The transition of surgical simulation training and its learning curve: a bibliometric analysis from 2000 to 2023.

BACKGROUND: Proficient surgical skills are essential for surgeons, making surgical training an important part of surgical education. The development of technology promotes the diversification of surgical training types. This study analyzes the changes in surgical training patterns from the perspective of bibliometrics, and applies the learning curves as a measure to demonstrate their teaching ability. METHOD: Related papers were searched in the Web of Science database using the following formula: TS=((training OR simulation) AND (learning curve) AND (surgical)). Two researchers browsed the papers to ensure that the topics of articles were focused on the impact of surgical simulation training on the learning curve. CiteSpace, VOSviewer and R packages were applied to analyze the publication trends, countries, authors, keywords and references of selected articles. RESULT: Ultimately, 2461 documents were screened and analyzed. The USA is the most productive and influential country in this field. Surgical endoscopy and other interventional techniques publish the most articles, while surgical endoscopy and other interventional techniques is the most cited journal. Aggarwal Rajesh is the most productive and influential author. Keyword and reference analyses reveal that laparoscopic surgery, robotic surgery, virtue reality (VR) and artificial intelligence (AI) were the hotspots in the field. CONCLUSION: This study provided a global overview of the current state and future trend in the surgical education field. The study surmised the applicability of different surgical simulation types by comparing and analyzing the learning curves, which is helpful for the development of this field.

Insights into the history and tendency of glycosylation and digestive system tumor: A bibliometric-based visual analysis.

BACKGROUND: Glycosylation, a commonly occurring post-translational modification, is highly expressed in several tumors, specifically in those of the digestive system, and plays a role in various cellular pathophysiological mechanisms. Although the importance and detection methods of glycosylation in digestive system tumors have garnered increasing attention in recent years, bibliometric analysis of this field remains scarce. The present study aims to identify the developmental trends and research hotspots of glycosylation in digestive system tumors. AIM: To find and identify the developmental trends and research hotspots of glycosylation in digestive system tumors. METHODS: We obtained relevant literature from the Web of Science Core Collection and employed VOSviewer 1.6.19 and CiteSpace (version 6.1.R6) to perform bibliometric analysis. RESULTS: A total of 2042 documents spanning from 1978 to the present were analyzed, with the research process divided into three phases: the period of obscurity (1978-1990), continuous development period (1991-2006), and the rapid outbreak period (2007-2023). These documents were authored by researchers from 66 countries or regions, with the United States and China leading in terms of publication output. Reis Celso A had the highest number of publications, while Pinho SS was the most cited author. Co-occurrence analysis revealed the most popular keywords in this field are glycosylation, expression, cancer, colorectal cancer, and pancreatic cancer. Furthermore, the Journal of Proteome Research was the most prolific journal in terms of publications, while the Journal of Biological Chemistry had the most citations. CONCLUSION: The bibliometric analysis shows current research focus is primarily on basic research in this field. However, future research should aim to utilize glycosylation as a target for treating tumor patients.

[Circular RNA-Encoded Proteins in Gastrointestinal Cancer:A Review].

Circular RNAs(CircRNAs)are a class of non-coding RNAs with a covalently closed-loop structure,high stability,and tissue specificity,with the production mechanisms different from linear RNAs.Recent studies have discovered that some CircRNAs can encode proteins via cap-independent translation mechanisms such as internal ribosome entry site,N6-methyladenosine,and rolling loop translation.The encoded proteins regulate homologous linear proteins or downstream signaling pathways via protein bait or other mechanisms,thereby exerting biological functions.Studies have shown that CircRNAs play a role in various diseases,especially in tumor progression,proliferation,invasion,and metastasis and immune regulation.Therefore,by elucidating the expression and roles of proteins encoded by CircRNAs in tumorigenesis and development,this paper is expected to provide new tumor markers and potential targets for tumor diagnosis and treatment.

High-Throughput Analysis of Leaf Chlorophyll Content in Aquaponically Grown Lettuce Using Hyperspectral Reflectance and RGB Images.

