Breast cancer (BC) is the most prevalent malignant tumor among women worldwide and a significant cause of cancer-related deaths in females. Recent studies have shown that lipid metabolism-related genes (LMRGs) exhibit prognostic potential in various types of tumors, including BC. Our study aimed to establish a novel model to predict the metastasis of BC. Clinical information and corresponding RNA data of patients with BC were downloaded from The Cancer Genome Atlas and Gene Expression Omnibus databases. Consensus clustering was performed to identify novel molecular subgroups. Estimation of Stromal and Immune Cells in Malignant Tumor Tissues using Expression, microenvironment cell populations counter, microenvironment cell populations counter, and single-sample gene set enrichment analyses were employed to determine the tumor immune microenvironment and immune status of the identified subgroups. Functional analyses, including Gene Ontology and gene set enrichment analyses, were conducted to elucidate the underlying mechanisms. A prognostic risk model was constructed using the Least Absolute Shrinkage and Selection Operator algorithm and multivariate Cox regression analysis. This study identified differential gene expression between patients with BC exhibiting metastasis and those without metastasis using public databases. Using the obtained data, we established predictive models based on six LMRGs. Furthermore, consensus clustering and prognostic score grouping analysis revealed that differentially expressed LMRGs influence tumor prognosis by regulating tumor immunity. To facilitate clinical application, we developed a nomogram integrating the risk model and clinical characteristics to accurately predict the prognosis of patients with BC. We developed and validated a novel signature associated with LMRGs for predicting disease-free survival in patients with BC. The expression of LMRGs correlates with the immune microenvironment of patients with BC, providing new insights and improved strategies for the diagnosis and treatment of BC.

ObjectiveThis study aimed to investigate the feasibility of using indocyanine green (ICG) near-infrared (NIR) imaging during lymphadenectomy for oesophageal cancer.MethodsEighty-seven patients with primary oesophageal cancer were enrolled in this study. All the enrolled patients received an endoscopic injection of ICG between 40 min and 23 h before surgery. Nodal dissection during surgery was performed under fluorescence imaging visualisation, with the NIR signal shown in purple. ICG+ or ICG− nodes were recorded station by station and were microscopically evaluated.ResultsEndoscopic peritumoral ICG injection was successfully performed in all patients. Major post-surgery complications included wound infection, pleural effusion, dysphonia, pneumonia and anastomotic fistula. No patients experienced ICG-related adverse events. A total of 2,584 lymph nodes were removed, and the mean number of lymph nodes for each patient was 29.70 ± 9.24. Most of the removed nodes (97.83%) were ICG+, and 3.32% of the ICG+ nodes were metastatic. No metastatic nodes were ICG− or belonged to an ICG− lymph node station. The time from ICG injection to surgery did not affect the number of harvested lymph nodes.ConclusionsThe use of ICG-NIR imaging during oesophageal cancer surgery can enhance the visualisation of lymph nodes during surgery. It is a feasible, safe and helpful technique for lymphadenectomy.

Pain is one of the most severe complications affecting the quality of life of cancer patients. Although substantial progress has been made in the diagnosis and treatment of cancer, the neurobiological mechanism of cancer pain is still unclear. In the present study, we identified the critical role of CXC chemokine 2 (CXCL2), released by Schwann cells after being activated by cancer cells, in maintaining cancer-induced macrophage infiltration and the resulting mechanical hypersensitivity and persistent spontaneous nociception. In vitro, Schwann cells cocultured with breast cancer cells exhibited a significant increase in CXCL2 expression; in addition, conditioned medium from Schwann cells activated by breast cancer cells had a similar effect to recombinant CXCL2 in terms of inducing macrophage migration. Targeting CXCL2 signaling by both CXC chemokine receptor 2 (CXCR2) antagonist pharmacological blockade and anti-CXCL2 mAb immunological blockade robustly prevented conditioned medium-induced macrophage migration. In vivo, both application of recombinant CXCL2 and perineural breast cancer cell implantation resulted in mechanical hypersensitivity and persistent spontaneous nociception in mice, along with increased macrophage infiltration into the sciatic nerves. Similar to the in vitro results, inhibition of CXCL2/CXCR2 signaling or conditional knockdown of CXCL2 in sciatic nerve Schwann cells effectively attenuated breast cancer cell-induced mechanical hypersensitivity, persistent spontaneous nociception, and macrophage recruitment in the sciatic nerve. Mechanistically, we found that redox effector factor-1 (Ref-1) secreted by breast cancer cells activated hypoxia inducible factor-1α (HIF-1α) expression and inhibited reactive oxygen species (ROS) production in Schwann cells, ultimately inducing CXCL2 expression in Schwann cells. In brief, the present study expands new insights into cancer pain mechanisms from promising animal models to provide new strategies for the control of cancer pain.

