OBJECTIVES:To investigate the effects of miR-183-5p overexpression on proliferation, invasion, migration, and ferroptosis of triple-negative breast cancer (TNBC) cells and the role of Kelch-like protein 24 (KLHL24) in mediating these effects. METHODS:Bioinformatics analyses were conducted to screen differentially expressed genes in breast cancer (BRCA) and predict the target gene of miR-183-5p. RT-qPCR was used to verify miR-183-5p expression in normal breast epithelial and TNBC cell lines. Dual-luciferase reporter assay was performed to confirm direct binding of miR-183-5p to 3'-UTR of KLHL24. Western blotting was used to detect KLHL24 expression in different TNBC cells after transfection with miR-183-5p-overexpressing plasmids. MDA-MB-231 cells were co-transfected with NC-miR and NC-KLHL24, oe-miR-183-5p and NC-KLHL24, NC-miR and oe-KLHL24, or oe-miR-183-5p and oe-KLHL24 plasmids, and the changes in cell proliferation, migration and invasion were examined using EdU, Transwell, and wound healing assays. Western blotting was used to detect the changes in expressions of ferroptosis-related proteins (GPX4, SLC7A11, and Nrf2), and ROS, LPO, MDA, and GSH levels in the transfected cells were determined. RESULTS:The expression of miR-183-5p was significantly elevated in BRCA tissues and TNBC cell lines, and MDA-MB-231 cells showed the highest miR-183-5p expression. Dual-luciferase reporter assay confirmed the direct binding of miR-183-5p to 3'-UTR of KLHL24. Overexpression of miR-183-5p significantly downregulated KLHL24 expression. In TNBC cells, miR-183-5p overexpression obviously promoted cell proliferation, invasion, and migration, upregulated the expressions of GPX4, SLC7A11 and Nrf2, reduced the levels of ROS, LPO and MDA, and increased the level of GSH (P<0.0001); these effects were significantly reversed by co-transfection of the cells with KLHL24-overexpressing plasmids. CONCLUSIONS:Overexpression of miR-183-5p enhances TNBC cell proliferation, invasion, migration and inhibits ferroptosis by negatively regulating KLHL24.

OBJECTIVES:To explore the molecular mechanism by which lncRNA SNHG15 regulates proliferation, invasion and migration of lung adenocarcinoma cells. METHODS:The lncRNA microarray chip dataset GSE196584 and LncBase were used to predict the lncRNAs that interact with miR-30b-3p, and their association with patient prognosis were investigated using online databases, after which lncRNA nucleolar RNA host gene 15 (SNHG15) was selected for further analysis. The subcellular localization of lncRNA SNHG15 and its expression levels in normal human lung epithelial cells and lung adenocarcinoma cell lines were detected using fluorescence in situ hybridization and qRT-PCR. In cultured A549 cells, the changes in cell proliferation, migration, and invasion following transfection with a SNHG15 knockdown plasmid (sh-SNHG15), a miR-30b-3p inhibitor, or their co-transfection were assessed with EdU, wound healing, and Transwell assays. Bioinformatics analyses were used to predict the regulatory relationship between lncRNA SNHG15 and COX6B1, and the results were verified using Western blotting and rescue experiments in A549 cells transfected with sh-SNHG15, a COX6B1-overexpressing plasmid, or both. RESULTS:LncRNA SNHG15 was shown to target miR-30b-3p, and the former was highly expressed in lung adenocarcinoma, and associated with a poor patient prognosis. LncRNA SNHG15 was localized in the cytoplasm and expressed at higher levels in A549 and NCI-H1299 cells than in BEAS-2B cells. In A549 cells, lncRNA SNHG15 knockdown significantly inhibited cell migration, invasion and proliferation, and these changes were reversed by miR-30b-3p inhibitor. A regulatory relationship was found between lncRNA SNHG15 and COX6B1, and their expression levels were positively correlated (r=0.128, P=0.003). MiR-30b-3p knockdown obviously decreased COX6B1 expression in A549 cells, and COX6B1 overexpression rescued the cells from the inhibitory effects of lncRNA-SNHG15 knockdown. CONCLUSIONS:LncRNA SNHG15 may compete with COX6B1 to bind miR-30b-3p through a ceRNA mechanism to affect proliferation, migration, and invasion of lung adenocarcinoma cells.