Chlorophyll content reflects plants' photosynthetic capacity, growth stage, and nitrogen status and is, therefore, of significant importance in precision agriculture. This study aims to develop a spectral and color vegetation indices-based model to estimate the chlorophyll content in aquaponically grown lettuce. A completely open-source automated machine learning (AutoML) framework (EvalML) was employed to develop the prediction models. The performance of AutoML along with four other standard machine learning models (back-propagation neural network (BPNN), partial least squares regression (PLSR), random forest (RF), and support vector machine (SVM) was compared. The most sensitive spectral (SVIs) and color vegetation indices (CVIs) for chlorophyll content were extracted and evaluated as reliable estimators of chlorophyll content. Using an ASD FieldSpec 4 Hi-Res spectroradiometer and a portable red, green, and blue (RGB) camera, 3600 hyperspectral reflectance measurements and 800 RGB images were acquired from lettuce grown across a gradient of nutrient levels. Ground measurements of leaf chlorophyll were acquired using an SPAD-502 m calibrated via laboratory chemical analyses. The results revealed a strong relationship between chlorophyll content and SPAD-502 readings, with an R2 of 0.95 and a correlation coefficient (r) of 0.975. The developed AutoML models outperformed all traditional models, yielding the highest values of the coefficient of determination in prediction (Rp2) for all vegetation indices (VIs). The combination of SVIs and CVIs achieved the best prediction accuracy with the highest Rp2 values ranging from 0.89 to 0.98, respectively. This study demonstrated the feasibility of spectral and color vegetation indices as estimators of chlorophyll content. Furthermore, the developed AutoML models can be integrated into embedded devices to control nutrient cycles in aquaponics systems.

Lactylation of METTL16 promotes cuproptosis via m6A-modification on FDX1 mRNA in gastric cancer.

Cuproptosis, caused by excessively high copper concentrations, is urgently exploited as a potential cancer therapeutic. However, the mechanisms underlying the initiation, propagation, and ultimate execution of cuproptosis in tumors remain unknown. Here, we show that copper content is significantly elevated in gastric cancer (GC), especially in malignant tumors. Screening reveals that METTL16, an atypical methyltransferase, is a critical mediator of cuproptosis through the m6A modification on FDX1 mRNA. Furthermore, copper stress promotes METTL16 lactylation at site K229 followed by cuproptosis. The process of METTL16 lactylation is inhibited by SIRT2. Elevated METTL16 lactylation significantly improves the therapeutic efficacy of the copper ionophore- elesclomol. Combining elesclomol with AGK2, a SIRT2-specific inhibitor, induce cuproptosis in gastric tumors in vitro and in vivo. These results reveal the significance of non-histone protein METTL16 lactylation on cuproptosis in tumors. Given the high copper and lactate concentrations in GC, cuproptosis induction becomes a promising therapeutic strategy for GC.

A bibliometric study and visualization analysis of ferroptosis-inducing cancer therapy.

Ferroptosis is a form of regulated cell death that was first formally proposed a decade ago. While its role in cancer cell death was initially understudied, it has recently gained considerable interest from researchers. In recent years, a growing number of studies have focused on the role of ferroptosis in cancer progression, with the goal of developing novel ferroptosis-inducing cancer therapies. This study aims to present the developmental trend and hotspots of research on ferroptosis-inducing cancer therapy using bibliometric analysis. A literature search was conducted using the Web of Science Core Collection on October 1st, 2022, to retrieve articles and reviews pertaining to ferroptosis and cancer published from 2012 to 2022. Microsoft Excel 2016, VOSviewer 1.6.18 and CiteSpace (version 6.1. R6) were utilized to conduct the bibliometric analysis of publication trends, authorship, and citation networks, with a focus on identifying countries, institutions, journals, and authors contributing to the field. These analyses were used to predict future trends in this area. A total of 2839 articles were identified and extracted for analysis. The number of publications has increased almost every year, with a sharp increase after 2018. China produced the most publications in this area, followed by the United States. Central South University was the institution that published the most papers. Frontiers in Oncology was the journal with the highest number of publications, while Cell had the greatest impact factor. Daolin Tang was the most productive author and Dixon SJ was the most influential author. Co-occurrence and burst analyses of keywords and references were conducted to identify the developmental trends and hotspots in ferroptosis-inducing cancer therapy research. Main research directions have shifted from investigating the mechanism of ferroptosis to developing novel ferroptosis-targeting cancer therapies. Emerging topicsfocus on the role of ferroptosis in solid tumor therapy. Based on our bibliometric analysis, we predict that research on ferroptosis in cancer therapy will continue to be a hot topic in the future, with a growing number of treatment modalities related to ferroptosis being developed. Our study provides valuable insights into the current state and future trends of research in this field, serving as a useful guide for researchers seeking to make important contributions in this area.