Drug resistance in breast cancer (BC) is a clinical challenge. Exploring the mechanism and identifying a precise predictive biomarker for the drug resistance in BC is critical. Three first-line drug (paclitaxel, doxorubicin and tamoxifen) resistance datasets in BC from GEO were merged to obtain 1,461 differentially expressed genes for weighted correlation network analysis, resulting in identifying ATRX as the hub gene. ATRX is a chromatin remodelling protein, therefore, ATRX-associated transcription factors were explored, thereby identifying the network of AR, GLI3 and GATA2. GO and KEGG analyses revealed immunity, transcriptional regulation and endocrinotherapy/chemotherapy resistance were enriched. Moreover, CIBERSORT revealed immunity regulation was inhibited in the resistance group. ssGSEA showed a significantly lower immune status in the ATRX-Low group compared to the ATRX-High group. Furthermore, the peaks of H3K9me3 ChIP-seq on the four genes were higher in normal tissues than in BC tissues. Notably, the frequency of ATRX mutation was higher than BRCA in BC. Moreover, depressed ATRX revealed worse overall survival and disease-free survival in the human epidermal growth factor receptor 2 (HER2)-/hormone receptor (HR)+ BC. Additionally, depressed ATRX predicted poor results for patients who underwent endocrinotherapy or chemotherapy in the HER2-/HR+ BC subgroup. A nomogram based on ATRX, TILs and ER exhibited a significantly accurate survival prediction ability. Importantly, overexpression of ATRX significantly inhibited the IC50 of the three first-line drugs on MCF-7 cell. Thus, ATRX is an efficient predictive biomarker for endocrinotherapy and chemotherapy resistance in HER2-/HR+ BC and acts by suppressing the AR, GLI3 and GATA2 transcriptional network.

Objective: To investigate the carcinogenesis of sulfide-quinone oxidoreductase（SQRDL） in different tumors. Methods:（1）The potential carcinogenic effects of SQRDL in 33 kinds of tumors were analyzed from five aspects: gene expression, sur vival prognosis, genetic alteration, immuno-infiltration and SQRDL-related gene enrichment according to The Cancer Genome Atlas, gene expression omnibus and other databases.（2）The difference of SQRDL expression between breast cancer and normal tissues was verified by immunohistochemistry. Results: It was found that SQRDL was highly expressed in a variety of tumors including breast cancer and uterine corpus endometrial carcinoma. In some tumors represented by pancreatic adenocarcinoma,there was a significant correlation between the expression of SQRDL and the pathological stage of the tumor. The high expression of SQRDL was associated with poor prognosis, such as significantly shortening the overall survival of brain lower grade glioma. Notably, overall survival in mesothelioma and disease-free survival in rectum adenocarcinoma were associated with low expression of SQRDL. The study found that the mutation rate of SQRDL was the highest in skin cutaneous melanoma. In some tumors, such as colon adenocarcinoma and uterine corpus endometrial carcinoma, the S343 phosphorylation level of SQRDL is higher. The analysis showed that in lymphoid neoplasm diffuse large B-cell lymphoma, and testicular germ cell tumors and pheochromocytoma and paraganglioma, the SQRDL expression correlated with cancer-associated fibroblast infiltra-tion levels. In addition, SQRDL is mainly involved in cell apoptosis and biosynthesis. Finally, immunohistochemical validation of breast cancer was obtained. Conclusion: SQRDL may act as a tumor promoter in the majority of the tumours investigated and may be a potential marker of cancer prognosis.

