with The Cancer Genome Atlas (TCGA) data, and the level of DTL was confirmed by immunohistochemistry. The functions of DTL1 and upstream E2F1 were evaluated by a Western blot, MTT, transwell, and xenograft in HCC cell lines. Results: The elevated mRNA expression of the CUL4 complex, including CUL4B, DDB1 (Damage Specific DNA Binding Protein 1), and DTL, was associated with the overall survival of HCC patients. We also found that the DTL protein was elevated in HCC tissues, and patients with highly expressed DTL and nucleus-located DTL had a poorer survival time. DTL knockdown significantly inhibited cancer proliferation, migration, and invasion. Further experiments showed that E2F1 was an upstream regulatory molecule of DTL, which was bound to the promoter of DTL, promoting the expression of DTL. Conclusion: The study results demonstrate that E2F1-DTL signaling promotes the growth, migration, and invasion of HCC cells, which provides new insights and a potential biological target for future HCC therapies

目的 研究结直肠癌(CRC)组织中肿瘤相关巨噬细胞(TAMs)标志物CD68和肿瘤干细胞(CSCs)标志物CD166表达变化,探讨其与CRC患者临床病理特征及预后的关系.方法 选取2014年1月至2019年10月CRC患者148例,取术中切除癌组织和配对的癌旁正常组织(距癌组织边缘>5 cm),应用免疫组化SABC法检测CD68+TAMs与CD166+CSCs的表达.比较癌组织与癌旁正常组织CD68+TAMs、CD166+CSCs阳性表达率;比较不同临床病理特征CRC患者癌组织CD68+TAMs、CD166+CSCs表达水平,Spearman相关法分析癌组织CD68+TAMs、CD166+CSCs表达的相关性;Kaplan-Meier法及Log-Rank检验比较CD68+TAMs与CD166+CSCs无高表达组、单一高表达组及均高表达组的5年生存率;多因素Cox回归分析CRC患者预后不良的影响因素.结果 CRC患者癌组织CD68+TAMs、CD166+CSCs阳性表达率均高于癌旁正常组织(P<0.05).CD68+TAMs、CD166+CSCs表达水平与肿瘤大小、淋巴结转移、TNM分期及分化程度密切相关,差异均有统计学意义(P<0.05),且二者的表达水平呈正相关(r=0.777,P<0.01).CD68+TAMs、CD166+CSCs无高表达组、单一高表达组、均高表达组的5年生存率依次降低,差异有统计学意义(P<0.05).肿瘤大小、淋巴结转移、TNM分期、CD68+TAMs和CD166+CSCs联合分组与患者的总生存期有关(P<0.05),且淋巴结转移、TNM分期、CD68+TAMs和CD166+CSCs联合分组为影响患者总生存期的独立因素(P<0.05).结论 CD68+TAMs与CD166+CSCs在CRC的发生发展中可能起协同促进作用,联合检测二者可进一步提高对CRC患者预后的评估价值,并指导临床进行更为精准的治疗.

目的 探讨缝隙连接蛋白43(Connexin43,Cx43)的表达与胃癌患者临床病理特征及预后的相关性.方法 通过免疫组化检测68例胃癌及癌旁胃正常组织(离肿瘤切缘>5 cm)中Cx43的表达,分析Cx43表达与临床病理特征的相关性.采用Kaplan-Meier构建总生存曲线及无病生存曲线,用Cox回归分析评价胃癌患者预后的独立影响因素.结果 胃癌组织中Cx43阳性表达率为51.47％,低于癌旁胃正常组织的95.58％(P<0.001).Cx43表达水平与肿瘤最大直径(P=0.004)、肿瘤浸润深度存在显著相关(P=0.012).此外,Cox回归分析表明,Cx43表达水平、肿瘤最大直径、肿瘤分化程度及浸润深度是胃癌患者预后的独立影响因素.结论 Cx43表达水平与胃癌患者临床病理特征和预后有关,可作为胃癌患者潜在的预后指标.

Abstract Hepatocellular carcinoma (HCC) is one of the most common malignant tumors in the world and accounts for approximately 90% of primary liver cancer. Recently, denticleless E3 ubiquitin protein ligase homolog (DTL) exhibited increasing expression in several cancers, while its function and regulatory mechanism is still unclear. By bioinformatics analysis, this study demonstrated the elevated mRNA expression of DTL complex including DTL, CUL4B (Cullin 4B) and DDB1 (Damage Specific DNA Binding Protein 1) were associated with the overall survival of HCC patients. Subsequently data showed DTL protein was also elevated in HCC tissues, patients with high expression and nucleus location had poor prognosis. Knocking-down DTL significantly inhibited the cancer proliferation, migration and invasion. Further experiments revealed E2F1 (E2F Transcription Factor 1) is an upstream regulatory molecule of DTL, which could bind to DTL promoter and promoted DTL expression. E2F1-DTL signaling axis promoted the growth, migration and invasion of HCC cells. Totally, this study not only enriches the regulatory mechanism of E2F1 and DTL, but also provides a new theoretical basis and potential biological target for the treatment of liver cancer in the future.

