Splenic metastases are uncommon in solid malignancies, and isolated splenic metastases are even more rare. Current research believes that both anatomical and immunological factors contribute to the rarity of splenic metastasis. We reported a rare case of metachronous isolated splenic metastasis of sigmoid carcinoma in a 58-year-old male. The combination of splenectomy, chemotherapy, and targeted therapy plus anti-PD-1 antibody helped the patient achieve tumor-bearing survival for 32 months. This study reviewed cases of isolated splenic metastasis from colorectal cancer, emphasizing the importance of comprehensive treatment in the treatment of solitary splenic metastasis to reduce the risk of development of new metastasis.

Background:Gastric cancer (GC) represents a considerable health risk, characterized by a poor 5-year survival rate of approximately 8%. Using data from The Cancer Genome Atlas (TCGA), this study investigated the function of calcium signaling-related genes in the context of GC. Methods:The RNA sequencing data and clinical characteristic data of GC patients were retrieved from TCGA database. A comprehensive analysis was conducted to identify the prognostic genes, and a significant correlation was found between these genes and the calcium signaling pathways related to GC. Results:The univariate Cox regression analysis identified 829 prognostic genes, primarily related to the calcium signaling pathway, focal adhesion, extracellular matrix (ECM)-receptor interaction, and cancer-associated pathways, all of which may significantly affect GC. Through consensus clustering, two distinct molecular subtypes of GC were identified [Cluster 1 (C1) and Cluster 2 (C2)] based on the genes associated with calcium signaling. Notably, C2 may serve as a prognostic indicator of risk, potentially reflecting the progression of clinical symptoms. The Gene Ontology (GO) analysis of biological processes revealed that these genes were significantly involved in cell-matrix adhesion, calcium ion homeostasis, and cell-substrate adhesion in the high-risk C1 cohort. Similarly, the Kyoto Encyclopedia of Genes and Genomes analysis indicated that the differentially expressed genes were largely associated with the pathways related to ECM-receptor interactions, focal adhesion, vascular smooth muscle contraction, cancer-related proteoglycans, and calcium signaling pathways in the high-risk C1 group. Further, there were significant differences in the immune activity of the two calcium signaling-related GC groups. The least absolute shrinkage and selection operator regression analysis identified 10 genes associated with calcium signaling in GC (i.e., PDE1B, NGF, FGF1, ADRA1B, TACR1, CXCR4, GNAS, EDNRB, EGF, and ERBB4). The accuracy of the prognostic model was assessed by a receiver operating characteristic curve analysis, yielding areas under the curve of 0.639 for 1 year, 0.707 for three years, and 0.674 for 5 years. Conclusions:We established an innovative signature associated with calcium signaling that serves as a reliable prognostic indicator for GC. Our findings may pave the way for enhanced diagnostic and therapeutic approaches in the context of GC.

OBJECTIVES:This study aimed to comprehensively investigate the molecular landscape of gastric cancer (GC) by integrating various bioinformatics tools and experimental validations. METHODS:GSE79973 dataset, limma package, STRING, UALCAN, GEPIA, OncoDB, cBioPortal, DAVID, TISIDB, Gene Set Cancer Analysis (GSCA), tissue samples, RT-qPCR, and cell proliferation assay were employed in this study. RESULTS:Analysis of the GSE79973 dataset identified 300 differentially expressed genes (DEGs), from which COL1A1, COL1A2, CHN1, and FN1 emerged as pivotal hub genes using protein-protein interaction network analysis. Subsequent validation across The Cancer Genome Atlas (TCGA) datasets confirmed their up-regulation in GC tissues compared to normal controls. Promoter methylation analysis revealed decreased methylation levels of these hubs in GC tissues, suggesting their potential role in tumorigenesis. Mutational analysis using cBioPortal showcased frequent mutations in these genes, particularly FN1, further highlighting their significance in GC pathogenesis. Survival analysis indicated their correlation with reduced overall survival rates among GC patients, supported by the development of a robust prognostic model. Prediction of hub-associated miRNAs and gene enrichment analysis provided insights into their regulatory mechanisms and downstream pathways, implicating their involvement in extracellular matrix remodeling and cell migration. Drug sensitivity analysis revealed correlations between hub gene expression and drug response, while RT-qPCR validation confirmed their upregulation in clinical GC samples. Finally, functional assays demonstrated the impact of FN1 knockdown on cellular proliferation, colony formation, and wound healing capacities. CONCLUSION:Overall, this study elucidates the crucial role of COL1A1, COL1A2, CHN1, and FN1 in GC pathogenesis and underscores their potential as diagnostic markers and therapeutic targets.