目的 探讨甘油三酯(TG)与前白蛋白(PAB)比值(TPR)对乳腺癌(BC)预后的预测价值.方法 回顾性分析自2010 年1 月至2014 年12 月于南通市肿瘤医院行手术治疗的171 例非晚期BC患者的临床资料.根据随访期间生存情况将患者分为死亡组(n =81)与生存组(n =90).比较两组患者的临床病理特征.采用Cox回归分析探讨影响患者预后的危险因素.采用受试者工作特征(ROC)曲线确定TPR对患者预后的预测价值.利用Kaplan-Meier法对高PAB组与低PAB组、高TG组与低TG组、高TPR组与低TPR组进行生存分析.结果 生存组患者肿瘤直径>2cm比例、淋巴结转移阳性比例、雌激素受体阴性比例、孕激素受体阴性比例、人表皮生长因子受体-2 阳性比例、组织学分级Ⅲ级比例、临床病理分期Ⅲ期比例、TG、TPR低于死亡组,PAB高于死亡组,两组比较,差异有统计学意义(P<0.05).多因素Cox回归分析结果显示,肿瘤直径、淋巴结转移、雌激素受体、TPR是BC患者死亡的独立危险因素(P<0.05).TPR预测患者死亡的ROC曲线下面积为0.696,敏感度为0.739,特异度为0.636,截断值为0.03157.高PAB组患者总存活率、无进展存活率与低PAB组比较,差异有统计学意义(P<0.05).高TG组患者总存活率、无进展存活率与低TG组比较,差异有统计学意义(P<0.05).高TPR组患者总存活率、无进展存活率与低TPR组比较,差异有统计学意义(P<0.05).结论 高TPR是非晚期BC患者预后不良的预测因素,对BC患者的预后具有一定的预测价值.

目的:探讨CT扫描联合硫氧还蛋白还原酶(thioredoxin reducatse,TR)检测对孤立性肺结节(solitary pulmonary nodule,SPN)良恶性的诊断价值.方法:回顾性分析 89 例孤立性肺结节患者的临床资料,其中恶性结节 46例(恶性组),良性结节43 例(良性组).比较两组患者SPN CT征象及血清TR水平,比较CT扫描、TR检测、CT联合TR检测 3 种方法诊断SPN的敏感度、特异度、准确度、阳性预测值和阴性预测值.结果:恶性组毛刺征、分叶征、胸膜凹陷征、血管集束征阳性率高于良性组,结节最大长径大于良性组,血清TR水平高于良性组,差异均有统计学意义(P＜0.05).诊断SPN的敏感度、特异度、准确度CT检查分别为 78.3%、88.4%和 83.1%,血清TR水平分别为 37.0%、86.0%和 60.7%,联合检查分别为82.6%、86.0%和 84.3%.联合检查及单独CT诊断SPN敏感度、准确度高于TR检测,差异均有统计学意义(P＜0.05).结论:CT扫描及CT联合血清TR检测对SPN的诊断价值优于TR检测,TR检测可以有效辅助CT扫描对SPN的定性诊断.

