Abstract Background Gastric cancer (GC) is a common digestive tract cancer whose high heterogeneity and invasiveness lead to a low survival rate. Therefore, it is necessary to explore the potential molecular mechanism of GC. Methods Three genes and one miRNA expression microarray dataset were downloaded from the GEO database. The gene expression profiles of the cancer group and normal group were compared in each dataset, and differentially expressed genes (DEGs) and miRNAs were identified with GEO2R. GO enrichment and KEGG pathway analysis of DEGs were performed with the R package clusterProfiler. The interaction network of DEGs was visualized with Cytoscape, and clusters and key genes were identified. According to the key DEGs, a prognostic risk model of GC was established by Cox regression. The patients were subdivided into high-risk and low-risk groups based on the median value of the risk score, and the model performance was evaluated by ROC curve and survival analyses. The risk model was combined with clinicopathological features to establish a nomogram, and a calibration chart was used to evaluate the prediction accuracy of the nomogram. The ROC curve was drawn to predict the ability of genes to differentiate tumour tissues from normal tissues. The starBase database was used to construct a regulatory network consistent with the miRNA–mRNA hypothesis. The expression of COL1A2 was analysed by immunohistochemistry/immunocytochemistry (IHC/ICC) in 150 patients with gastric cancer and a GC cell line. The correlations between COL1A2 expression and clinical features were analysed. Results A total of 106 DEGs and 113 differentially expressed miRNAs were identified from the gastric cancer dataset. PPI network screening revealed the two most significant modules and identified the dominant gene. A prognostic risk model composed of six prognostic genes (COL1A2, COL1A1, COL3A1, SPARC, LUM and BGN) was constructed by Cox regression analysis. The prognosis of the high-risk group was poor (P < 0.001). ROC curve analysis (AUC = 0.732) showed that the model better predicted the 5-year survival rate of patients. In addition, the six prognostic genes had appropriate diagnostic ability for GC. A potential ceRNA network of model genes in GC was constructed through the starBase database. IHC showed that COL1A2 was highly expressed in gastric cancer and GC cells. COL1A2 expression was significantly correlated with lymph node metastasis. Conclusion This study reveals the potential biomarkers and related pathways of GC and provides a theoretical basis for the diagnosis and prognosis prediction of GC.

Tumor resection is a commonly used treatment method in clinical practice. With the increasing refinement of tumor surgery, the application of robotic-assisted surgery in clinical procedures has expanded. However, effective indicators for evaluating surgical efficacy and postoperative prognosis remain limited. This study introduced the systemic immune-inflammatory index (SII) to evaluate perioperative inflammatory responses and postoperative recovery following robotic and conventional laparoscopic surgery. A total of 81 patients who underwent robotic-assisted gastrointestinal tumor resection and 81 patients who underwent conventional laparoscopic gastrointestinal tumor resection were included. SII was calculated using the formula: platelet count × (neutrophil count/lymphocyte count). Postoperative SII, neutrophil-to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio (PLR) increased after surgery, peaked on postoperative day 3, and gradually returned toward baseline by postoperative day 7. From postoperative day 3 onward, SII and NLR values in the robotic surgery group were significantly lower than those in the laparoscopic surgery group (P < 0.05), and these differences remained significant on postoperative days 5 and 7 (P < 0.05). PLR values were significantly lower in the robotic surgery group on postoperative day 3 only (P < 0.05), whereas no significant differences were observed on postoperative days 5 or 7 (P > 0.05). Patients in the robotic surgery group also demonstrated improved postoperative recovery indicators, including earlier ambulation, earlier postoperative exhaust and feeding, lower average drainage volume and shorter postoperative hospital stay. These findings suggest that SII may serve as a useful indicator for evaluating postoperative inflammatory status and perioperative recovery following minimally invasive gastric cancer surgery.