S100A8/A9 proteins are members of EF-hand calcium-binding proteins secreted by neutrophils and activated monocytes. S100A8/A9 has cell growth-promoting activity at low concentrations by binding to the receptor for advanced glycation end products (RAGE). In this study, we report for the first time that S100A8/A9 promoted the invasion of breast cancer cells depending on RAGE. In addition, RAGE binding to S100A8/A9 promoted the phosphorylation of LIN-11, Isl1, and MEC-3 protein domain kinase, as well as cofilin. This phosphorylation is a critical step in cofilin recycling and actin polymerization. Interestingly, RAGE binding to S100A8/A9 enhanced cell mesenchymal properties and induced epithelial–mesenchymal transition. Mechanistically, RAGE binding to S100A8/A9 stabilized Snail through the NF-κB signaling pathway. Based on these observations, RAGE expression in breast cancer cells was associated with lymph node and distant metastases in patients with invasive ductal carcinoma. Moreover, RAGE binding to S100A8/A9 promoted lung metastasis in vivo. In summary, our in vitro and in vivo results indicated that RAGE binding to S100A8/A9 played an important role in breast cancer invasion/metastasis. This study identified both RAGE and S100A8/A9 as potential anti-invasion targets for therapeutic intervention in breast cancer.

The study is aimed to establish a predictive model of double-J stent encrustation after upper urinary tract calculi surgery. We collected the clinical data of 561 patients with indwelling double-J tubes admitted to a hospital in Shandong Province from January 2019 to December 2020 as the modeling group and 241 cases of indwelling double-J tubes from January 2021 to January 2022 as the verification group. Univariate and binary logistic regression analyses were used to explore risk factors, the risk prediction equation was established, and the receiver operating characteristic (ROC) curve analysis model was used for prediction. In this study, 104 of the 561 patients developed double-J stent encrustation, with an incidence rate of 18.5%. We finally screened out BMI (body mass index) > 23.9 (OR = 1.648), preoperative urine routine white blood cell quantification (OR = 1.149), double-J tube insertion time (OR = 1.566), postoperative water consumption did not reach 2000 ml/d (OR = 8.514), a total of four factors build a risk prediction model. From the ROC curve analysis, the area under the curve (AUC) was 0.844, and the maximum Oden index was 0.579. At this time, the sensitivity was 0.735 and the specificity was 0.844. The research established in this study has a high predictive value for the occurrence of double-J stent encrustation in the double-J tube after upper urinary tract stone surgery, which provides a basis for the prevention and treatment of double-J stent encrustation.

Triple-negative breast cancer (TNBC) is a pathological subtype of breast cancer (BC) with high malignancy, strong invasiveness and poor prognosis. Long non-coding RNA (LncRNA) plays an important role during tumorigenesis. We identified that Linc00707 was upregulated in TNBC tissues by TCGA database and RT-qPCR assay, compared with normal breast tissues and other subtypes of BC. Linc00707 promoted TNBC cells proliferation, migration and invasion. Furthermore, we found that knockdown of Linc00707 influenced autophagy via PI3K/AKT/mTOR signaling pathway in TNBC cells. Linc00707 affected the progress of TNBC cells through affecting autophagy. Further mechanistic experiments confirmed that Linc00707 could competitively bind with miR-423-5p to up-regulate MARCH2 expression, ultimately promoting TNBC progression and autophagy through PI3K/AKT/mTOR pathway. In conclusion, we demonstrate that Linc00707 is a key molecule in tumor progression and may be an effective target for patients with TNBC.