Background: Colorectal adenocarcinoma [COAD] is a prevalent and lethal form of cancer. Understanding the molecular mechanisms underlying COAD progression is crucial for developing effective diagnostic and therapeutic strategies Methods: This study aims to explore wound healing-related genes in COAD and their potential roles in tumorigenesis and prognosis using in silico and in vitro methodology Results: A set of 70 genes associated with the "wound healing" term ere extracted from the Gene Ontology [GO] database [GO:0042060] and a protein-protein interaction [PPI] network was constructed using the STRING database. The PPI network was analyzed with the CytoHubba plugin in Cytoscape, identifying four major hub genes: MMP2, FN1, NF1, and PTK7. We then analyzed the expression of these hub genes across 16 COAD cell lines and nine normal colon cell lines using RT-qPCR, finding significant overexpression in COAD cell lines. ROC curve analysis confirmed the diagnostic potential of these genes, with MMP2, FN1, and NF1 showing high AUC values. Expression validation using the TCGA COAD cohort, OncoDB, and HPA databases corroborated these findings, highlighting the overexpression and high protein levels of these genes in COAD. Promoter methylation analysis indicated lower methylation levels in COAD samples, suggesting dysregulation through epigenetic mechanisms. Genetic alteration analysis via cBioPortal revealed a spectrum of mutations, with FN1 being the most frequently mutated. Prognostic analysis using a KM plotter showed that high expression of the hub genes is associated with poorer overall survival [OS] and disease-free survival [DFS]. Functional state correlations via CancerSEA suggested that these genes promote cell cycle, proliferation, metastasis, and stemness in COAD. Expression analysis in immune cells and drug sensitivity analyses highlighted the roles of MMP2, FN1, and NF1 in macrophages and drug resistance. A miRNA-mRNA network constructed using miRNet identified hsa-miR-200a-3p as a central regulator. Finally, functional assays in HCT116 cells demonstrated that knockdown of MMP2 and FN1 reduced proliferation, colony formation, and wound healing, suggesting these genes as potential therapeutic targets in COAD. Conclusion: In conclusion, our study identifies MMP2, FN1, NF1, and PTK7 as key wound healing-related hub genes in COAD.

BACKGROUND:Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2) is implicated in various cancers, but its role in modulating ferroptosis and tumor cell behavior in non-small cell lung cancer (NSCLC) remains unclear. OBJECTIVES:This study aimed to investigate how IGF2BP2-mediated N6-methyladenosine (m6A) modification of solute carrier family 7 member 11 (SLC7A11) affects ferroptosis and NSCLC cell viability. MATERIAL AND METHODS:NSCLC H1299 cells were transfected with either IGF2BP2 or SLC7A11 plasmids and corresponding siRNAs. Expression levels of IGF2BP2, SLC7A11 and ferroptosis markers were analyzed using reverse transcription real-time quantitative polymerase chain reaction (RT-qPCR) and western blot. Cell viability was assessed using the Cell Counting Kit-8 (CCK-8) assay. Reactive oxygen species (ROS) and lipid peroxidation levels were measured with flow cytometry and biochemical kits. The RNA immunoprecipitation (RIP) and mRNA stability assays were utilized to explore the interaction between IGF2BP2 and SLC7A11. RESULTS:IGF2BP2 expression was significantly upregulated in H1299 cells. Overexpression of IGF2BP2 enhanced cell viability and decreased ferroptosis, whereas its knockdown resulted in reduced cell viability and increased ferroptotic activity. IGF2BP2 enhanced SLC7A11 mRNA stability through m6A modification, and SLC7A11 overexpression reversed the effects of IGF2BP2 knockdown. This interaction increased cell viability and reduced ROS and lipid peroxidation. CONCLUSIONS:IGF2BP2 plays a critical role in NSCLC by stabilizing SLC7A11 mRNA via m6A modification, promoting cell proliferation and suppressing ferroptosis. Targeting the IGF2BP2-SLC7A11 axis may offer a promising therapeutic strategy for NSCLC.