Exosomal ACADM sensitizes gemcitabine-resistance through modulating fatty acid metabolism and ferroptosis in pancreatic cancer.

This study aimed to evaluate the potential of exosomes from cancer cells to predict chemoresistance in pancreatic cancer (PC) and explore the molecular mechanisms through RNA-sequencing and mass spectrometry. We sought to understand the connection between the exosomal Medium-chain acyl-CoA dehydrogenase (ACADM) level and the reaction to gemcitabine in vivo and in patients with PC. We employed loss-of-function, gain-of-function, metabolome mass spectrometry, and xenograft models to investigate the effect of exosomal ACADM in chemoresistance in PC. Our results showed that the molecules involved in lipid metabolism in exosomes vary between PC cells with different gemcitabine sensitivity. Exosomal ACADM (Exo-ACADM) was strongly correlated with gemcitabine sensitivity in vivo, which can be used as a predictor for postoperative gemcitabine chemosensitivity in pancreatic patients. Moreover, ACADM was found to regulate the gemcitabine response by affecting ferroptosis through Glutathione peroxidase 4 (GPX4) and mevalonate pathways. It was also observed that ACADM increased the consumption of unsaturated fatty acids and decreased intracellular lipid peroxides and reactive oxygen species (ROS) levels. In conclusion, this research suggests that Exo-ACADM may be a viable biomarker for predicting the responsiveness of patients to chemotherapy.

Deubiquitinase UCHL5 stabilizes ELK3 to potentiate cancer stemness and tumor progression in pancreatic adenocarcinoma (PAAD).

Aberrant ubiquitin-proteasome system (UPS) contributes to tumorigeneisis or drug resistance of Pancreatic Adenocarcinoma (PAAD). Previous studies have implicated the deubiquitinase UCHL5 was abnormally expressed in multiple malignancies. However, little was reported about the specific roles of UCHL5 in PAAD. We aimed to identify the biological roles of UCHL5 in PAAD and demonstrate its prognostic significance. Differential analysis revealed that UCHL5 expressed highly in tumors versus normal tissues, like TCGA-PAAD, GSE28735, GSE15471 and collected samples. Patients with high UCHL5 expressions had worse survival outcomes relative to those with low UCHL5 levels. Experimental assays showed that UCHL5 overexpression could significantly enhance cell proliferation, colony formation and self-renewal capacities. UCHL5 could also promote PAAD migration in vitro and in vivo. Mechanistically, UCHL5 could directly deubiquitinate and stabilize ELK3 proteins. UCHL5 relied on accumulated ELK3 proteins to drive cell growth, stem-like properties and migration abilities. In addition, enrichment analysis based on RNA-seq data implicated that ELK3 mainly correlated with Notch1 signaling and ELK3 could notably elevate ELK3 mRNA levels. UCHL5 could thus promote self-renewal abilities of PAAD and targeting ELK3 could inhibit the stemness features. In contrast, UCHL5 deficiency could suppress PAAD stemness features, and ectopic expression of ELK3 could rescue this effect. Last of all, we utilized the UCHL5 inhibitor, b-AP15, to treat PAAD cells and found that b-AP15 could inhibit the growth of PAAD cells in a dose-dependent manner. Collectively, our study uncovered the underlying mechanisms of UCHL5/ELK3/Notch1 axis in PAAD progression and stemness maintaince, shedding light on individualized treatment and risk stratification for PAAD patients.

Long noncoding RNA negative regulator of antiviral response contributes to pancreatic ductal adenocarcinoma progression via targeting miR-299-3p.

BACKGROUND: Pancreatic ductal cancer (PDAC) has high malignancy and poor prognosis. Long noncoding RNAs (lncRNAs) are associated with high levels of malignancy, including PDAC. However, the biological and clinical significance of negative regulator of antiviral response (NRAV) in PDAC is unclear. AIM: To study the regulatory role of lncRNA NRAV in PDAC. METHODS: GEPIA analyzed lncRNA NRAV and miRNA (miR-299-3p) expression levels in PDAC tissues and measured them in PDAC cells by quantitative measurements in real time. The specific role of NRAV and miR-299-3p in cell proliferation and transfer potential was evaluated by cell formation analysis, Cell Counting Kit-8 and Transwell analysis. The relationship between NRAV and miR-299-3p was studied by predictive bioinformatics, RNA immunoassay, and fluorescence enzyme analysis. In vivo experiments included transplantation of simulated tumor cells under naked mice. RESULTS: The expression level of lncRNA NRAV was higher in both tumor tissues and cell lines of PDAC and was negatively associated with the clinical survival of PDAC patients. Functionally, overexpression of NRAV promoted cell proliferation and metastasis of PDAC cells, while knockdown of NRAV reversed these effects. Finally, NRAV was performed as a molecular sponge of miR-299-3p. Moreover, overexpression of miR-299-3p could reverse the promoting effects of NRAV on cell proliferation and metastasis of PDAC cells. CONCLUSION: NRAV facilitates progression of PDAC as a molecular sponge of miR-299-3p and may be a potential molecular marker for diagnosis and treatment of PDAC.