Objective To explore the concentration and integrity of circulating free DNA（cfDNA） in plasma, and its diagnostic value for benign and malignant pulmonary nodules. Methods According to pathological diagnosis results, the patients were divided into benign pulmonary nodules group（60 cases） and malignant pulmonary nodule group（50 cases）, and another 30 healthy examiners in the same period were selected as control group. Plasma carcinoembryonic antigen（CEA） and cytokeratin fragment 19（Cyfra21-1） expression levels were detected by enzyme-related immunosorbent assay（ELISA）. The cfDNA level and cfDNA integrity were detected by quantitative real-time polymerase chain reaction（qRT-PCR）. Receiver operating characteristic（ROC） curve was drawn, and the diagnostic value of cfDNA, CEA and Cyfra21-1 in NSCLC was analyzed by ROC curve, and the diagnostic efficacy of each index and their combination was compared. Results Compared with the benign pulmonary nodule group [385.43（176.45, 704.55）, 0.37（0.26, 0.59） ng/mL, 2.67（1.36, 5.45） ng/mL, 2.74（1.43, 3.96） ng/mL], the plasma levels of cfDNA [1 154.83（452.85,1 642. 31） ng/m L],cf DNA integrity[0. 68（ 0. 47,0. 91） ng/m L],CEA[7. 93（ 3. 21,10. 31） ng/m L]and Cyfra21-1 [5. 75（ 2. 85,8. 12） ng/m L]in the malignant pulmonary nodule group were significantly increased（ P ＜ 0. 05）. Plasma cf DNA concentration and integrity showed no significant correlation with gender,age,smoking or not,tumor diameter,pathological type,TNM stage,degree of tumor differentiation and lymph node metastasis in lung cancer patients（ P ＞ 0. 05）. ROC curve showed that area under the curve,sensitivity and specificity of plasma cf DNA concentration and cf DNA integrity were higher or larger than those of CEA and Cyfra21-1,the sensitivity and specificity of plasma cf DNA concentration and cf DNA integrity combined with CEA and Cyfra21-1 in the diagnosis of NSCLC were higher than those of their single detection of plasma cf DNA concentration,cf DNA integrity,CEA,Cyfra21-1（ P ＜ 0. 05）. Conclusion Plasma cf DNA and its integrity have certain clinical value in the diagnosis of benign and malignant pulmonary nodules,and can be used as molecular biological indicators for the auxiliary diagnosis of benign and malignant pulmonary nodules.

Esophageal squamous cell carcinoma (ESCC) is a major histological subtype of esophageal cancer with a poor prognosis. Although several serum metabolomic investigations have been reported, ESCC tumor-associated metabolic alterations and predictive biomarkers in sera have not been defined. Here, we enrolled 34 treatment-naive patients with ESCC and collected their pre- and post-esophagectomy sera together with the sera from 34 healthy volunteers for a metabolomic survey. Our comprehensive analysis identified ESCC tumor-associated metabolic alterations as represented by a panel of 12 serum metabolites. Notably, postoperative abrosia and parenteral nutrition substantially perturbed the serum metabolome. Furthermore, we performed an examination using sera from carcinogen-induced mice at the dysplasia and ESCC stages and identified three ESCC tumor-associated metabolites conserved between mice and humans. Notably, among these metabolites, the level of pipecolic acid was observed to be progressively increased in mouse sera from dysplasia to cancerization, and it could be used to accurately discriminate between mice at the dysplasia stage and healthy control mice. Furthermore, this metabolite is essential for ESCC cells to restrain oxidative stress-induced DNA damage and cell proliferation arrest. Together, this study revealed a panel of 12 ESCC tumor-associated serum metabolites with potential for monitoring therapeutic efficacy and disease relapse, presented evidence for refining parenteral nutrition composition, and highlighted serum pipecolic acid as an attractive biomarker for predicting ESCC tumorigenesis.

