The crosstalk between cancer-associated fibroblasts (CAFs) and tumor cells presents a formidable barrier to treating digestive malignancies, yet the molecular syntax governing this interaction is often overlooked. Recent studies have highlighted the indispensable function of non-coding RNAs (ncRNAs), which act not merely as bystanders but as architects of stromal remodeling. Here, we dissect how ncRNAs dictate the heterogeneity and function of CAFs, regulating fibroblast activation, metastatic niche formation, drug resistance, and metabolic reprogramming. We further examine how the exosomal transfer of ncRNAs reshapes the immune landscape, engineering a tumor-permissive microenvironment. Current clinical observations indicate, however, that indiscriminate depletion of CAFs is often counterproductive, underscoring the necessity of "stromal normalization." Targeting specific ncRNA master regulators to reprogram activated CAFs to a quiescent state-rather than destroying them-provides robust mechanistic support for the stromal normalization paradigm previously proposed.

Cachexia is associated with adverse clinical outcomes in patients with gastric cancer (GC); therefore, a convenient and reliable method for monitoring cachexia is essential. This study aimed to evaluate the utility of the cachexia index (CXI) as a biomarker for estimating cancer cachexia and health-related quality of life (HRQoL) in GC patients. The CXI was calculated as the skeletal muscle index (SMI) × serum albumin / neutrophil–lymphocyte ratio (NLR). Diagnosis of cachexia was based on Asian Working Group for Cachexia (AWGC) criteria and Fearon’s criteria. Univariate and multivariate logistic regression analyses were carried out to identify potential risk factors related to cancer cachexia and HRQoL respectively. Receiver Operating Characteristics (ROC) analysis was conducted to evaluate the diagnostic value in identifying cancer cachexia, and the area under the ROC curve (AUC) was calculated. This study comprised a total of 431 patients diagnosed with GC, including 309 males (71.7

Background: Low muscle mass was significantly correlated with poor clinical outcomes in cancer patients. This study aimed to compare the differences between bioelectrical impedance analysis (BIA) and computed tomography (CT) in measuring skeletal muscle mass and detecting low muscle mass in patients with gastric cancer (GC). Method: This cross-sectional study included a total of 302 consecutive patients diagnosed with GC at our institution from October 2021 to March 2023. CT images were analyzed at the L3 level to obtain the crosssectional area of skeletal muscle, which was subsequently used for calculating whole-body skeletal muscle mass via the Shen equation and skeletal muscle tissue density. BIA was utilized to measure skeletal muscle mass using the manufacturer's proprietary algorithms. Skeletal muscle mass (kg) was divided by height squared (m(2)) to obtain skeletal muscle index (SMI, kg/m(2)). Pearson's correlation coefficient was performed to assess the correlation between SMI measured by BIA and CT. The agreement between the two methods was assessed using Bland -Altman analyses. The clinically acceptable agreement was defined as the 95% limits of agreement (LOA) for the percentage bias falling within +/- 10%. The area under the receiver operating characteristic curve (AUC) was used to evaluate the performance of BIA in identifying low muscle mass. Results: A total of 59 patients (19.5%) were identified as having low muscle mass based on CT analysis, whereas only 19 patients (6.3%) met the criteria for low muscle mass according to BIA analysis. BIA-measured SMI showed a strong positive correlation with CT-measured SMI in all patients (r = 0.715, P < 0.001). With Bland -Altman analysis, there was a significant mean bias of 1.18 +/- 0.96 kg/m(2) (95% CI 1.07-1.29, P < 0.001) between SMI measured by BIA and CT. The 95% LOA for the percentage bias ranged from -7.98 to 33.92%, which exceeded the clinically acceptable range of +/- 10%. A significant difference was observed in the mean bias of SMI measured by BIA and CT between patients with and without GLIM malnutrition (1.42 +/- 0.91 kg/m(2) versus 0.98 +/- 0.96 kg/m(2), P < 0.001). The cut -off values for BIA-measured SMI in identifying low muscle mass using CT as the reference were 10.11 kg/m(2) for males and 8.71 kg/m(2) for females (male: AUC = 0.840, 95% CI: 0.772-0.908; female: AUC = 0.721, 95% CI: 0.598-0.843 ). Conclusions: Despite a significant correlation, the values of skeletal muscle mass obtained BIA and CT cannot be used interchangeably. The BIA method may overestimate skeletal muscle mass in GC patients compared to CT, especially among those with GLIM malnutrition, leading to an underestimation of low muscle mass prevalence. (c) 2024 Elsevier Inc. All rights reserved.