Gastric cancer (GC) development is influenced by crosstalk between tumor cells and host immune elements. Circ_0000372 has potential as an oncogene. This research aimed to investigate the circ_0000372 mechanism in GC. Circ_0000372 expressions were evaluated via the GSE194384 database. The overall survival of GC patients was determined via the Kaplan-Meier Survival Curve. Gene relationships were assessed using the Chi-square test. Circ_0000372 functions in GC were evaluated with qRT-PCR, Cell Counting Kit-8 analysis, 5-ethynyl-2’-deoxyuridine analysis, Transwell, Western blot, co-culture of peripheral blood mononuclear cells (PBMCs) and GC cells, flow cytometry, and ELISA. Meanwhile, the circ_0000372 mechanism was examined by RNA pull-down, dual-luciferase reporter assay, and Spearman Correlation Analysis. Finally, the circ_0000372 impact on tumor-bearing mice was analyzed by immunohistochemistry and western blot assays. Elevated circ_0000372 levels were detected in GC. Patients with raised circ_0000372 levels had a poor prognosis. Besides, circ_0000372 expressions were interrelated to TNM stage and lymph node metastasis. Silencing circ_0000372 repressed GC cell proliferation and invasion. Silencing circ_0000372 reduced immune escape with reduced PD-L1 protein levels and increased CD8 + T cell percentage. Moreover, circ_0000372 positively regulated PD-L1 expression via miR-488-3p, and circ_0000372 knockdown restrained GC cell proliferation, invasion, and immune escape by derepressing PD-L1 via sponging miR-488-3p. The interference of circ_0000372 also reduced GC tumor formation, tumor weight, and PD-L1 level with elevated IFN-γ level in vivo. A high circ_0000372 level indicated a GC poor prognosis. Silencing circ_0000372 suppressed cell proliferation, invasion, and immune escape by derepressing PD-L1 via sponging miR-488-3p.

Epithelioid inflammatory myofibroblastic sarcoma (EIMS) is an extremely rare and aggressive form of inflammatory myofibroblastic tumor. Clinically, it has a high risk of relapse and peripheral organ infiltration, and it responds poorly to conventional chemotherapy. Anaplastic lymphoma kinase (ALK) inhibitors are currently the most effective targeted therapy for EIMS. This report discusses a typical case of abdominal EIMS in a 43-year-old woman. The tumors recurred rapidly within one month after surgery. Alectinib was promptly administered upon diagnosis. However, the patient developed a severe allergic reaction to the medication. After a comprehensive assessment and symptomatic treatment, her condition stabilized, leading to a favorable prognosis. This study summarizes cases of abdominal EIMS, highlights the successful use of Alectinib for treatment, and discusses the management of medication-related complications.

Rectal cancer is one of the most malignant tumors, and postoperative recurrence and metastasis are the main reasons for treatment failure. Lymph node metastasis is the main metastatic pathway of rectal cancer. The present study aimed to investigate the role of lateral lymph node dissection (LLND) in patients with rectal cancer using a meta-analysis. Articles in Chinese and English related to the application of LLND in patients with rectal cancer were retrieved and eligible studies were selected for data analysis. Evaluation indicators included the 5-year survival rate, recurrence rate, urinary system function and operation time. The random-effects model was utilized for the analysis. A total of 10 studies that met the eligibility criteria were selected, comprising 2,272 patients, including 1,101 cases in the LLND group and 1,171 cases in the non-LLND group. No significant difference was found between the two groups in terms of local recurrence rate, 5-year disease-free survival (DFS) rate, and DFS rate at the follow-up. It is noteworthy that cases in the LLND group had no significantly longer overall survival, but had a higher 5-year survival rate. However, cases in the LLND group had a longer operation time and worse urinary dysfunction. The results remained consistent throughout separate analyses for different research quality sources. The present meta-analysis showed that LLND provided a specific advantage in prolonging survival time. However, it was associated with prolonged operation time and an increased incidence of urinary dysfunction.