目的 探讨血清清蛋白/球蛋白比值(AGR)和外周血血小板/淋巴细胞比值(PLR)与食管鳞状细胞癌(ESCC)患者总体生存期(OS)的关系,评估AGR联合PLR对ESCC患者预后的预测价值.方法 选择2014年3月至2017年3月因食管癌于该院接受根治性手术治疗的125例ESCC患者为研究对象,并根据患者术前实验室检查结果计算AGR和PLR.通过受试者工作特征(ROC)曲线分析AGR和PLR预测ESCC患者OS的cut-off值.采用Kaplan-Meier曲线评估AGR与PLR对ESCC患者的预后价值.采用单变量、多变量Cox回归分析ESCC患者OS的独立预测指标.结果 ROC曲线分析显示,AGR与PLR预测患者OS的cut-off值分别为1.57和126.80,曲线下面积(AUC)分别为0.653(95％CI:0.556～0.750)和0.647(95％CI:0.548～0.747).生存分析表明,AGR≤1.57组OS(22.0个月,95％CI:14.2～29.8)短于AGR>1.57组(43.0个月,95％CI:36.1～49.9),差异有统计学意义(χ2=10.743,P=0.001).PLR>126.80组OS(23.0个月,95％CI:10.9～35.1)明显短于PLR≤126.80组(43.0个月,95％CI:36.2～49.8),差异有统计学意义(χ2=8.983,P=0.003).单变量、多变量Cox分析进一步证实AGR≤1.57与PLR>126.80是ESCC患者OS短的独立预测指标(P<0.05).根据AGR和PLR的cut-off值,设计了一个AGR联合PLR评分(APS评分):AGR>1.57且PLR≤126.80为0分;AGR≤1.57且PLR>126.80为1分;AGR≤1.57且PLR>126.80为2分.0、1、2分组OS分别为49.0个月(95％CI:36.0～60.9),36.0个月(95％CI:22.1～49.9)和13.0个月(95％CI:9.1～16.9),差异均有统计学意义(P<0.05).结论 术前AGR与PLR是预测ESCC患者预后的有效血液学指标.

目的:分析术中喉返神经监测在微创McKeown食管切除术中的应用价值.方法:回顾性分析南通市肿瘤医院2020年1月-2021年1月进行微创McKeown食管切除术治疗食管鳞状细胞癌患者78例,其中使用喉返神经监测的纳入研究组(38例);未接受喉返神经监测的纳入对照组(40例).比较两组手术指标、并发症,分析肌电图(EMG)波形异常诊断术后声带麻痹的价值.结果:研究组的喉返神经暴露时间、双侧喉返神经旁淋巴结清扫时间短于对照组,术中出血量少于对照组(P<0.05);两组住院时间比较,差异无统计学意义(P>0.05).研究组并发症发生率为13.16％,低于对照组的42.50％(P<0.05).EMG波形异常诊断术后声带麻痹的特异度为82.4％,敏感度为100％,阳性预测值为40.0％,阴性预测值为100％,准确率为84.2％.结论:喉返神经监测用于微创McKeown食管切除术可减少手术时间和出血量,降低术后并发症发生风险,其中EMG波形异常诊断声带麻痹敏感度和特异度较高.

目的：探索微创食管癌根治术（minimally invasive esophagectomy, MIE）中，应用吲哚菁绿（indocyanine green,ICG）近红外光成像技术，对食管癌手术中淋巴引流成像效果的影响因素。方法 ：收集2020年10月—2021年10月行荧光腔镜MIE入组患者120例，术前均行胃镜下食管肿瘤周围ICG黏膜下注射，分为ICG注射浓度对比组（ICG浓度对比组） 39例和ICG注射间隔时间显影组（ICG间隔时间组） 81例，观察比较两组淋巴引流的显影效果。结果：（1）ICG浓度对比组：ICG低浓度（2.5 mg/mL）胃镜下食管肿瘤周围黏膜下注射较高浓度（5 mg/mL）更易染色成功（P=0.001）。（2）ICG间隔时间组：胃镜下自ICG溶液（2.5 mg/mL）注射至荧光腔镜MIE的间隔时间会影响淋巴引流成像效果。ICG最佳显示间隔时间为143 min，其灵敏度为84.7%，特异度为93.3%，受试者工作特征曲线下面积为0.945,95%CI:0.895～0.995（P＜0.001）。结论：ICG近红外光成像技术可用于荧光腔镜MIE术中的淋巴引流成像。低浓度ICG（2.5 mg/mL）术前胃镜下食管肿瘤周围黏膜下注射可获得较高的染色成功率；胃镜下ICG注射到接受手术的间隔时间与成像效果有关，最佳时间间隔为143 min。

Circ_0020123 was highly expressed in NSCLC tissues and cell lines, and knockdown of circ_0020123 abolished cell growth, migration and invasion in vitro and hindered tumor growth in nude mice. Mechanically, circ_0020123 directly targeted miR-940, and KIAA1522 was a target of miR-940. Thereafter, a series of rescue experiments showed that circ_0020123 served its biological functions by miR-940/KIAA1522 axis. In all, circ_0020123 acted as an oncogene to promote the tumorigenesis of NSCLC via miR-940/KIAA1522 axis, suggesting a potential therapeutic target for NSCLC treatment.