This study aimed to compare three objective nutritional screening tools for identifying GLIM-defined malnutrition in patients with gastric cancer (GC). Objective nutritional screening tools including geriatric nutritional risk index (GNRI), prognostic nutritional index (PNI), and controlling nutritional status (CONUT) score, were evaluated in patients with GC at our institution. Malnutrition was diagnosed according to the GLIM criteria. The diagnostic value of GNRI, PNI, and COUNT scores in identifying GLIM-defined malnutrition was assessed by conducting Receiver Operating Characteristic (ROC) curves and calculating the area under the curve (AUC). Additionally, sensitivity, specificity, accuracy, positive predictive value (PPV), and negative predictive value (NPV) were determined. The Kappa coefficient (k) was used to assess agreement between three objective nutritional screening tools and GLIM criteria. A total of 316 patients were enrolled in this study, and malnutrition was diagnosed in 151 (47.8

Background: Patients with gastric cancer (GC) are more likely to experience malnutrition and muscle wasting. This study aims to investigate the potential of phase angle (PhA) as a screening tool for identifying malnutrition and sarcopenia in GC patients, as well as its association with short-term outcomes after radical gastrectomy. Methods: This cross-sectional study enrolled patients diagnosed with GC at The Affiliated People's Hospital of Jiangsu University from October 2021 to September 2022. PhA was measured using bioelectrical impedance analysis. Computed tomography scan images were analyzed for body composition at the level of the third lumbar vertebra. Malnutrition was diagnosed using Global Leadership Initiative on Malnutrition (GLIM) criteria. Sarcopenia diagnosis was based on the Asian Working Group for Sarcopenia (AWGS) 2019 criteria. Results: A total of 248 patients with GC were analyzed, including 188 patients who underwent radical gastrectomy. Of these, 71.4 % (n = 177) were male and 28.6 % (n = 71) were female and the median overall age was 68 years (IQR: 61-72 years). According to GLIM criteria, 49.2 % (n = 122) of patients were malnourished and 19.8 % (n = 49) had sarcopenia based on AWGS criteria. A one-degree decrease in PhA was significantly associated with GLIM malnutrition (Odds Ratio [OR] = 8.108, 95 % CI:3.181-20.665) and sarcopenia (OR = 2.903, 95 % CI:1.170-7.206). PhA exhibited fair to good diagnostic accuracy in identifying GLIM malnutrition (male: AUC = 0.797; female: AUC = 0.816) and sarcopenia (male: AUC = 0.814; female: AUC = 0.710). Low PhA (OR = 3.632, 95 % CI: 1.686-7.824) and operation time (OR = 2.434, 95 % CI:1.120-5.293) were independently associated with the risk of postoperative complications. Conclusions: PhA can serve as a reliable screening tool for identifying patients at risk of malnutrition, sarcopenia, and postoperative complications in GC. (c) 2023 European Society for Clinical Nutrition and Metabolism. Published by Elsevier Ltd. All rights reserved.