Objective:To compare the lymph node tracing of indocyanine green (ICG) and nanocarbon in laparoscopic right hemicolectomy.Methods:Fifty-two patients with right colon cancer were randomly divided into two groups: ICG group and nanocarbon group at Peking University International Hospital between Oct 2020 and Jul 2022. Sentinel lymph node (SLN) mapping and standard oncologic resection was performed. The micrometastasis was to detect when the routine SLN pathological test was negative.Results:In ICG group, the detection rate of SLN was 100%, the sensitivity was 93%, the false negative rate was 7%, and the accuracy was 96%,which were better than nanocarbon group (92%,57%,43%,77%). The number of SLN and positive SLN detected in ICG group were significantly higher than nanocarbon group [(3.2±0.7) vs. (2.6±1.1), t=4.424, P=0.020; (1.2±1.2) vs.(0.5±0.8), t=15.176, P=0.013]. The SLN biopsy accuracy of patients with BMI ≥24 kg/m 2 and tumor diameter ≥3 cm in ICG group was significantly higher than nanocarbon group (90% vs. 44%, χ 2=7.935, P=0.005; 90% vs.57%, χ 2=4.309, P=0.038). The detection rate of micrometastasis in SLN of ICG group was significantly different from nanocarbon group (35% vs. 15%, χ 2=5.853, P=0.016). Conclusion:ICG fluorescence imaging is superior to nanocarbon in SLN biopsy during laparoscopic radical right hemicolectomy, especially when patients' BMI ≥24 kg/m 2 and tumor diameter ≥3 cm.

Objective:To investigate the effects of Nuclear factor interleukin 3regulator (NFIL3) on proliferation and invasion of human breast cancer cells.Methods:we successfully established cell models of NFIL3 over-expression and knockdown in breast cancer cell lines BT549 and Hs578T respectively (Shanghai cell bank of Chinese Academy of Sciences) thought lentiviral vectorsand validated by fluorescence quantitative polymerase chain reaction and Western blotting. Methyl thiazolyl tetrazolium assay (MTT) test cell proliferation, Transwell assays, Subcutaneous tumor bearing and tail vein lung metastasis in nude mice, were verified the proliferation and invasion of NFIL3 in breast cancer cells. Data between sample groups expressed by mean±standard deviation, and comparison between groups performed by T-test and One-way ANOVA test. Results:MTT cell proliferation assay demonstrated that NFIL3 over-expression significantly promoted cell proliferation (BT549-control 4.37±0.27 vs. BT549-NFIL3 5.98±0.31, t=6.783, P<0.01; Hs578T-control 4.75±0.32 vs. Hs578T-NFIL3 6.05±0.39, t=4.463, P<0.05), and NFIL3 knockdown significantly inhibited cell proliferation (BT549-PLKO 4.17±0.20 vs. BT549-sh1 2.83±0.29, t=6.557, P<0.01; BT549-PLKO 4.17±0.20 vs. BT549-sh2 3.11±0.17, t=4.943, P<0.01; Hs578T-PLKO 4.11±0.31 vs. Hs578T-sh1 3.11±0.21, t=12.540, P<0.01; Hs578T-PLKO 4.11±0.31 vs. Hs578T-sh2 3.01±0.23, t=10.930, P<0.01). Transwell assay showed that NFIL3 over-expression significantly promoted cell migration (BT549-control 198.00±28.03 vs. BT549-NFIL3 397.0±52.1, t=10.640, P<0.01; Hs578T-control 294±32.01 vs. Hs578T-NFIL3 598±46.11, t=17.130, P<0.01), and oNFIL3 knockdown significantly inhibited cell migration (BT549-PLKO 178±23.11 vs. BT549-sh1 41.01±15.12, t=9.820, P<0.01; BT549-PLKO 178±23.11 vs. BT549-sh2 56.1±24.27, t=10.430, P<0.01; Hs578T-PLKO 197.6±21.13 vs. Hs578T-sh1 69.8±19.96, t=8.403, P<0.01; Hs578T-PLKO 197.6±21.13 vs. Hs578T-sh2 58.0±14.26, t=8.042, P<0.01). Transwell assay showed that NFIL3 over-expression significantly promoted cell invasion (BT549-control 74.6±23.14 vs. BT549-NFIL3 142.5±28.3, t=5.874, P<0.01; Hs578T-control 103.2±28.14 vs. Hs578T-NFIL3 183.7±22.14, t=7.110, P<0.01), and oNFIL3 knockdown significantly inhibited cell invasion (BT549-PLKO 89.13±19.86 vs. BT549-sh1 37.45±15.63, t=9.062, P<0.01; BT549-PLKO 89.13±19.86 vs. BT549-sh2 50.17±17.12, t=8.067, P<0.01; Hs578T-PLKO 135.1±16.52 vs. Hs578T-sh1 47.1±16.3, t=6.747, P<0.01; Hs578T-PLKO 135.1±16.52 vs. Hs578T-sh2 58.45±14.13, t=6.598, P<0.01). NFIL3 over-expression significantly promoted subcutaneous tumor growth in nude mice [Hs578T-control (0.126±0.017) g vs. Hs578T-NFIL3 (0.301±0.098) g, t=3.934, P<0.01], and NFIL3 knockdown significantly inhibited subcutaneous tumor growth in nude mice [Hs578T-PLKO (0.19±0.078) g vs. Hs578T-sh (0.04±0.019) g, t=4.168, P<0.01]. NFIL3 over-expression increased the number of lung metastases in nude mice (Hs578T-control 1.45±0.98 vs. Hs578T-NFIL3 4.12±1.79, t=4.137, P<0.01), while NFIL3 knockdown reduced the number of lung metastases in nude mice (Hs578T-PLKO 1.53±1.21 vs. Hs578T-sh 0.34±0.27, t=3.035, P<0.05). Conclusion:NFIL3 promotes proliferationand invasion ofbreast cancer cells.