Lung adenocarcinoma (LUAD) is a malignant tumor that occurs in the lungs. Numerous reports have substantiated the participation of long non-coding RNAs (lncRNAs) in the tumorigenesis of LUAD. Previously, lncRNA alpha-2-macroglobulin antisense RNA 1 (A2M-AS1) was confirmed to be an important regulator in the biological processes of LUAD and dysregulation of A2M-AS1 was associated with non-small cell lung cancer (NSCLC) progression. However, the precise mechanism of A2M-AS1 in LUAD has not been elucidated. Therefore, our study was designed to investigate the detailed molecular mechanism of A2M-AS1 in LUAD. Herein, the expression of lncRNA A2M-AS1, microRNA (miRNA) miR-587, and bone morphogenetic protein 3 (BMP3) in LUAD cell lines and tissues were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting. The viability, proliferation, migration and invasion of LUAD cells were tested by cell counting kit-8 (CCK-8), colony formation and Transwell assays. In vivo tumor growth was investigated by xenograft animal experiment. Interactions among A2M-AS1, miR-587 and BMP3 were measured by RNA pulldown and luciferase reporter assays. In this study, A2M-AS1 was downregulated in LUAD tissues and cells and related to poor prognosis in LUAD patients. A2M-AS1 overexpression suppressed LUAD cell proliferation, migration and invasion in vitro and inhibited tumor growth in vivo. Mechanistically, A2M-AS1 directly bound with miR-587 to promote BMP3 expression in LUAD cells. Low expression of BMP3 was found in LUAD tissues and cells and was closely correlated with poor prognosis in LUAD patients. BMP3 deficiency reserved the inhibitory influence of A2M-AS1 overexpression on LUAD cell behaviors. Overall, A2M-AS1 inhibits cell growth and aggressiveness via regulating the miR-587/BMP3 axis in LUAD. Keywords Lung adenocarcinoma , alpha-2-macroglobulin antisense RNA 1 , miR-587 , bone morphogenetic protein 3

Background Esophageal cancer is the most prevalent digestive system tumor. Due to a lack of characteristic symptoms and early diagnosis, a confirmed esophageal cancer is typically detected at a progressively harmful stage. Therefore, it is critical to investigate the molecular mechanisms governing the formation and progression of esophageal cancer in order to identify new treatment targets for esophageal cancer early detection. Methods We first screened the differentially expressed gene LINC00240 in the TCGA database. Multivariate analysis and Cox regression were performed, and a nomogram was constructed for internal validation. The correlation between LINC00240 and immune cells was analyzed using the TIMER database. The possible mechanism of action was explored through GSEA enrichment analysis. Then, in 43 esophageal cancer tissues, paracancour tissues, and cell lines, the LINC00240 expression was found. Transwell assays, CCK-8, and clone formation assays were utilized to assess the impact of LINC00240 on the metastasis of esophageal cancer cells. The binding activity of LINC00240 to downstream miRNAs was assessed using the luciferase reporter gene. Results TCGA database showed that LINC00240 expression was increased in cancer tissues compared to adjacent tissues. The C-index of the nomogram is 0.712 (0.666–0.758), and the prediction model has good accuracy. According to the TIMER database, the LINC00240 expression is linked to immune infiltration and may be crucial in encouraging the immune escape of tumor cells. Gene enrichment analysis depicts that LINC00240 could influence the biological events of esophageal cancer by taking part in pathways such as affecting the cell cycle. LINC00240 expression was substantially greater in the plasma of esophageal cancer patients (3.94 ± 1.55) than in the normal control group (2.13 ± 0.89). Plasma expression of LINC00240 was linked to the degree of differentiation (P=0.0345) and TNM stage (P=0.0409). Knocked down LINC00240 inhibited esophageal cancer cells proliferation, lone formation, and invasion. LINC00240 might bind itself to miR-26a-5p and influence its expression. MiR-26a-5p inhibitor can dramatically limit the ability of LINC00240 knockdown on plate colony formation and relocation of esophageal cancerous cells was demonstrated in colony formation and migration experiments. Conclusion LINC00240 expression is elevated in esophageal cancerous tissues, and knocking down LINC00240 decreases esophageal cancer cell proliferation, clone formation, invasion, and migration via miR-26a-5p. As a result, LINC00240 could be a novel target for esophageal cancer patients' early diagnosis and treatment.