Correction to "Genome-wide CRISPR-Cas9 screening identifies that hypoxia-inducible factor-1a-induced CBX8 transcription promotes pancreatic cancer progression via IRS1/AKT axis".

[This corrects the article on p. 1709 in vol. 13, PMID: 34853645.].

Exosomal MicroRNA signature acts as an efficient biomarker for non-invasive diagnosis of gallbladder carcinoma.

Through a three-step study that relies on biomarker discovery, training, and validation, we identified a set of five exosomal microRNAs (miRNAs) that can be used to evaluate the risk of gallbladder carcinoma (GBC), including miR-552-3p, miR-581, miR-4433a-3p, miR-496, and miR-203b-3p. When validated in 102 GBC patients and 112 chronic cholecystitis patients from multiple medical centers, the AUC of this combinatorial biomarker was 0.905, with a sensitivity of 81.37% and a specificity of 86.61%. The performance of this biomarker is superior to that of the standard biomarkers CA199 and CEA and is suited for GBC early diagnosis. The multi-clinicopathological features and prognosis of GBC patients were significantly associated with this biomarker. After building a miRNA-target gene regulation network, cell functions and signaling pathways regulated by these five miRNAs were examined. This biomarker signature can be used in the development of a noninvasive tool for GBC diagnosis, screening and prognosis prediction.

Towards a fast and generalized microplastic quantification method in soil using terahertz spectroscopy.

Extensive investigation of microplastic abundance in soil environment calls for rapid, accurate, efficient and harmonized quantification methods. Development of rapid quantification method requires made-to-measure soil samples with additions of standard polymers. Existing rapid quantification methods ignore the gap between standard polymers in laboratory and household microplastics in soil environment. Here, terahertz (0.6-1.67 thz) and NIR (950-1660 nm) spectroscopy were compared to explore a fast, accurate and potentially generalizable microplastic quantification method in soil. Soil sample was spiked with two standard polymers (polyvinyl chloride (PVC) and polystyrene (PS)) and their additive-containing household microplastics. Two standard sample sets and two household sample sets were prepared in concentrations ranging from 0.5 to 10%. Nine commonly used preprocessing methods and three machine learning algorithms were coupled to develop methods. Models were constructed by training sets from standard sample sets. When models transferred to household samples, prediction error (RMSE) of proposed terahertz method (Wdenosie_PLSR) only increased by 0.4% for PVC and 0.19% for PS, yet that of the NIR method increased by 1.49% and 1.16% respectively. The proposed terahertz method presented a detection limit around 1.12% and the NIR method showed a detection limit around 3.24%. Overall, our results suggest that compared with NIR method, the proposed terahertz method is not only more accurate but also demonstrate stronger generalizability to bridge the gaps between standard PVC/PS polymers and household PVC/PS microplastics. We also propose MMD heatmap for diagnosing spectral preprocessing methods to further improve method efficiency.

Advances in infrared spectroscopy combined with artificial neural network for the authentication and traceability of food.

The authentication and traceability of food attract more attention due to the increasing consumer awareness regarding nutrition and health, being a new hotspot of food science. Infrared spectroscopy (IRS) combined with shallow neural network has been widely proven to be an effective food analysis technology. As an advanced deep learning technology, deep neural network has also been explored to analyze and solve food-related IRS problems in recent years. The present review begins with brief introductions to IRS and artificial neural network (ANN), including shallow neural network and deep neural network. More notably, it emphasizes the comprehensive overview of the advances of the technology combined IRS with ANN for the authentication and traceability of food, based on relevant literature from 2014 to early 2020. In detail, the types of IRS and ANN, modeling processes, experimental results, and model comparisons in related studies are described to set forth the usage and performance of the combined technology for food analysis. The combined technology shows excellent ability to authenticate food quality and safety, involving chemical components, freshness, microorganisms, damages, toxic substances, and adulteration. As well, it shows excellent performance in the traceability of food variety and origin. The advantages, current limitations, and future trends of the combined technology are further discussed to provide a thoughtful viewpoint on the challenges and expectations of online applications for the authentication and traceability of food.