目的 探讨AT富交互域3A(ARID3A)对结肠癌细胞化疗敏感性的影响及其作用机制.方法 在人结肠癌细胞系HCT116和SW1116中构建ARID3A过表达或敲低细胞系,设置HCT116-PLVX/SW1116-PLVX过表达对照组、HCT116-ARID3A/SW1116-ARID3A过表达组、HCT116-ARID3A-sh1/SW1116-ARID3A-sh1敲减组、HCT116-ARID3A-sh2/SW1116-ARID3A-sh2敲减组和HCT116-SH/SW1116-SH敲减对照组.应用MTT实验检测5-FU作用于各组后的抑制效率.蛋白质谱检测筛选下游调控基因醛酮还原酶家族1成员C3(AKR1C3),采用qRT-PCR和蛋白质印迹法检测ARID3 A过表达或敲减对AKR1C3表达的影响.采用双荧光素酶报告基因和染色质免疫沉淀(ChIP)实验分析ARID3A对AKR1C3的调控作用.进一步构建AKR1C3过表达或敲低细胞系,再次应用MTT实验检测其对5-FU的敏感性.结果 与对照组相比,HCT116-ARID3A过表达组(F药物浓度=151.300,P<0.001;FARID3A=11.980,P=0.003;F药物浓度×ARID3A=5.250,P=0.005)和SW1116-ARID3A过表达组(F药物浓度=404.902,P<0.001;FARID3A=215.901,P<0.001;F药物浓度×ARID3A=3.185,P=0.023)细胞受5-FU的抑制效率增加,药物和ARID3 A表达水平的作用效应存在交互作用.而敲减ARID3 A后,相较于对照组细胞表现出了对5-FU敏感性的降低,均P<0.05.进一步筛选出ARID3 A的下游靶基因AKR1C3,qRT-PCR实验结果显示,在过表达ARID3A的HCT116和SW1116细胞中,AKR1C3的mRNA水平均低于相应对照组细胞(HCT116:0.395±0.054 vs 1.000±0.162,t=6.147,P=0.004;SW1116:0.250±0.017 vs 1.000±0.332,t=3.911,P=0.017);而在ARID3A敲减细胞中则相反,即AKR1C3的mRNA水平高于相应对照组细胞(HCT116:2.886±0.421 vs 1.000±0.080,t=7.621,P=0.002;SW1116:2.990±0.851 vs 1.000±0.148,t=3.909,P=0.016).在过表达ARID3A的HCT116和SW1116细胞中,AKR1C3的蛋白水平均低于相应对照组细胞(HCT116:0.780±0.010 vs 1.000±0.012,t=19.630,P=0.004;SW1116:0.130±0.012 vs 0.240±0.029,t=4.880,P=0.032).而在ARID3A敲减细胞中则相反,即AKR1C3的蛋白水平均高于相应对照组细胞(HCT116:1.630±0.040 vs 1.030±0.026,t=18.140,P=0.005;SW1116:1.070±0.153 vs 0.450±0.033,t=5.590,P=0.031).并进一步明确ARID3A与AKR1C3结合并发挥其对AKR1C3的转录抑制作用.在HCT116和SW1116细胞中,过表达AKR1C3后,相较于对照组细胞均表现出了对5-FU敏感性的减弱,药物和AKR1C3表达水平的作用效应存在交互作用,均P<0.05.而敲减AKR1 C3后,相较于对照组细胞表现出了对5-FU敏感性的增强,均P<0.05.结论 ARID3A通过抑制结肠癌细胞中的耐药相关基因AKR1C3促进结肠癌细胞对化疗药物5-FU的敏感性.