Blastic plasmacytoid dendritic cell neoplasm (BPDCN) is a rare and highly aggressive hematologic malignancy that commonly presents with skin involvement and may also involve the bone marrow, peripheral blood, and lymph nodes. The coexistence of BPDCN with a primary solid tumor is extremely uncommon and poses substantial diagnostic and therapeutic challenges. We report a 70-year-old man who was first diagnosed with BPDCN after excision of a left forearm lesion and later developed recurrent hematemesis during chemotherapy. Subsequent endoscopic evaluation revealed a bleeding cardia lesion, and repeat biopsy confirmed poorly differentiated gastric cardia adenocarcinoma. After multidisciplinary evaluation, radical gastrectomy was performed first to control tumor-related bleeding, after which systemic chemotherapy for BPDCN was resumed. This case suggests that, in BPDCN patients who develop hematemesis, progressive anemia, or weight loss during treatment, prompt evaluation for a second primary gastrointestinal malignancy is warranted, and control of active tumor-related bleeding may need to precede hematologic therapy.

Aberrant DNA methylation (DNAm) is the most well-defined epigenetic hallmark in gastric cancer (GC), which may be associated with a variety of risk factors exposure. In this study, leveraging the multi-omics data of Genome-wide association studies (GWAS), methylation quantitative trait locus (mQTL) and expression quantitative trait locus (eQTL) collected from The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression (GTEx) Project and Gene Expression Omnibus (GEO) database, a joint analysis of cox proportional hazard regression and Summary-data-based Mendelian randomization (SMR) analysis were adapted to investigate the causal associations of DNAm, gene expression and the GC prognosis. The results showed the causal association of hypermethylation of cg16007185, down-regulation of TMX1, and poorer prognosis of GC patients. Mendelian randomization (MR) analysis revealed that exposure to PCB-99, a type of polychlorinated biphenyl, might lead to the hypermethylation of cg16007185. Mediation analysis showed the borderline mediation role of TMX1 in the association between cg16007185 and GC survival, with an indirect effect (IE) of 5.24

Aims: This study investigates the mechanisms underlying acquired resistance to FGFR tyrosine kinase inhibitor (FGFR-TKI) in gastric cancer (GC), focusing on the interplay between ferroptosis and lipid metabolism of tumor cells. Methods: We constructed FGFR-TKI-resistant cell lines from GC cells. RNA sequencing was performed to identify differentially expressed genes (DEGs) related to ferroptosis and assess lipid metabolism in resistant cells. GC microenvironment lipid profile was characterized by HPLC-MS/MS lipidomics. The effects of CHAC1 and cholesterol synthesis modulation on ferroptosis and FGFR-TKI resistance were assessed using in vitro and in vivo models. Results: We found that FGFR-TKI can induce ferroptosis in FGFR-TKI-sensitive cells, while resistant cells exhibit decreased sensitivity to ferroptosis due to reduced CHAC1 expression, a key glutathione-specific degrading enzyme. Overexpression of CHAC1 enhances FGFR-TKI cytotoxicity. Additionally, cholesterol accumulation in resistant cells, associated with diminished stearic acid (SA) uptake, confers FGFR-TKI-induced ferroptosis resistance. In vivo studies show that CHAC1 overexpression or cholesterol synthesis inhibition can reverse FGFR-TKI resistance, which is dependent on ferroptosis. Conclusions: Dysregulated lipid homeostasis downregulated CHAC1-mediated ferroptosis, leading to FGFR-TKI resistance in gastric cancer. Overexpression of CHAC1 or inhibiting cholesterol synthesis presents promising therapeutic strategies to overcome FGFR-TKI resistance in GC.