Genome-wide CRISPR-Cas9 screening identifies that hypoxia-inducible factor-1a-induced CBX8 transcription promotes pancreatic cancer progression via IRS1/AKT axis.

BACKGROUND: Pancreatic cancer (PC) is one of the most lethal malignancies worldwide. It is known that the proliferation of PC cells is a critical process in the disease. Previous studies have failed to identify the key genes associated with PC cell proliferation, using bioinformatic analysis, genome-wide association studies, and candidate gene testing. AIM: To investigate the function of the chromobox 8 (CBX8)/receptor substrate 1 (IRS1)/AKT axis in PC. METHODS: A genome-wide CRISPR-Cas9 screening was performed to select genes that could facilitate PC cell proliferation. Quantitative reverse transcription-polymerase chain reaction was used to detect the expression of CBX8 in PC tissues and cells. The regulatory roles of CBX8 in cell proliferation, migration, and invasion were verified by in vivo and in vitro functional assays. RESULTS: CBX8 was upregulated in PC tissues and shown to drive PC cell proliferation. Higher expression of CBX8 was correlated with worse outcomes of PC patients from two independent cohorts comprising a total of 116 cases. CBX8 was also proved to serve as a promising therapeutic target for a PC xenograft model. We demonstrated that hypoxia-inducible factor (HIF)-1a induced CBX8 transcription by binding to the promoter of CBX8. CBX8 efficiently activated the PI3K/AKT signaling by upregulating insulin IRS1. CONCLUSION: CBX8 is a key gene regulated by HIF-1α, and activates the IRS1/AKT pathway, which suggests that targeting CBX8 may be a promising therapeutic strategy for PC.

Development and Validation of the Individualized Prognostic Nomograms in Patients With Right- and Left-Sided Colon Cancer.

BACKGROUND: The overall survival (OS) of patients diagnosed with colon cancer (CC) varied greatly, so did the patients with the same tumor stage. We aimed to design a nomogram that is capable of predicting OS in resected left-sided colon cancers (LSCC) and right-sided colon cancers (RSCC), and thus to stratify patients into different risk groups, respectively. METHODS: Records from a retrospective cohort of 577 patients with complete information were used to construct the nomogram. Univariate and multivariate analyses screened risk factors associated with overall survival. The performance of the nomogram was evaluated with concordance index (c-index), calibration plots, and decision curve analyses for discrimination, accuracy, calibration ability, and clinical net benefits, respectively, which was further compared with the American Joint Committee on Cancer (AJCC) 8th tumor-node-metastasis (TNM) classification. Risk stratification based on nomogram scores was performed with recursive partitioning analysis. RESULTS: The LSCC nomogram incorporated carbohydrate antigen 12-5 (CA12-5), age and log odds of positive lymph nodes (LODDS), and RSCC nomogram enrolled tumor stroma percentage (TSP), age and LODDS. Compared with the TNM classification, the LSCC and RSCC nomograms both had a statistically higher C-index (0.837, 95% CI: 0.827-0.846 and 0.780, 95% CI 0.773-0.787, respectively) and more clinical net benefits, respectively. Calibration plots revealed no deviations from reference lines. All results were reproducible in the validation cohort. CONCLUSIONS: An original predictive nomogram was constructed and validated for OS in patients with CC after surgery, which had facilitated physicians to appraise the individual survival of postoperative patients accurately and to identify high-risk patients who were in need of more aggressive treatment and follow-up strategies.

The novel circSLC6A6/miR-1265/C2CD4A axis promotes colorectal cancer growth by suppressing p53 signaling pathway.