目的 探讨Runt相关转录因子3(RUNX3)在结直肠癌组织中的表达,分析其与结直肠癌患者临床病理特征及预后的关系.方法 选择2017年2月至2020年6月郑州大学附属洛阳市中心医院胃肠外科收治的100例结直肠癌患者为研究对象,取患者术中留取的结直肠癌组织及距离癌组织边缘5 cm以上的癌旁组织标本,采用免疫组织化学染色法检测结直肠癌组织和癌旁组织中RU N X3蛋白的表达,蛋白免疫印迹法检测结直肠癌组织、癌旁组织及人正常结肠上皮细胞NCM460和结肠癌细胞系HCT-116、SW-480细胞中RUNX3蛋白相对表达量.采用Kaplan-Meier绘制生存率曲线,Log-rank检验和Cox回归分析癌症患者的预后影响因素.结果 结直肠癌组织中RUNX3蛋白高表达率为35.0％(35/100),癌旁组织中RUNX3蛋白高表达率为74.0％(74/100);结直肠癌组织中RUNX3蛋白高表达率显著低于癌旁组织(χ2=30.670,P<0.05).结直肠癌组织中RUNX3蛋白相对表达量显著低于癌旁组织(t=2.904,P<0.05);结肠癌细胞系HCT-116和SW-480细胞中RUNX3蛋白相对表达量均显著低于正常结肠上皮细胞NCM460(t=-14.738、-8.082,P<0.05);结肠癌细胞系HCT-116中RUNX3蛋白相对表达量与SW-480细胞比较差异无统计学意义(t=0.554,P>0.05).结直肠癌组织中RUNX3表达水平与患者淋巴结转移、远处转移及肿瘤TNM分期有关(P<0.05),与患者的性别、年龄、肿瘤直径、位置、大体分型、浸润深度及分化程度无关(P>0.05).Kaplan-Meier生存分析结果显示,结直肠癌组织中RUNX3低表达患者生存率为60.0％(39/65),高表达患者生存率为71.4％(25/35);高表达患者生存率显著高于低表达患者(χ2=4.413,P<0.05).单因素Cox回归分析结果显示,肿瘤浸润深度、有无淋巴结转移、有无远处转移、肿瘤TNM分期及RUNX3表达水平与患者生存有关(P<0.05);多因素Cox回归分析结果显示,有无远处转移、肿瘤TNM分期及RUNX3表达水平是影响患者生存的独立危险因素(P<0.05).结论 RUNX3在结直肠癌组织中呈低表达,其与结直肠癌发生、发展及不良预后有关,可作为判定患者预后的潜在指标.

Background:Studies have confirmed that Caudal Type Homeobox 2 (CDX2) plays a tumor suppressor role in colorectal cancer (CRC) and as a prognostic and predictive marker for colorectal cancer. The epithelial to mesenchymal transition (EMT) is a transdifferentiation process, providing migratory and invasive properties to cancer cells during tumor progression. However, the role of CDX2 during the activation of EMT in CRC maintains controversial.Aim:To investigate whether CDX2 is associated with EMT in CRC.Methods:Forty-six CRC patients were included in the study. Expressions of CDX2, E-cadherin, and N-cadherin in all CRC patients were detected by IHC. ROC assays were applied to detect cut-off points for IHC scores to distinguish high and low expressions of CDX2 in 46 CRC samples. The prognostic value of CDX2 was statistically analyzed. MTT, Western blot, invasion, and migration assays in vitro were employed to explore the function of CDX2.Results:We observed that high expressions of CDX2 and E-cadherin as well as low expressions of N-cadherin were significantly correlated with favorable prognosis. The levels of CDX2 protein exhibited a positive associated with E-cadherin while negative correlation with N-cadherin. Then, the low expression of CDX2 and high expression of CA199 in combination are positively related with poor prognosis. Overexpression of CDX2 reduced expression of MMP-2 and diminished cell proliferation, invasion, and migration, while knockdown CDX2 enhanced MMP-2 expression and increased cell proliferation, invasion, and migration in HCT-116 cells. CDX2 was correlated with expression of EMT markers. Overexpression of CDX2 suppressed the EMT markers indicating that CDX2 suppresses CRC cell viability, invasion, and metastasis through inhibiting EMT. Finally, we found that the expression of CDX2 was negatively associated with Th1 cells, macrophages, Th2 cells, cytotoxic cells, T cells, and T helper cells.Conclusions:These results indicated CDX2 as prognostic biomarkers involved in immunotherapy response for CRC. CDX2 loss promotes metastasis in CRC through a CDX2-dependent mechanism.