COL12A1, a collagen type XII alpha 1 chain, has an instrumental role in the extracellular matrix (ECM), but its effect on gastric cancer (GC) and clinical significance remain unclear. In this study, co-expressed differentially expressed genes (co-DEGs) were identified using Venn diagrams based on datasets from The Cancer Genome Atlas (TCGA) and the Gene Expression Omnibus (GEO) for gastric cancer RNA sequencing. Intersections between co-DEGs and TCGA prognosis-related genes were used to pinpoint genes that were differentially associated with prognosis. COL12A1 emerged as a key candidate gene. We analyzed COL12A1 expression in human GC tissues and explored its association with various clinicopathological parameters. Survival analysis, including overall survival (OS) and disease-free survival (DFS), was conducted using TCGA data, and a prognostic nomogram was constructed. The relative protein-encoding gene expression was assessed via immunohistochemistry (IHC) analysis of four downloaded datasets, along with PCR experiments. COL12A1-related DEGs were further identified using the LinkedOmics database, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. Multiple databases were analysed for the relationship between COL12A1 and methylation. Immune cell infiltration was evaluated through CIBERSORT and TIMER databases, revealing a strong correlation between COL12A1 expression and immune cell presence in the tumor microenvironment. Single-cell expression analysis using TISCH provided further insights into the cellular context of COL12A1 expression. TISCH was used to analyse the single-cell expression of COL12A1. Finally, this work examined the correlation of COL12A1 with drug sensitivity via the RNAactDrug database. COL12A1 overexpression in gastric cancer was detected and foundto be closely related to clinicopathological features. GO/KEGG functional enrichment analysis revealed that COL12A1 was associated with pathways such as extracellular structure organization, extracellular matrix organization and the collagen-containing extracellular matrix. Analysis of several databases revealed that COL12A1 was associated with gene mutation and methylation. Additionally, as revealed by CIBERSORT profiling and TIMER database analysis, COL12A1 expression is related to immune cell infiltration. Correlation analysis via the RNAactDrug website revealed that COL12A1 is associated with drug sensitivity. In conclusion, COL12A1 is significantly overexpressed in gastric cancer and is associated with tumor progression, immune infiltration, and drug sensitivity. These findings suggest that COL12A1 may serve as a potential diagnostic and therapeutic biomarker for gastric cancer.

Gastric cancer is one of the most common malignant tumours, with limited treatment options and poor prognosis in its advanced stages. In recent years, breakthroughs in tumour immunotherapy have led to immune checkpoint inhibitors becoming a new class of clinical oncology drugs. Programmed death receptor-1 (PD-1) and programmed death-ligand 1 (PD-L1) play significant roles in inhibiting T cell responses and tumour immune escape. PD-1/PD-L1 inhibitors can significantly improve the prognosis of patients with advanced gastric cancer. Moreover, the combination of administering PD-1/PD-L1 inhibitors along with chemotherapy, radiotherapy, targeted therapy, and other immunotherapies may further enhance therapeutic efficacy. However, some scientific issues need to be urgently resolved in the immunotherapy of gastric cancer, including the suboptimal efficacy of PD-1/PD-L1 inhibitor monotherapy, high incidence of immune-related adverse events, and the absence of definitive biomarkers for effectively screening treatment-sensitive populations. This article reviews the mechanism of action, therapeutic advances, adverse effects, and putative predictive biomarkers of PD-1/PD-L1 inhibitors in the treatment of advanced gastric cancer.

While Phorbol-12-myristate-13-acetate-induced protein 1 (Noxa/PMAIP1) assumes a pivotal role in numerous tumors, its clinical implications and underlying mechanisms of gastric cancer (GC) are yet enigmatic. In this investigation, our primary objective was to scrutinize the clinical relevance and potential mechanisms of Noxa in gastric cancer. Immunohistochemical analysis was conducted on tissue microarrays comprising samples from a meticulously characterized cohort of 84 gastric cancer patients, accompanied by follow-up data, to assess the expression of Noxa. Additionally, Noxa expression levels in gastric cancer clinical samples and cell lines were measured through quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot analysis. The effect of Noxa expression on the prognosis of patients with gastric cancer was evaluated using Kaplan–Meier survival. Further insight into the role of Noxa in driving gastric cancer progression was gained through an array of experimental techniques, including cell viability assays (CCK8), plate cloning assays, transwell assays, scratch assays, and real-time cell analysis (RTCA). Potential upstream microRNAs (miRNAs) that might modulate Noxa were identified through rigorous bioinformatics analysis, substantiated by luciferase reporter assays and Western blot experiments. Additionally, we utilized RNA sequencing, qRT-PCR, and Western blot to identify proteins binding to Noxa and potential downstream target. Finally, we utilized BALB/c nude mice to explore the role of Noxa in vivo. Our investigation unveiled a marked downregulation of Noxa expression in gastric cancer and underscored its significance as a pivotal prognostic factor influencing overall survival (OS). Noxa overexpression exerted a substantial inhibitory effect on the proliferation, migration and invasion of GC cells. Bioinformatic analysis and dual luciferase reporter assays unveiled the capacity of hsa-miR-200b-3p to interact with the 3′-UTR of Noxa mRNA, thereby orchestrating a downregulation of Noxa expression in vitro, consequently promoting tumor progression in GC. Our transcriptome analysis, coupled with mechanistic validation, elucidated a role for Noxa in modulating the expression of ZNF519 in the Mitophagy-animal pathway. The depletion of ZNF519 effectively reversed the oncogenic attributes induced by Noxa. Upregulation of Noxa expression suppressed the tumorigenesis of GC in vivo. The current investigation sheds light on the pivotal role of the hsa-miR-200b-3p/Noxa/ZNF519 axis in elucidating the pathogenesis of gastric cancer, offering a promising avenue for targeted therapeutic interventions in the management of this challenging malignancy.