BACKGROUND: Colorectal cancer (CRC) is one of the most frequent malignancy and a leading cause of cancer-related deaths. Therefore, further researches are required to identify novel and more effective diagnoses and to identify molecular targets in treatment of CRC. METHODS: C2CD4A expression in CRC tissues and cell lines was detected by qRT-PCR and western blot. The biological functions of C2CD4A were performed both in vitro and in vivo. Western blot, cDNA array, IP-MS, Co-immunoprecipitation assay, and Ubiquitination assay were used to analyze the interaction between C2CD4A and p53. Bioinformatics analysis, FISH, RNA sequencing, luciferase reporter assay, RNA immunoprecipitation, RNA pull-down and rescue experiments, were deployed to detect upstream regulation mechanism of C2CD4A. RESULTS: C2CD4A was elevated in CRC tissues compared with adjacent normal colorectal tissues. C2CD4A knockdown significantly promoted cell apoptosis and with inhibited proliferation in vitro, and tumorigenicity in vivo, whereas C2CD4A overexpression led to opposite effects. Moreover, circSLC6A6 was upregulated and shown to positively regulate C2CD4A expression via sponging miR-1265. Fundamentally, C2CD4A inhibited p53 signaling pathway through interacting with p53 and increasing its ubiquitination and degradation. CONCLUSION: Our results identified that circSLC6A6/miR-1265/C2CD4A axis, which was involved in CRC via the p53 signaling pathway, may serve as a therapeutic target for CRC.

Low expression of KIF20A suppresses cell proliferation, promotes chemosensitivity and is associated with better prognosis in HCC.

This study analysed the microarray datasets from Gene Expression Omnibus (GEO) database, and aimed to identify novel potential hub genes associated with the progression of HCC via bioinformatics analysis and experimental validation. The common differentially expressed genes (DEGs) from five GEO datasets were screened using GEO2R tool. The expression and survival analysis of hub genes in HCC were performed using Gene Expression Profiling Interactive Analysis, UALCAN and Kaplan-Meier plotter tools. In vitro functional assays were used to determine the caspase-3, -9, cell proliferation and chemo-sensitivity of HCC cells. A total of 177 common DEGs were identified between normal liver and HCC tissues among these datasets. Functional enrichment and PPI network analysis identified 22 hub genes from the common DEGs. The mRNA expression of 22 hub genes was all significantly up-regulated in HCC tissues compared to that in normal liver tissues. Further survival analysis showed that 10 hub genes predicted poor prognosis of patients with HCC. More importantly, the in vitro functional studies demonstrated that KIF20A knockdown suppressed the HCC cell proliferation and promoted the chemosensitivity of HCC cells to cisplatin and sorafenib. In conclusion, the present study identified a total of 177 common DEGs among 5 GEO microarray datasets and found that 10 hub genes could predict the poor prognosis of patients with HCC using the comprehensive bioinformatics analysis. Furthermore, KIF20A silence suppressed cell proliferation and enhanced chemosensitivity in HCC cells. Further studies may be required to determine the mechanistic role of these hub genes in HCC progression.

hsa-miR-15b-5p regulates the proliferation and apoptosis of human vascular smooth muscle cells by targeting the ACSS2/PTGS2 axis.

A previous bioinformatic analysis from our group predicted that the interaction of microRNA (miRNA/miR)-15b with the acyl-CoA synthetase short chain family member 2 (ACSS2) gene was important for the development of abdominal aortic aneurysm (AAA). Apoptosis of aortic vascular smooth muscle cells (VSMCs) is a pathological feature of AAA. The present study aimed to explain the roles of miR-15b/ACSS2 in AAA by exploring their effects on the proliferation and apoptosis of aortic VSMCs. Human aortic VSMCs (T/G HA-VSMC cell line) were divided into six groups and were transfected with miR-15b-5p mimics, mimic negative control (NC), miR-15b-5p inhibitors, inhibitor NC, miR-15b-5p mimics+pcDNA3.1 and miR-15b-5p mimics+ACSS2-overexpessing vector. CCK-8 assay was used to determine cell proliferation. Annexin V-FITC/PI staining and flow cytometry assays were used to measure cell apoptosis. Dual-luciferase reporter assays were used to confirm the targeted relationship between miR-15b-5p and ACSS2. Reverse transcription-quantitative PCR and/or western blotting were used to examine the expression levels of miR-15b-5p, ACSS2 and prostaglandin-endoperoxide synthase 2 (PTGS2). Following transfection of T/G HA-VSMCs with mimics and inhibitors to respectively upregulate and downregulate miR-15b-5p, the results demonstrated that overexpression of miR-15b-5p inhibited cell proliferation and promoted cell apoptosis; silencing of miR-15b-5p obtained the opposite results. ACSS2 may be a direct target of miR-15b-5p, since the luciferase activity of a ACSS2 wild-type vector, but not that of a ACSS2 mutant reporter, was significantly inhibited by miR-15b-5p mimics compared with controls. Additionally, the expression levels of ACSS2 and its downstream gene PTGS2 were significantly reduced or increased following transfection with miR-15b-5p mimics or inhibitors, respectively. Furthermore, overexpression of ACSS2 reversed the antiproliferative and proapoptotic effects of miR-15b-5p mimics by blocking the production of PTGS2 protein. In conclusion, miR-15b-5p may promote the apoptosis and inhibit the proliferation of aortic VSMCs via targeting the ACSS2/PTGS2 axis. The present study provided preliminary evidence indicating that the miR-15b-5p/ACSS2/PTGS2 axis may be a potential target for the treatment of AAA.