Monoclonal antibodies (MABs) to a new drug Dalargin (Tyr-D-Ala-Gly-Phe-Leu-Arg) enhancing ulcer healing have been produced. Dalargin is a synthetic analog of Leu-enkephalin. With about 40 compounds tested in competition radioimmunoassay it has been shown that specificity of the MABs is directed against the N-terminal tetrapeptide of the molecule. The MABs are sensitive to amino acid substitutions in any of the positions of the fragment and have no cross-reactivity with endogenous opioids. Their further application in pharmacokinetic studies in humans and for characterization of opioid receptors is discussed.

目的 分析紧密连接蛋白6(CLDN6)在人胰腺癌组织中的表达及其与胰腺癌患者临床病理特征的关系,探究其对人胰腺癌细胞增殖及相关上皮细胞-间充质转化(EMT)蛋白表达的影响.方法 选取2014年1月至2018年6月在郑州大学附属洛阳中心医院行手术切除的50例胰腺癌组织及癌旁组织,免疫组织化学法及qRT-PCR法检测50例胰腺癌组织及对应癌旁组织中CLDN6的表达情况,分析其与患者临床病理特征及预后的相关性;qRT-PCR法检测胰腺癌细胞株(AsPC-1、BxPC-3、Capan-1、PANC-1、HPAC、Hs 766T、MIA Paca-2)及正常胰腺导管上皮细胞株HPDE中CLDN6的表达.胰腺癌细胞株脂质体转染CLDN6 siRNA沉默基因,qRT-PCR检测转染情况;MTT法、平板克隆实验检测各胰腺癌细胞增殖及克隆形成能力;Western blotting检测上皮型钙黏蛋白(E-cadherin)、神经型钙黏蛋白(N-cad-herin)、波形纤维蛋白(VIM)及纤维连接蛋白(FN)的表达水平.结果 胰腺癌组织中CLDN6表达水平为(19.44±1.22),明显高于癌旁组织的(1.35±0.71),差异有统计学意义(P=0.001),其表达水平与患者年龄、性别、肿瘤大小、病理学类型、肿瘤部位及CA19-9水平无关(P>0.05),而与TNM分期、肿瘤分化程度及淋巴结转移有关(P<0.05).CLDN6阳性表达胰腺癌患者的中位生存期为8.993个月,短于阴性表达者的18.402个月,差异有统计学意义(P<0.05).各胰腺癌细胞株中CLDN6表达量均高于HPDE细胞株(均P<0.05),成功构建沉默CLDN6的胰腺癌细胞AsPC-1-si-CLDN6、BxPC-3-si-CLDN6,转染CLDN6 siRNA沉默质粒的AsPC-1及BxPC-3细胞的增殖能力及克隆形成能力较转染前明显降低,E-cadherin表达明显增高,而N-cadherin、VIM及FN表达明显降低(均P<0.05).结论 CLDN6在胰腺癌中高表达,且与患者临床特征及预后相关,其可促进人胰腺癌细胞增殖及克隆形成,机制可能与其促进上皮细胞-间充质转化有关.

目的 探讨含自水解酶域蛋白5(ABHD5)过表达对结肠癌HCT116细胞侵袭、迁移以及单磷酸腺苷活化蛋白激酶(AMPK)/雷帕霉素靶体蛋白(mTOR)通路的影响.方法 应用UALCAN数据库资料分析ABHD5 mRNA在结肠癌组织中的表达及其与结肠癌患者临床病理特征之间的关系.体外培养结肠癌HCT116细胞,转染ABHD5重组质粒并分为对照组、阴性转染组和ABHD5转染组,采用实时荧光定量PCR(qRT-PCR)方法检测各组HCT116细胞中ABHD5 mRNA的表达;CCK-8法检测各组HCT116细胞增殖情况;Transwell法检测细胞侵袭和迁移能力;蛋白免疫印迹法检测侵袭蛋白基质金属蛋白酶9(MMP-9)、E-钙黏附蛋白(E-cadherin)、Snail、AMPK/mTOR 通路蛋白 p-AMPK、AMPK、p-mTOR 和 mTOR 的表达情况.结果 UALCAN数据库资料分析结果表明,与正常结肠组织比较,ABHD5 mRNA在结肠癌组织中的相对表达量降低,且其在腺癌和N1分期中分别低于黏液腺癌(P＜0.05)及N0分期(P＜0.05).与对照组和阴性转染组比较,ABHD5转染组的ABHD5mRNA表达升高(P＜0.05),HCT116细胞增殖抑制率升高(P＜0.05),HCT116细胞迁移和侵袭细胞数目减少(P＜0.05),蛋白 MMP-9、Snail、p-mTOR 和 mTOR 表达降低,蛋白 E-cadherin、p-AMPK 和 AMPK 表达升高(P＜0.05).结论 ABHD5过表达能够抑制结肠癌细胞HCT116的侵袭和迁移,且激活AMPK,抑制mTOR的表达,ABHD5可能通过影响AMPK/mTOR通路在抑制结肠癌的过程中发挥作用.