BACKGROUND:Effective noninvasive biomarkers of gastric cancer (GC) are critical for early detection and improvement of prognosis. We performed genome-wide long non-coding RNA (lncRNA) microarray analysis to identify and validate novel GC biomarkers depending on a high-risk population cohort. METHODS:LncRNA profiles were described using the Human LncRNA Microarray between GC and control plasma samples. The differential candidate lncRNAs were validated in two stages by quantitative reverse transcription polymerase chain reaction (qRT-PCR). We further evaluated the joint effect between the GC-associated lncRNA and Helicobacter pylori (H. pylori) infection on the risk of cardia and non-cardia GC, respectively. RESULTS:Different lncRNA expression profiles were identified between GC and control plasma with a total of 1206 differential lncRNAs including 470 upregulated and 736 downregulated in GC compared with the control group. The eight significantly upregulated lncRNAs (RP11-521D12.1, AC011995.3, RP11-5P4.3, RP11-244 K5.6, RP11-422 J15.1, CTD-2306 M5.1, CTC-428G20.2, and AC009133.20) in GC cases both in the present study and a similar microarray screening study by our collaborative team were selected for a two-stage validation. After the large sample size validation, the subjects with higher expression of RP11-244 K5.6 showed a significantly increased risk of GC with an adjusted odds ratio (OR) as 2.68 and 95% confidence interval (CI) as 1.15-6.24. Joint effects between RP11-244 K5.6 expression and H. pylori infection on the risk of GC were evaluated with no statistical significance. CONCLUSIONS:Our study found different lncRNA expression profiles between GC and control plasma and preliminarily identified RP11-244 K5.6 as a potential noninvasive biomarker for GC screening.

Abstract COL12A1 has an instrumental role in the extracellular matrix (ECM), but its effect on gastric cancer (GC) as well as the clinical significance remains unclear. The co-expression differential genes (co-DEGs) were acquired from Venn diagrams via The Cancer Genome Atlas (TCGA) as well as Gene Expression Omnibus (GEO) stomach RNAseq dataset. Intersection between co-DEGs and TCGA prognosis-related genes was used to to pinpoint genes differentially associated with prognosis. The COL12A1 gene was selected as the key factor for the present work. COL12A1 level within human GC was analyzed in relation to its clinicopathological characteristics, and the TCGA database was adopted for plotting overall survival (OS) together with disease-free survival (DFS) curves, and the prognostic column. The relative protein gene expression was assessed by Human Protein Atlas (HPA) database, four downloaded datasets, along with PCR experiments. Differentially expressed genes (DEGs related to COL12A1 were detected via LinkedOmics, and subject to GO as well as KEGG analysis based on related genes. The cBioPortal and Catalogue of Somatic Mutations in Cancer databases were first utilized for the expression and identification of COL12A1-correlated mutation analysis. Multiple databases were analyzed for the relationship between COL12A1 and methylation. COL12A1 was examined using the Tumor Immune Estimation Resource (TIMER) database for identifying association of COL12A1 gene level with stomach adenocarcinoma-infiltrating immune cells. Finally, this work examined correlation of COL12A1 with drug sensitivity with RNAactDrug database. COL12A1 over-expression within gastric cancer was detected, which was closely related to clinicopathological features. GO/KEGG functional enrichment analysis revealed that COL12A1 was associated with pathways like extracellular structure organization, extracellular matrix organization and collagen-containing extracellular matrix. The analysis of several databases revealed that COL12A1 was associated with gene mutation and methylation. Additionally, as revealed by CIBERSORT profiling and TIMER database, COL12A1 expression related to immune cell infiltration. Correlation analysis through the RNAactDrug website revealed that COL12A1 is associated with drug sensitivity. COL12A1 can be a diagnostic and therapeutic biomarker for GC, which may be associated with tumor immune infiltration and drug sensitivity.