Lung adenocarcinoma (LUAD) is a malignant tumor that occurs in the lungs. Numerous reports have substantiated the participation of long non-coding RNAs (lncRNAs) in the tumorigenesis of LUAD. Previously, lncRNA alpha-2-macroglobulin antisense RNA 1 (A2M-AS1) was confirmed to be an important regulator in the biological processes of LUAD and dysregulation of A2M-AS1 was associated with non-small cell lung cancer (NSCLC) progression. However, the precise mechanism of A2M-AS1 in LUAD has not been elucidated. Therefore, our study was designed to investigate the detailed molecular mechanism of A2M-AS1 in LUAD. Herein, the expression of lncRNA A2M-AS1, microRNA (miRNA) miR-587, and bone morphogenetic protein 3 (BMP3) in LUAD cell lines and tissues were detected by real-time quantitative polymerase chain reaction (RT-qPCR) and western blotting. The viability, proliferation, migration and invasion of LUAD cells were tested by cell counting kit-8 (CCK-8), colony formation and Transwell assays. In vivo tumor growth was investigated by xenograft animal experiment. Interactions among A2M-AS1, miR-587 and BMP3 were measured by RNA pulldown and luciferase reporter assays. In this study, A2M-AS1 was downregulated in LUAD tissues and cells and related to poor prognosis in LUAD patients. A2M-AS1 overexpression suppressed LUAD cell proliferation, migration and invasion in vitro and inhibited tumor growth in vivo. Mechanistically, A2M-AS1 directly bound with miR-587 to promote BMP3 expression in LUAD cells. Low expression of BMP3 was found in LUAD tissues and cells and was closely correlated with poor prognosis in LUAD patients. BMP3 deficiency reserved the inhibitory influence of A2M-AS1 overexpression on LUAD cell behaviors. Overall, A2M-AS1 inhibits cell growth and aggressiveness via regulating the miR-587/BMP3 axis in LUAD.

目的:研究术前老年营养风险指数(geriatric nutritional risk index,GNRI)对食管鳞癌患者术后预后的影响.方法:共纳入接受食管鳞癌根治术的患者152例,根据GNRI值,分为营养风险组(GNRI<92)(n=56)和营养无风险组(GNRI≥92)(n=96).采用Kaplan-Meier法Log-rank检验比较两组患者的生存曲线.采用Cox回归分析方法分析与预后相关的指标.结果:两组患者的血清白蛋白水平、体质量指数、预后营养指数比较差异均有统计学意义(均P<0.05).营养风险组发生吻合口瘘8例(14.3％),营养无风险组4例(4.2％),差异有统计学意义(P=0.026).营养风险组患者术后5年无病生存率和总体生存率分别为17.9％和19.9％,营养无风险组分别为34.4％和42.6％,差异均有统计学意义(均P=0.008,0.004).术前GNRI可作为患者无病生存及总体生存的独立预后因素(P<0.05).结论:术前GNRI低与食管鳞癌患者术后预后不良密切相关,可作为一种简易方便的评估食管鳞癌患者术后预后的指标.