Prognostic implications of ENE and LODDS in relation to lymph node-positive colorectal cancer location.

BACKGROUND: Extranodal extension (ENE) and log odds of positive lymph nodes (LODDS) are associated with the aggressiveness of both colon and rectal cancers. The current study evaluated the clinicopathological significance and the prognostic impact of ENE and LODDS in the colon and rectal patients independently. METHODS: The clinical and histological records of 389 colorectal cancer (CRC) patients who underwent curative surgery were reviewed. RESULTS: For the ENE system, 244 patients were in the ENE1 group and 145 in the ENE2 system. Compared with the ENE1 system, the patients included in the ENE2 system were prone to nerve invasion (P < 0.001) and vessel invasion (P < 0.001) with higher TNM (P = 0.009), higher T category (P = 0.003), higher N category (P < 0.001), advanced differentiation (P = 0.013), more number of positive lymph nodes (NPLN) (P < 0.001), more lymph node ratio (LNR) (P < 0.001), and a higher value of LODDS (P < 0.001). ENE was more frequent in patients with left and rectal than right cancer. For the LODDS system, 280 patients were in the LODDS1 group, and 109 in the LODDS2 group. Compared to the LODDS1 group, the patients included in the LODDS2 group were more prone to nerve invasion (P = 0.0351) and vessel invasion (P < 0.001) with a higher rate of N2 stage, less NDLN (P < 0.001), more NPLN (P < 0.001), more LNR (P < 0.001), and a higher value of ENE (P < 0.001). Based on the results in the univariable analysis, the N, NPLN, LNR, LODDS, and ENE were separately incorporated into five different Cox regression models combined with the same confounders. The multivariable Cox regression analysis demonstrated that all the five staging systems were independent prognostic factors for overall survival. CONCLUSION: The current study confirmed that the LODDS stage is an independent influence on the prognosis of both CRC and CC patients. ENE is an independent influencing factor on the prognosis of both CRC and CC patients, and the prognostic impact of extracapsular lymph node was observed in both CRC and CC. The frequency of ENE increases from the proximal (right) to the distal (left) colon as well as the rectum. Therefore, combining ENE and LODDS into the current TNM system to compensate for the inadequacy of pN staging needs further investigation.

Aberrant Non-Coding RNA Expressed in Gastric Cancer and Its Diagnostic Value.

Gastric cancer (GC) is one of the digestive tract malignancies with high invasion and mortality rates. Recent studies have reported that non-coding RNAs (ncRNAs) seem to play a crucial part in many tumors. Due to their high stability, ncRNAs may used as novel biomarkers to predict the occurrence and prognosis of GC. Here, we measured miRNA, lncRNA and cirRNA expression profiles of GC patients by using microarray and RNA-sequencing data from tissue samples. The diagnosis prediction model based on the ncRNA signatures and clinical features was evaluated by circulating and tissue validation and ROC analysis. Nine miRNAs and eight lncRNAs were obtained from the microarray analysis. Six miRNAs (miR-550a-5p, miRNA-936, miR-1306-3p, miR-3185, miR-6083, miR-6792-3p) and three lncRNAs (lnc-MB21D1-3:5, lnc-PSCA-4:2 and lnc-ABCC5-2:1) were abnormally expressed in circulating and tissue samples compared with normal control (NC), which was closely related to clinical pathology and survival time of GC patients; circRNA sequencing and qRT-PCR revealed four circRNAs (circASHL2, circCCDC9, circNHSL1 and cirMLLT10) were abnormally expressed in GC tissues and parts of them were negative relationship with their predicted binding miRNAs. These ncRNAs might act as promising molecular markers for the diagnosis and prognosis of gastric cancer.