Gastric cancer is one of the most common malignancies of the digestive system with high mortality rates. Recent studies have demonstrated that circRNAs are novel noncoding RNAs that play vital roles in the tumorigenesis and development of gastric cancer. Our study found a novel circRNA, namely, hsa_circ_0107595 (also called circABCA5), that is overexpressed in gastric cancer based on circRNA sequencing. qPCR demonstrated its overexpression in gastric cancer specimens. The overexpression or knockdown of circABCA5 in gastric cancer cell lines was achieved by lentiviral-mediated transfection. All MTS, EdU, Transwell and migration assays and xenograft experiments demonstrated that circABCA5 could promote gastric cancer proliferation, invasion, and migration in vitro and in vivo. Mechanistically, both RIP and RNA pulldown assays confirmed that circABCA5 could bind to the SPI1 protein, upregulate SPI1 expression, and promote its nuclear translocation. SPI1 could further promote the malignant phenotype of gastric cancer by activating IL6/JAK2/STAT3 signaling. In addition, EIF4A3 could directly bind to circABCA5, promoting its stability and expression. Our study reveals that circABCA5 plays a vital role in the diagnosis and prognosis of gastric cancer and may even be developed as a molecular target for the treatment of gastric cancer.

Objective: To discuss the feasibility and safety of modified side overlap with fundoplication by Yamashita (mSOFY) in laparoscopic proximal gastrectomy. Methods: Using the method of descriptive case series study, the clinical data of 9 patients with upper gastric cancer who successfully performed mSOFY anastomosis from March 2022 to October 2022 in the Affiliated Huaian No.1 People's Hospital of Nanjing Medical University were retrospectively analyzed.The reconstruction steps of mSOFY anastomosis are as follows: (1) Make a small incision on the right side of the esophageal stump and in front of the anterior wall of the gastric stump; (2) The 45mm linear cutting stapler is placed into the preset anastomosis of the esophagus and the remnant stomach, and the esophagus is rotated 90° counterclockwise along the axis, so that the right wall of the esophagus is anastomosed with the remnant stomach, and the stomach wall is sutured to the left side of the esophagus; (3) The common opening of esophagus and remnant stomach was sutured with inverted suture; (4)Suture the left and lower sides of the esophagus with the remnant stomach to make the esophagus flat against the stomach wall; (5) Open the sutured common opening: due to the pressure of the false dome, the posterior wall of the lower esophageal segment was compressed into a valve-like structure. We mainly observing the postoperative reflux and nutritional improvement of the patients, and recording the intraoperative situation and postoperative complications. Results: Nine patients with upper gastric cancer who completed laparoscopic proximal gastrectomy (mSOFY anastomosis) did not have conversion to laparotomy or intraoperative / postoperative complications. The operation time was (169.4±10.4) minutes, the anastomotic reconstruction time was (51.7±7.1) minutes, the intraoperative bleeding volume was (98.9±43.4) ml, and the number of lymph nodes dissected was (27.2±6.7). The patient recovered well after operation, without any complaints related to reflux esophagitis. Postoperative gastrointestinal radiography showed that the anastomosis was smooth, without stenosis and leakage. The serum albumin [(41.6±3.4) L vs. (39.9±2.6) L], prealbumin [(211.3±38.6) mg/L vs. (205.3±36.0) mg/L], and hemoglobin levels [(126.7±13.2) g/L vs. (121.0±9.7) g/L] of patients before and one month after surgery have no statistically significant differences (all P>0.05). Conclusion: mSOFY anastomosis can be used as one of the safe and feasible reconstruction methods in laparoscopic proximal gastrectomy.