Objective:To explore the expression of vasohibin-1 (VASH1) and vascular endothelial growth factor A (VEGF-A) and clinical significance of VASH1 in gastric carcinoma.Methods:The expression of VASH1 and VEGF-A were detected by immunohistochemistry in formalin-fixed and paraffin-embedded sections in 56 pairs of gastric cancer and corresponding paraneoplastic tissue specimens. The correlation between the expression of VASH1, VEGF-A, clinicopathological parameters and prognosis were analyzed.Results:VASH1 and VEGF-A expression was significantly higher in gastric cancer tissues than normal paraneoplastic tissues. VASH1 and VEGF-A protein were expressed in 79% and 82% of gastric cancer tissues, respectively. A positive correlation was found between Vasohibin-1 and VEGF-A expression in gastric cancer tissues. VASH1 expression has significant positive correlation with TNM stage, tumor stromal invasion, tumor gross types and distant metastasis. Patients with high VASH1 expression had significantly worse overall survival (OS) and progression-free survival (PFS) than those with low VASH1 expression.Conclusion:VASH1 might be a clinically relevant predictor of patients in gastric cancer.

Abstract Background Aging is the major risk factor for most human cancers. We aim to develop and validate a reliable aging-related gene pair signature (ARGPs) to predict the prognosis of gastric cancer (GC) patients. Methods The mRNA expression data and clinical information were obtained from two public databases, The Cancer Genome Atlas (TCGA) dataset, and Gene Expression Omnibus (GEO) dataset, respectively. The best prognostic signature was established using Cox regression analysis (univariate and least absolute shrinkage and selection operator). The optimal cut-off value to distinguish between high- and low-risk patients was found by time-dependent receiver operating characteristic (ROC). The prognostic ability of the ARGPS was evaluated by a log‐rank test and a Cox proportional hazards regression model. Results The 24 ARGPs were constructed for GC prognosis. Using the optimal cut-off value − 0.270, all patients were stratified into high risk and low risk. In both TCGA and GEO cohorts, the results of Kaplan–Meier analysis showed that the high-risk group has a poor prognosis (P < 0.001, P = 0.002, respectively). Then, we conducted a subgroup analysis of age, gender, grade and stage, and reached the same conclusion. After adjusting for a variety of clinical and pathological factors, the results of multivariate COX regression analysis showed that the ARGPs is still an independent prognostic factor of OS (HR, 4.919; 95% CI 3.345–7.235; P < 0.001). In comparing with previous signature, the novel signature was superior, with an area under the receiver operating characteristic curve (AUC) value of 0.845 vs. 0.684 vs. 0.695. The results of immune infiltration analysis showed that the abundance of T cells follicular helper was significantly higher in the low-risk group, while the abundance of monocytes was the opposite. Finally, we identified and incorporated independent prognostic factors and developed a superior nomogram to predict the prognosis of GC patients. Conclusion Our study has developed a robust prognostic signature that can accurately predict the prognostic outcome of GC patients.

Objective:To analyze the clinicopathological features and prognostic factors of alpha‐fetoprotein‐producing gastric carcinoma (AFPGC).Methods:A retrospective analysis was made on 2 671 GC patients admitted from Jan 1998 to Dec 2018 , AFPGC patients and matching AFP negative GC cases were enrolled and their clinicopathological features and prognostic factors were analyzed. The survival curve was drawn by Kaplan-Meier method. Log-rank test was used to test the significance, Univariate analysis was performed by using COX proportional hazard model.Results:There were 98 AFPGC in this study accounting for 4.5% of all GC of the corresponding time period. The proportion of male to female was 2.16∶1, the average age was (65±12) years. The serum AFP levels significantly decreased after operation in most patients (median: 52 ng/ml vs. 5 ng/ml, Ｚ=-2.736, P=0.001). Serum AFP and CEA levels in patients with AFPGC before treatment were significantly higher than that in patients with AFP negative GC (both P<0.05) . Vascular invasion(62.71% vs. 40.68%) and liver metastasis (31.63% vs .6.12%) were more likely to occur in AFPGC groups (both P<0.05). However, there was no significant difference between the two groups in tumor size, location, differentiation and lymph node metastasis (all P>0.05). The prognosis of AFPGC was significant pooer than that in AFP negative GC ( P<0.05). Prognosis of AFPGC patients was significantly correlated with preoperative serum AFP level, TNM stage, lymph node metastasis, simultaneous liver metastasis and vascular invasion (all P<0.05) . COX multivariate survival analysis found that preoperative serum AFP level was independent risk factors of patients with AFPGC ( P<0.05). Conclusion:AFPGC is a special GC charactering poor prognosis .