目的 分析Hsa-miR-29c在胃癌组织中的表达及其作用机制,并探讨其与胃癌患者临床病理学特征及预后间的关系.方法 通过慢病毒转染法建立过表达Hsa-miR-29c的MKN28细胞及MKN45细胞(转染组),并设立空载慢病毒对照组(阴性对照组),采用实时荧光聚合酶链式反应(qRT-PCR)法检测转染后2组细胞内Hsa-miR-29c的表达情况,采用CCK-8法及平板克隆实验检测2组细胞的增殖及克隆形成能力,采用蛋白印迹法(Western blot)检测2组细胞中细胞外基质蛋白1(extracellular matrix protein 1,ECM1)、Ⅰ 型胶原(Col Ⅰ)、平滑肌肌动蛋白(α-SMA)、基质金属蛋白酶2(MMP-2)和金属蛋白酶组织抑制物1(TIMP-1)的表达.采用qRT-PCR法及免疫组织化学法检测70胃癌组织及其癌旁组织中Hsa-miR-29c的表达,并分析其与胃癌临床病理学特征及预后间的关系.结果 本研究成功构建稳定表达Hsa-miR-29c的胃癌细胞株,转染后MKN28细胞及MKN45细胞内Hsa-miR-29c的表达水平均高于同种细胞的阴性对照组(P＜0.05),且细胞增殖及克隆形成能力低于同种细胞的阴性对照组(P＜0.05).与同类型细胞的阴性对照组比较,转染后MKN28细胞及MKN45细胞内Col Ⅰ和TIMP-1的表达水平升高(P＜0.05),而ECM1、α-SMA和MMP-2的表达水平降低(P＜0.05).胃癌组织中Hsa-miR-29c的表达水平低于癌旁组织(P＜0.05),其表达阳性率与患者年龄、性别及病理学类型均无关(P＞0.05),而与肿瘤直径、TNM分期、分化程度及淋巴结转移有关(P＜0.05).Hsa-miR-29c阴性表达胃癌患者的中位生存期较阳性表达者明显缩短(P=0.029).结论 Hsa-miR-29c在胃癌组织中的表达下调,且与患者的临床病理学特征及预后相关.过表达Hsa-miR-29c可抑制胃癌细胞增殖,其机制可能与抑制细胞外基质(ECM)信号通路有关.

Correction for 'Biological behavior exploration of a paclitaxel-eluting poly-l-lactide-coated Mg-Zn-Y-Nd alloy intestinal stent in vivo' by Zhanhui Wang et al., RSC Adv., 2020, 10, 15079-15090. DOI: ; 10.1039/c9ra10156j

As a new type of intestinal stent, the MAO/PLLA/paclitaxel/Mg-Zn-Y-Nd alloy stent has shown good degradability, although its biocompatibility in vitro and in vivo has not been investigated in detail. In this study, its in vivo biocompatibility was evaluated by animal study. New Zealand white rabbits were implanted with degradable intestinal Mg-Zn-Y-Nd alloy stents that were exposed to different treatments. Stent degradation behavior was observed both macroscopically and using a scanning electron microscope (SEM). Energy dispersion spectrum (EDS) and histological observations were performed to investigate stent biological safety. Macroscopic analysis showed that the MAO/PLLA/paclitaxel/Mg-Zn-Y-Nd stents could not be located 12 days after implantation. SEM observations showed that corrosion degree of the MAO/PLLA/paclitaxel/Mg-Zn-Y-Nd stents implanted in rabbits was significantly lower than that in the PLLA/Mg-Zn-Y-Nd stent group. Both histopathological testing and serological analysis of in vivo biocompatibility demonstrated that the MAO/PLLA/paclitaxel/Mg-Zn-Y-Nd alloy stents could significantly inhibit intestinal tissue proliferation compared to the PLLA/Mg-Zn-Y-Nd alloy stents, thus providing the basis for designing excellent biodegradable drug stents.