Background: STAD ranked 5th most common in the incidence of malignant tumors and 3rd most common in the death rate of cancer worldwide. CXC chemokines affect the biological progress of various tumors, resulting in therapeutic failure. The role of CXCL2 in STAD was still a mystery. Methods: The expression, prognostic value, and clinical function of CXCL2 were analyzed using several online bioinformatics tools and clinical tissues. Results: CXCL2 level was significantly upregulated in STAD tissues. Strong correlation was obtained between CXCL2 level and immune cells as well as immune biomarkers. High CXCL2 expression in STAD was correlated with a favorable prognosis. Further analysis revealed that CXCL2, pTNM stage and age were independent factors affecting the prognosis of STAD patients. A predictive nomogram indicated that the calibration plots for the 1-year, 3-year and 5-year OS rates were predicted relatively well compared with an ideal model in the entire cohort. Validation analysis revealed that CXCL2 expression was upregulated in STAD and high CXCL2 level had a better overall survival. CXCL2 was associated with resistance to numerous drugs or small molecules in STAD. Conclusions: We identified CXCL2 as a novel therapeutic target and associated with immune infiltration in STAD.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (https://www.elsevier.com/about/our-business/policies/article-withdrawal). This article has been retracted at the request of the Editor-in-Chief and authors. Following the publication of the above article, the Editor was notified by a concerned reader that the authors supplied duplicated images. Specifically, that in Fig. 5 A, both FACS panels are identical and in Fig 5E, two different proteins (HK2 and PDK1) have the same western blot. After checking the data in relation with Fig. 5A and E, the authors have confirmed that the two pictures indeed have the problems of duplication. The authors reported that this problem came from the authors' unintentional behavior, which may be due to a copy and paste error in the manner of image processing. The authors sincerely apologize for the inconvenience caused to our Editors and readers. Due to this duplication error, the authors and Editor have made the decision to retract this paper.

目的:研究长链非编码RNA(long non-coding RNA,lncRNA)SPATA3-AS1在胃癌患者癌组织和血浆中的表达及临床意义,并进一步探讨其对胃癌细胞株的影响及其潜在机制.方法:采用实时荧光定量PCR(qRT-PCR)检测80例胃癌及癌旁组织、29例胃癌患者和29例健康者血浆中SPATA3-AS1的表达水平;对胃癌患者SPATA3-AS1表达与其临床病理特征行统计学分析.敲减SPATA3-AS1,分别转染胃癌AGS、HGC-27细胞,采用细胞增殖、克隆形成、Transwell实验及流式细胞术分别检测细胞增殖、迁移、侵袭和凋亡;采用qRT-PCR检测肿瘤相关基因mRNA的表达水平.结果:SPATA3-AS1在胃癌组织中呈高表达,其表达与淋巴结转移、肿瘤TNM分期、肿瘤浸润深度及肿瘤预后相关;胃癌患者血浆中SPATA3-AS1也呈高表达,其表达与淋巴结转移、肿瘤直径、肿瘤TNM分期呈正相关.血浆中SPATA3-AS1表达水平诊断胃癌ROC曲线下面积为0.788.敲减SPATA3-AS1后,胃癌AGS、HGC-27细胞增殖及移动活力减弱,细胞凋亡能力增强.同时N-钙黏蛋白、Twist1、Snail mRNA表达下调而E-钙黏蛋白mRNA表达上调.结论:SPATA3-AS1在胃癌患者癌组织及血浆中呈高表达并与其预后相关;敲减SPATA3-AS1后胃癌细胞增殖、迁移及侵袭等能力均受到抑制,细胞凋亡增强,可能与对上皮间质转化过程的调控有关.