BACKGROUND:Lung adenocarcinoma (LUAD) is the most common type of non-small cell lung cancer, and any change of miRNAs expression will affect the degree of target regulation, thus affecting intracellular homeostasis. This study verified that miR-186-5p could inhibit the proliferation, migration and invasion of LUAD cells by regulating PRKAA2.METHODS:Previous investigations found that the expression of miR-186-5p was markedly suppressed in LUAD. Bioinformatics method is used to predict the target protein related to ferroptosis downstream and inquire about its expression level in LUAD and its influence on the survival of patients. Double luciferase verified the binding site of PRKAA2 and miR-186-5p. Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were used to detect the expression of PRKAA2. The effects of miR-186-5p of LUAD cells as well as the mechanism by which miR-186-5p inhibits Fer-1's sensitivity to ferroptosis were confirmed by EdU, Transwell, and scratch assays. The effect of miR-186-5p on the amount of reactive oxygen species (ROS) in LUAD cells was discovered using ROS experiment. Malondialdehyde (MDA) and glutathione (GSH) experiments were used to detect the effects of miR-186-5p and PRKAA2 on ferroptosis index of LUAD cells. The concentration of lipid ROS (L-ROS) in LUAD cells were measured using the L-ROS tests to determine the effects of miR-186-5p and PRKAA2.RESULTS:The expression of PRKAA2 is up-regulated, and a high level of PRKAA2 expression was associated with a poor prognosis for patients with LUAD. Overexpression of miR-186-5p decreased the gene and protein expression of PRKAA2. By promoting ferroptosis, miR-186-5p overexpression prevented lung cancer cells from proliferating, invading, and migrating. ROS could be produced in higher amounts in LUAD cells due to miR-186-5p. Overexpression of miR-186-5p and knockdown PRKAA2 up-regulated MDA content and reduced GSH content in LUAD cells, respectively. miR-186-5p could increase the content of L-ROS and promote the ferroptosis sensitivity of LUAD cells by targeting PRKAA2.CONCLUSIONS:miR-186-5p promotes ferroptosis of LUAD cells through targeted regulation of PRKAA2, thus inhibiting the proliferation, invasion and migration of LUAD.
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Aim To investigate the molecular mechanism of miR-326 inhibiting breast cancer invasion and metastasis by regulating EphB3 expression.Methods RTFQ-PCR was used to examine the expression o miR-326 in normal breast epithelial cells and breas cancer cells and the transfection efficiency of miR-326overexpression plasmid.EdU cell proliferation assay and Transwell assay were used to examine the changes in proliferation,migration and invasion ability of different subgroups of cells.Dual luciferase assay was used to verify the presence of binding sites for miR-326 and EphB3.Western blot was used to detect the expression of EphB3 in breast cancer cells after overexpression of miR-326.Results RTFQ-PCR results showed that miR-326 was lowly expressed in breast cancer cells and successfully transfected （P＜0.05）.EdU proliferation assay and Transwell assay results showed that overexpression of miR-326 in breast cancer cells inhibited proliferation,migration and invasive ability （P＜0.05）.The results of dual luciferase assay showed that miR-326 could interact with the 3’-UTR of EphB3 （P＜0.05）.Western blot and Transwell assays showed that miR-326 could negatively regulate EphB3 to inhibit invasive metastasis of breast cancer cells （P＜0.05）.Conclusions MiR-326 acts as a cancer suppressor genes in the development of breast cancer and suppresses the invasion and metastasis of breast cancer cells by regulating the expression of EphB3.

Objective To explore the biological function and involve the signal transduction pathways of the target gene, through the target gene prediction and bioinformatics analysis of hsa-miR-340-5p.Methods The conservation of miR-340-5p sequence among different species was analyzed by using RNAcentral and miRBase databases online. The target genes of hsa-miR-340-5p were predicted by using online databases as DIANA-microT, Target Scan, miRWalk and miRDB, respectively. Then, venny2.1 was used to draw the venn map to get the set of intersection target genes. The set of intersection target genes was analyzed by gene ontology（GO） function annotation, Kyoto encyclopedia of genes and genomes signaling pathways（KEGG Pathway） enrichment analysis, protein interaction（PPI） network construction and key（hub） gene screened.Results Through comparative sequence analysis, the mature sequence of miR-340-5p was highly conservative among 8 different species was found. After using four miRNA target genes online databases prediction, there were 92 intersection target genes sets with binding sites of hsa-miR-340-5p, accounting for 1.9% of the total predicted target genes were found. Go functional annotation analysis showed that the hsa-miR-340-5p intersection target gene sets were mainly enriched in the nucleoplasm, focal adhesion and cell-cell junction, and simultaneously participated in many biological processes and molecular functions, such as the positive regulation of transcription from RNA polymeraseⅡ promoter, transcription from RNA polymeraseⅡ promoter and protein binding, and so on. KEGG Pathway enrichment analysis showed that the hsa-miR-340-5p intersection target gene sets were mainly enriched in 7 signaling pathways, such as proteoglycans in cancer, pathways in cancer and human T-cytotropic virus type Ⅰ（HTLV-Ⅰ） infection, and so on. Based on the PPI network construction of hsa-mir-340-5p intersection target gene set, the top 10 hub genes of degree value were screened, which were recombinant mothers against decapentaplegic homolog（SMAD）2, Wnt family member（WNT）3, recombinant activin A receptor type 1C（ACVR1C）, F-box only prote（FBXO）30, defective in cullin neddylation（DCUN1D）1, PH domain interacting proteins（PHIP）, CUB and Sushi multi-domain（CSMD）3, recombinant sorting nexin（SNX）9, human immunodeficiency virus type I enhancer binding protein（HIVEP）2 and RWD domain proteins（RWDD）2A.Conclusions The target genes regulated by hsa-mir-340-5p are involved in a variety of biological processes, such as cancer, inflammation and so on.