Objective:To explore the function and mechanism of LIN28 homolog A (LIN28A) mRNA depend on non-coding manner in the development of colon cancer.Methods:Establish colon cancer cell lines over expressing LIN28A mRNA and LIN28A protein in HCT116 and SW1116 cells, and verified by fluorescence quantitative polymerase chain response (PCR) and western blotting experiments. The cell counting kit (MTT) and transwell experiment was used to analyze the metastasis ability of the cells. Mass spectrometry was used to detect the protein changes caused by non-coding LIN28A mRNA over expression and screen functional target molecules. We verify the effect of LIN28A mRNA on target molecules expression and construct the cells which the target molecule to detect the function of its on colon cancer. Data comparison between groups was performed by t test. Results:The cell metastasis ability of the non-coding functional LIN28A mRNA was significantly higher than that of the control (HCT116 migration: 1.065±0.323 vs. 2.768±0.249, t=8.345, P<0.05; SW1116 invasion: 1.034±0.117 vs. 1.458±0.056, t=6.600, P<0.05; HCT116 migration: 1.055±0.319 vs. 2.026±0.165, t=6.387, P<0.05; SW1116 invasion: 0.941±0.100 vs. 2.103±0.111, t=16.48, P<0.05), but its proliferation ability did not change significantly. Methionyl aminopeptidase 2 (METAP2) is one of the up-regulated metastasis regulators identified by mass spectrum in LIN28A mRNA over expressing cells. LIN28A knockdown significantly reduced METAP2 expression than that of the control (HCT116-si#1: 1.003±0.052 vs. 0.937±0.044, t=1.371, P>0.05; si#2: 1.003±0.052 vs. 0.503±0.015, t=13.11, P<0.05; SW1116-si#1: 1.005±0.071 vs. 0.993±0.075, t=0.1623, P<0.05; si#2: 1.005±0.071 vs. 0.809±0.052 t=3.141, P<0.05). The roles of METAP2 were consistent with LIN28A mRNA, the metastasis ability of METAP2 knockdown was significantly lower than that of the control (HCT116 migration and invasion: 1.000±0.055 vs. 0.420±0.070, t=14.60, P<0.05; 1.000±0.176 vs. 0.200±0.009, t=8.942, P<0.05; SW1116 migration and invasion: 1.026±0.152 vs. 0.350±0.078, t=7.933, P<0.05; 0.982±0.238 vs. 0.487±0.030, t=4.851, P<0.05). Conclusion:Non-coding LIN28A mRNA promotes colon cancer cell metastasis by regulating METAP2.

Objective:To study the relation ship between the branch patterns of inferior mesenteric artery (IMA) and imaging pelvic measurement parameters for anastomotic leakage (AL) after anterior resection (AR) of rectal cancer.Methods:Five hundred thirty-four patient were enrolled from Jan 2008 to Dec 2018 at the General Surgery Department of Guizhou Provincial People's Hospital. The AL related imaging risk factors were analyzed by chi-square test or Fisher's exact test.Results:AL was found in 36 (6.7%) patients. AL related mortality rate was 11.1% (4/36) compared to 0.4% (2/498) in those without the complications of no AL cases ( P<0.001). Seven pelvic imaging measurement results were attained in 412 patients including anteroposterior diameter of the inlet of the pelvis, anteroposterior diameter of the outlet of the pelvis, upper edge of the symphysis pubis to the tip of the coccyx, sacrococcygeal distance angle from the lower edge of the pubis to the upper edge of the pubis to the sacral promontory, distance between the ischial spines and that of ischial tuberosity. Univariate analysis showed that there was no significant relationship between the above 7 pelvic measurement parameters and the occurrence of AL (all P>0.05). There was no significant relationship between branch patterns of IMA and AL after rectal cancer surgery ( P=0.712). Conclusion:AL as a severe postoperative complication in rectal cancer patients undergoing AR procedure were caused by multiple factors. Neither IMA branch patters nor pelvic imaging measurement seem to be related to the occurrence of AL after AR for rectal cancer.