目的 探讨LncRNA NPSR1-AS1在胃癌(gastric cancer,GC)中的表达及临床意义,分析其对胃癌细胞生物学行为的影响和作用机制.方法 收集86例胃癌患者癌组织及癌旁组织,另收集21例胃癌患者及体检健康者血浆标本,采用实时荧光定量PCR(RT-qPCR)检测各组LncRNA NPSR1-AS1的表达水平,并与患者临床病理资料进行相关性分析.siRNA敲减NPSR1-AS1后,采用细胞增殖试验、Transwell试验、流式细胞术检测癌细胞增殖、迁移、侵袭、凋亡能力,并用RT-qPCR检测肿瘤相关基因表达量的变化.结果 LncRNA NPSR1-AS1在胃癌组织中的表达水平显著升高,且与肿瘤大小(t=11.02,P<0.01)、淋巴结转移(t=2.30,P<0.05)、TNM分期(t=3.55,P<0.01)、肿瘤血管或神经侵袭(t=3.10,P<0.05)显著相关;血浆LncRNA NPSR1-AS1筛查胃癌的ROC曲线下面积(AUCROC)为0.696.LncRNA NPSR1-AS1敲减后可使GSK-3β(t=16.15,P<0.01)和E-cadherin(t=10.17,P<0.01)表达上调,β-catenin(t=4.869,P<0.05)、N-cadherin(t=3.77,P<0.05)、Snail(t=9.372,P<0.01)和MMP2(t=15.57,P<0.01)表达下调.结论 LncRNA NPSR1-AS1敲减可抑制胃癌细胞增殖、迁移及侵袭并诱导其凋亡,其作用机制与上皮-间质转化(EMT)有关.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy). This article has been retracted at the request of the Editor-in-Chief and authors. Following the publication of the above article, the Editor was notified by a concerned reader that the authors supplied duplicated images. Specifically, that in Fig. 5A, both FACS panels are identical and in Fig. 5E, two different proteins (HK2 and PDK1) have the same western blot. After checking the data in relation with Fig. 5A and Fig. 5E, the authors have confirmed that the two pictures indeed have the problems of duplication. The authors reported that this problem came from the authors’ unintentional behavior, which may be due to a copy and paste error in the manner of image processing. The authors sincerely apologize for the inconvenience caused to our Editors and readers. Due to this duplication error, the authors and Editor have made the decision to retract this paper.

目的 探讨手辅助腹腔镜直肠癌根治术在直肠癌外科治疗中的临床应用价值.方法 分析52例施行手辅助腹腔镜直肠癌根治术(手辅助组)和49例施行腹腔镜直肠癌根治术(腹腔镜组)患者的临床资料,比较两组患者的切口长度、手术时间、术中出血量、淋巴结清扫数目、术后腹腔引流量、术后排气时间和术后住院时间的差异.结果 手辅助组和腹腔镜组均顺利完成手术.两组的病理检出淋巴结清扫数目、术后腹腔引流量、术后排气时间和术后住院时间比较,差异无统计学意义(P＞0.05).虽然手辅助组的手术切口长度长于腹腔镜组、术中出血量多于腹腔镜组,但手辅助组的手术时间明显少于腹腔镜组(P＜0.05).结论 手辅助腹腔镜直肠癌根治术疗效与腹腔镜直肠癌根治术相当,但操作难度降低,手术时间更短.

Objective To investigate the expression of triggering receptor-1 on myeloid cells (TREM-1) and inflammatory cytokines in acute lung injury (ALI) incurred by severe acute pancreatitis (SAP).Methods Twenty-four male SD rats were randomly (random number) divided into sham operation (SO) group,SAP group and SAP + LP17 (synthesized TREM-1) group (n =8 in each group),and SAP model was established by retrograde injection of sodium taurocholate into the bile-pancreatic duct.Twelve hours after modeling,all rats of three groups were sacrificed,and the pancreas and lung of rats were harvested.The histopathological changes of pancreas and lung tissue stained with hematoxylin-eosin staining (HE staining) were observed under light microscope.The lung tissue was marked with macrophage-specific antibody CD68 to detect macrophage infiltration by using immunohistochemistry.The expressions of TREM-1 mRNA、interleukin-1β (IL-1β) mRNA and tumor necrosis factor-α (TNF-α) mRNA in lung tissue were detected by fluorescence quantitative polymerase chain reaction (QRT-PCR method).The data were expressed as ((-x) ± s) and SPSS 17.0 software was used to make one-way ANOVA,and P ＜ 0.05 was considered to indicate significant difference.Results Compared with SO group and SAP + LP17 group,the injuries of pancreas and lung tissue in SAP group were significantly more severe (P ＜ 0.05).In SAP group,macrophage infiltration in lung tissue was more evident than that in SO group.Accordantly,the expression of TREM-1 mRNA,IL-1β mRNA and TNF-α mRNA of lung tissue in SAP group were significantly higher than those in SO group and SAP + LP17 group (P ＜ 0.01 or P ＜ 0.05).Conclusions The expression of TREM-1 in the lung injury caused by SAP was significantly higher.It might be an important inflammatory mediator in the mechanism of lung injury caused by SAP.LP17 effectively lowered the expression of TREM-1 and decreased the release of inflammatory cytokines,lessening the lung injury.