佛波醇-12-肉豆蔻酸-13-乙酸酯诱导蛋白-1(phorbol-12-myristate-13-acetate-induced protein 1,PMAIP1)是一种肿瘤抑制基因,是p53相关凋亡途径的重要介质.同时,PMAIP1也属于B淋巴细胞瘤-2基因(B-cell lympho-ma-2,Bcl-2)家族中促凋亡的 BH3-only亚家族成员之一,可以通过p53依赖途径或p53非依赖途径来影响细胞的增殖及凋亡过程,在肿瘤的发生、发展以及相应的治疗中发挥着重要作用.本文将对近年来PMAIP1基因在恶性肿瘤中的研究进展进行综述,以期为相应肿瘤的治疗带来一定的帮助.

The Hedgehog signaling pathway participates in the occurrence and progression of cancers including gastric cancer. We conducted this study to evaluate whether genetic variants in the Hedgehog signaling pathway genes would affect gastric cancer risk. Multi-marker Analysis of GenoMic Annotation (MAGMA) was used to investigate the aggregated genetic effects of single nucleotide polymorphisms (SNPs) assigned to candidate genes. The relationship between SNPs and gastric cancer risk was estimated by multivariate logistic regression analyses. Gene expression was calculated using databases obtained from The Cancer Genome Atlas (TCGA) and The Gene Expression Omnibus (GEO). Kaplan-Meier plotter was used to evaluate the association between gene expression with gastric cancer survival. Tumor Immune Estimation Resource 2.0 (TIMER 2.0) was applied to determine the correlation between selected gene expression and the immune cell infiltration degree. We identified that the G allele of rs2990912 in KIF27 was associated with higher gastric cancer risk, especially in the young and male subgroups. The expression of KIF27 in gastric cancer tissues was higher than that in normal tissues, leading to poor survival in gastric cancer patients. Besides, KIF27 expression was related to immune cell infiltration and positively correlated with PD-L1 expression. Our findings highlight the key role of genetic variation in the Hedgehog signaling pathway genes in gastric cancer susceptibility, which may provide important insights into the diagnosis, prognosis, and treatment of gastric cancer.

Epigenetic complex NuRD (nucleosome remodeling and deacetylase) engages in a range of basic cellular processes, including chromatin modification. Changes in the activity of NuRD complex can influence gastric cancer progression. Multivariate logistic regression analyses were used to estimate the association between single-nucleotide polymorphisms (SNPs) and gastric cancer risk. Expression quantitative trait loci (eQTL) analysis was used to analyze the relationship between the genotypes and gene expression levels using data from the genotype tissue expression project (GTEx). Gene expression was calculated using databases from The Cancer Genome Atlas (TCGA) and The Gene Expression Omnibus (GEO). Kaplan–Meier plotter was used to evaluate the association between gene expression and survival. SNP rs11064275 T allele in CHD4, rs892022 A allele and rs2033481 A allele in GATAD2A were found to contribute to the decreased risk of gastric cancer. The increase in the number of favorable alleles of these three SNPs was associated with a lower risk of gastric cancer. rs2033481 and rs892022 were substantially correlated with GATAD2A mRNA expression levels. Meanwhile, we detected that the CHD4 and GATAD2A mRNA expression was increased in gastric cancer tissues compared with the adjacent normal tissues. Furthermore, we found that patients with higher CHD4 or GATAD2A mRNA expression level had more advantageous overall survival. Our findings indicated that genetic variants in NuRD complex subunits encoding genes may be promising predictors of gastric cancer risk.

The purpose of our investigation is to explore the putative molecular mechanisms underpinning LINC00858 involvement in colon cancer. The expression of LINC00858 in TCGA data was identified using the GEPIA website. Colon cancer cancerous tissues were clinically collected. The expression of LINC00858, RAD21, and PCNP in colon tissues or cells was determined using RT-qPCR. The interactions among LINC00858, RAD21, and PCNP promoter region were determined by means of RNA pull down, RIP, and ChIP assays. Cell proliferative, apoptotic, invasive, and migrated capabilities were evaluated. Western blot was conducted to determine RAD21, PCNP, phosphorylated (p)-STAT3, STAT3, p-STAT5 and STAT5 and apoptosis related proteins. A nude mouse model of colon cancer was constructed and tumorigenesis of colon cancer cells was observed. LINC00858 was upregulated in cancerous tissues and cells. LINC00858 recruited the transcription factor RAD21. Overexpression of LINC00858 promoted the binding of RAD21 and PCNP promoter region, which increased the expression of PCNP. Silencing of RAD21 or PCNP reversed the promoting effect of LINC00858 on the disease initiation and development. PCNP silencing inhibited proliferative ability and promoted apoptotic ability of cancerous cells via STAT3/5 inhibition, which was reversed by colivelin-activated STAT3. In vivo experiments further verified that LINC00858 enhanced the tumorigenicity of colon cancer cells in vivo by regulating the RAD21/PCNP/STAT3/5 axis. It indicated the promoting role of LINC00858 in colon cancer progression though activating PCNP-mediated STAT3/5 pathway by recruiting RAD21.