Hepatocellular carcinoma (HCC) is a heterogeneous tumor with an increased incidence worldwide accompanied by high mortality and dismal prognosis. Emerging evidence indicates that mesenchymal stem cells (MSCs)-derived exosomes possess protective effects against various human diseases by transporting microRNAs (miRNAs or miRs). We aimed to explore the role of exosomal miR-15a derived from MSCs and its related mechanisms in HCC. Exosomes were isolated from transduced MSCs and co-incubated with Hep3B and Huh7 cells. miR-15a expression was examined by RT-qPCR in HCC cells, MSCs, and secreted exosomes. CCK-8, transwell, and flow cytometry were used to detect the effects of miR-15a or spalt-like transcription factor 4 (SALL4) on cell proliferative, migrating, invasive, and apoptotic properties. A dual-luciferase reporter gene assay was performed to validate the predicted targeting relationship of miR-15a with SALL4. Finally, in vivo experiments in nude mice were implemented to assess the impact of exosome-delivered miR-15a on HCC. The exosomes from MSCs restrained HCC cell proliferative, migrating, and invasive potentials, and accelerated their apoptosis. miR-15a was expressed at low levels in HCC cells and could bind to SALL4, thus curtailing the proliferative, migrating, and invasive abilities of HCC cells. Exosomes successfully delivered miR-15a to HCC cells. Exosomal miR-15a depressed tumorigenicity and metastasis of HCC tumors in vivo. Overall, exosomal miR-15a from MSCs can downregulate SALL4 expression and thereby retard HCC development.

The widespread prevalence of coronavirus disease-2019 (COVID-19) which is caused by severe respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, has resulted in a severe global public health emergency. However, there are no sensitive biomarkers to predict the disease prognosis of COVID-19 patients. Here, we have identified interleukin-8 (IL-8) as a biomarker candidate to predict different disease severity and prognosis of COVID-19 patients. While serum IL-6 become obviously elevated in severe COVID-19 patients, serum IL-8 was easily detectible in COVID-19 patients with mild syndromes. Furthermore, lL-8 levels correlated better than IL-6 levels with the overall clinical disease scores at different stages of the same COVID-19 patients. Thus, our studies suggest that IL-6 and IL-8 can be respectively used as biomarkers for severe COVID-19 patients and for COVID-19 disease prognosis.

BACKGROUND:Esophageal cancer (ESCA) constitutes one of the most common cancers worldwide. The identification of potential biomarkers is important to improving the diagnostic accuracy and treatment efficiency for patients with ESCA. In this study, we aimed to identify biomarkers related to ESCA progression through a comprehensive analysis of long non-coding RNAs (lncRNAs), microRNA (miRNAs), and mRNA expression profiles in ESCA.METHODS:Differentially expressed lncRNAs, miRNAs, and mRNAs (DElncRNAs, DEmiRNAs, and DEmRNAs, respectively) in ESCA samples compared with normal controls were obtained. A competing endogenous RNA (ceRNA) network consisting of interacting DElncRNAs, DEmiRNAs, and DEmRNAs was constructed using a combination of the miRCode and TargetScan databases. Relationships between RNAs in the ceRNA network and overall survival in patients with EC were explored through another independent ESCA dataset from The Cancer Genome Atlas.RESULTS:A total of 1,014 DElncRNAs, 3,677 DEmRNAs, and 35 DEmiRNAs were identified in ESCA samples compared with normal samples. Functional enrichment analysis indicated that the DEmRNAs were involved in cell activity, inflammatory response, and oxygen metabolism-related biological processes. A ceRNA network containing 5 DEmiRNAs, 582 DEmRNAs and 764 DElncRNAs was obtained. In the survival analysis, 39 genes were found to be significantly associated with overall survival in patients with EC, including GOLGA7, NFYB, TOP1, and TMTC3.CONCLUSIONS:Our study constructed a ceRNA network for ESCA for the first time, which will be helpful for the disease's diagnosis and treatment.