The long noncoding RNA (lncRNA) LUCAT1 was recently reported to be upregulated and to play an essential role in multiple cancer types, especially colorectal cancer (CRC), but the molecular mechanisms of LUCAT1 in CRC are mostly unreported. Here, a systematic analysis of LUACT1 expression is performed with data from TCGA database and clinic CRC samples. LUCAT1 is identified as a putative oncogene, which is significantly upregulated in CRC and is associated with poor prognosis. Loss of LUCAT1 restricts CRC proliferative capacities in vitro and in vivo. Mechanically, NCL is identified as the protein binding partner of LUCAT1 by using chromatin isolation by RNA purification coupled with mass spectrometry (ChIRP-MS) and RNA immunoprecipitation assays. We also show that NCL directly binds to LUCAT1 via its putative G-quadruplex-forming regions from nucleotides 717 to 746. The interaction between LUCAT1 and NCL interferes NCL-mediated inhibition of MYC and promote the expression of MYC. Cells lacking LUCAT1 show a decreased MYC expression, and NCL knockdown rescue LUCAT1 depletion-induced inhibition of CRC cell proliferation and MYC expression. Our results suggest that LUCAT1 plays a critical role in CRC cell proliferation by inhibiting the function of NCL via its G-quadruplex structure and may serve as a new prognostic biomarker and effective therapeutic target for CRC.

Purpose An increasing number of long non-coding RNAs (lncRNAs) are thought to be associated with gastric cancer (GC). A lncRNA subclass that promotes enhancer function is called enhancer RNA (eRNA). We aimed to identify an eRNA that can predict GC prognosis and response to immune checkpoint inhibitors (ICIs).Methods Kaplan–Meier survival analysis was utilized to screen eRNA which can predict the prognosis of GC (P <0.05). The method of Spearman correlation analysis was employed in the filtration of target genes related to eRNA (r> 0.4, P <0.001). According to the median of WAKMAR2 expression, the patients were subdivided into low expression group and high expression group. Subsequently, differences of immune checkpoint-related genes and immune cell infiltration between the two groups were further explored. Furthermore, we analyzed the correlation of WAKMAR2 with tumor mutation burden (TMB) and microsatellite instability (MSI) in GC and other types of cancer.Results WAKMAR2 and its target gene TNFAIP3 entered the subsequent analysis. Patients with high-WAKMAR2 expression had a favorable prognosis compared to patients with low-WAKMAR2 expression (P = 0.048). Immune checkpoint-related genes (PD-L1, CTLA4, PDCD1, LAG3) in the WAKMAR2 high-expression group were also highly expressed, except for B7-H3. In addition, infiltration levels of B cells naive, T cells CD8, T cells CD4 memory activated, as well as Macrophages M1 in high-WAKMAR2 group were greater than in low-WAKMAR2 group. Last, the expression of WAKMAR2 in GC was significantly correlated with TMB and MSI.Conclusion WAKMAR2, a new eRNA, is a promising biomarker that can be used to predict the overall survival (OS) of GC patients, and WAKMAR2 expression can be utilized to identify ICB responders in GC, providing new insights for immunotherapy strategies.

Cancer metastasis is a significant challenge in colorectal cancer (CRC) therapy. SET and MYND domain-containing protein 2 (SMYD2) is highly expressed in multiple cancers but is rarely studied in CRC. This study aims to identify whether abnormal expression of SMYD2 is associated with cancer metastasis in CRC. In this study, we demonstrated that SMYD2 not only promoted cell proliferation but also increased the metastatic ability of CRC. The expression of adenomatous polyposis coli 2 (APC2), an inhibitor of the Wnt/β-catenin pathway, was suppressed by SMYD2 overexpression. Overexpression of SMYD2 activated the Wnt/β-catenin pathway and then induced the epithelial-mesenchymal transition (EMT) program in CRC. Mechanistically, low APC2 expression in CRC cells was due to SMYD2-mediated DNA methylation modification. This modification might require synergism with DNMT1. In summary, our study provides new insights into SMYD2-related transcriptional regulation patterns and indicates that SMYD2 could be a potential therapeutic target for CRC patients.