Objective To detect the effect of Toll-like receptor 9(TLR9)agonist CPGoligonucleotide 1826(CPG-ODN1826)on the proliferation of pancreatic cancer PANC-1cells in vitro.Methods The PANC-1cells were divided into group A(intervened with CPG-ODN1826)and B(treated with culture medium as the control).The proliferation of PANC-1cells was analyzed by MTT assay,crystal violet test and soft agar colony formation test,respectively.The expressions of phosphorylated extracellular signal-regulated kinase(p-ERK)and phosphorylated c-Jun N-terminal kinase(p-JNK)were detected by Western blot.Results Compared with group B,the proliferation of PANC-1cells was promoted(P<0.05),the number of cell clone was increased(35.60±2.70vs.50.40±4.04)(P<0.05)and the expressions of p-ERK and p-JNK were enhanced(0.455±0.057vs.0.665±0.121and 0.301±0.028vs.0.656±0.051)in group A(P<0.05).Conclusion TLR9agonist CPG-ODN1826can promote the proliferation of pancreatic cancer cells.

目的 探讨胰腺星状细胞(PSCs)对胰腺癌细胞PANC-1迁移能力的影响.方法 从小鼠胰腺组织中分离PSCs后分为A组(共培养PSCs及PAN&1细胞)和B组(PANC-1细胞),均以Transwell小室培养24 h.细胞划痕及细胞迁移实验分别检测两组PANC-1细胞的迁徙距离和跨膜细胞数目,免疫荧光技术及Western blot测定两组PANC-1细胞中基质金属蛋白酶(MMP)2和MMP-9的表达.结果 培养24 h后,A组细胞迁移距离远于B组[(18.75±1.70) mm vs.(12.40±1.14) mm](P＜0.05),跨膜细胞数目多于B组[(137±24)个vs.(68±11)个](P＜0.05),MMP-2和MMP-9蛋白表达量均高于B组(0.84±0.08 vs.0.41±0.13和0.56±0.72 vs.0.31±0.12)(P＜0.05).结论 PSCs能够增强PANG1细胞迁移能力,促进PANC-1细胞中MMP2、MMP-9的表达.

近年来研究发现,胰腺纤维化及胰腺癌耐药与胰腺星状细胞(PSCs)有关,具体机制尚不清楚[1-3].有文献报道,肝星状细胞表达TLR-9,并通过TLR-9介导肝纤维化[4].

Objective:To establish a new method to isolate and culture mouse primary pancreatic stellate cells(PSCs).Methods:Based on techniques of isolating and culturing rat PSCs,we acquired purified PSCs from pancreatic tissue fragments via isolation,culture and passage.Oil red O staining,immunofluorescence as well as western blotting were performed to identify pancreatic stellate cells.Cell growth and vitality were validated by cell counting and trypan blue staining.Results:Primary PSCs were positive for oil red O staining;cells grew rapidly and began being activated from the third day.After passage,most of cells were activated.Immunofluorescence staining showed that α-smooth muscle actin(α-SMA) was positive expressed in activated PSCs.Western blotting showed that α-SMA and desmin were expressed in activated PSCs,and that the expression of desmin in fully activated PSCs was obviously higher(P0.05).Conclusion:This method can be successfully used to isolate mouse PSCs.The yield,purity and activity of PSCs were higher,and this new method could thus meet the research of pancreatic stellate cells in vitro.