目的 比较分析内镜下全层切除术(EFTR)与内镜下黏膜剥离术(ESD)在治疗直径≤10 mm直肠神经内分泌瘤的治疗效果.方法 回顾性选取2017年1月至2021年10月于南京医科大学附属淮安第一医院内镜下切除的直径≤10 mm直肠NETs患者49例为研究对象,其中EFTR组21例,ESD组28例.比较两组病灶大小、操作时间、组织学完全切除率、住院费用、住院时间等.结果 EFTR组和ESD组的年龄及性别在组间均衡.两组患者术中、术后均无出血、继发感染.两组的病灶大小及操作时间比较,差异无统计学意义(P>0.05).EFTR组的组织学完全切除率为100％,显著高于ESD组的82.1％(P<0.05).EFTR组的住院费用及住院时间均与ESD组相似,差异均无统计意义(P>0.05).结论 EFTR在切除≤10 mm直肠NETs的治疗中术中、术后出血及继发感染风险低,组织学完整切除率较ESD组高,是一种安全、有效的手术方式.

Long non-coding RNAs (lncRNAs) play important roles in a range of different human cancers. However, the role of lncRNA solute carrier organic anion transporter family member 4A1-AS1 (SLCO4A1-AS1) in colon cancer remains enigmatic. Hence, we aimed to explore the specific role of SLCO4A1-AS1 in colon cancer stem cells. Colon cancer-related differentially expressed lncRNA and mRNA were screened using microarray-based analysis, and the expression of SLCO4A1-AS1 and SLCO4A1 in colon cancer tissues was determined using reverse transcription quantitative polymerase chain reaction and western blot analysis. The interaction among SLCO4A1-AS1, microRNA-150-3p (miR-150-3p) and SLCO4A1 was verified using dual-luciferase reporter assay, RNA immunoprecipitation and RNA pull-down. Moreover, SLCO4A1-AS1, miR-150-3p and/or SLCO4A1 were overexpressed or depleted in colon cancer cells to detect their effects on migration, invasion, sphere formation, apoptosis and tumorigenesis abilities of colon cancer stem CD133+CD44+ cells using both in vitro and in vivo assays. SLCO4A1-AS1 and SLCO4A1 were screened as the differentially expressed lncRNA and mRNA in colon cancer tissues. SLCO4A1-AS1 was confirmed to competitively bind to miR-150-3p to elevate SLCO4A1 expression. Moreover, knockdown of SLCO4A1-AS1 decreased SLCO4A1 expression, thus inhibiting cell migration, invasion, sphere formation, and tumorigenesis abilities and enhancing the apoptosis of CD133+CD44+ cells. Collectively, these findings provide evidence demonstrating that depleting SLCO4A1-AS1 competitively binds to miR-150-3p, which downregulates SLCO4A1 expression, thus hindering colon cancer progression. This study reports that long non-coding RNA lncRNA SLCO4A1-AS1 regulates the characteristics of colon cancer stem cells. Moreover, SLCO4A1 targets miR-150-3p. LncRNA SLCO4A1-AS1 can be used as ceRNA to adsorb miR-150-3p and thus affect the expression of SLCO4A1. Mechanistically, miR-150-3p can downregulate SLCO4A1, thereby inhibiting migration, invasion, spheroidization and tumor formation of colon cancer stem cells. This study lays a theoretical foundation for in-depth understanding of the pathogenesis of colon cancer and points to new therapeutic targets.