目的 探讨miR-185-5p对小鼠乳腺癌PY8119细胞增殖、侵袭迁移能力的影响.方法 通过前期研究获得乳腺癌中表达显著下调的miR-185-5p,NCBI查询人源与鼠源miR-185-5p基因序列;EdU增殖实验、Transwell侵袭实验、划痕愈合实验、流式细胞术检测过表达和敲低miR-185-5p对PY8119细胞增殖、侵袭、迁移、凋亡能力的影响;利用C57BL/6小鼠建立皮下肿瘤模型和肺转移模型,观察过表达miR-185-5p对体内肿瘤增殖能力以及肺部转移情况的变化.结果 EdU增殖实验、Transwell侵袭实验、划痕愈合实验、流式细胞术结果分别显示,敲低miR-185-5p使PY8119细胞的增殖、侵袭、迁移能力显著增强,抑制细胞凋亡;而过表达miR-185-5p抑制PY8119细胞的增殖、侵袭、迁移能力,促进细胞凋亡;C57BL/6小鼠体内成瘤实验显示,过表达miR-185-5p减缓C57BL/6小鼠体内肿瘤生长速度;肺转移实验显示,过表达miR-185-5p抑制C57BL/6小鼠肺转移能力.结论 miR-185-5p作为抑癌基因抑制小鼠乳腺癌PY8119细胞体内外增殖、侵袭迁移的能力.

目的 探讨ICU肠外营养患者发生中心静脉导管相关血流感染的危险因素,为针对性干预提供参考.方法 将ICU 987例经中心静脉导管进行肠外营养的患者分为建模组708例、验证组279例,通过单因素和多因素分析危险因素并构建预测模型.结果 建模组708例中85例(12.01％)发生血流感染,病原菌以革兰阳性菌为主(占53.98％).筛选出APACHE Ⅱ评分、拔管时最高体温、白蛋白含量、营养液中加入谷氨酰胺、导管留置时间、肠外营养时间6项影响因素(均P＜0.05),构建风险预测模型.预测曲线和观察曲线具有较好的一致性,建模组及验证组ROC曲线下面积分别为0.816和0.847.结论 该模型能较好地预测ICU肠外营养患者发生中心静脉导管相关血流感染风险,可为预防性管理提供参考.

BACKGROUND:Lung adenocarcinoma (LUAD) is the most common clinical histological subtype of lung cancer and microRNAs (miRNAs) are a type of small non-coding RNAs which play a central role in cells. miR-30b-3p plays a key effect in many types of carcinoma, but there is still very little research on how it works in lung adenocarcinoma. The role and mechanism of miR-30b-3p in the proliferation and invasion of LUAD were explored in this study, to provide new targets for inhibiting the proliferation and invasion of LUAD.METHODS:NCBI database was used to screen out miRNA with obvious differential expression, and the differential expression and survival curve were searched by StarBase database. Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) was used to detect the relative expression of miR-30b-3p in each lung adenocarcinoma cell line. 5-ethynyl-2'-deoxyuridine (EdU) cell proliferation assay and Transwell invasion assay were used to detect the proliferation and invasion of A549 cells in each group. The target genes of miR-30b-3p were determined by the target gene prediction websites. Western blot assay was used to detect the expression of COX6B1 in each group of A549 cells. Double luciferase assay was used to verify the targeted binding relationship between miR-30b-3p and COX6B1.RESULTS:The expression of miR-30b-3p in lung adenocarcinoma tissues and lung adenocarcinoma cells was downregulated (P<0.05). Low expression levels of miR-30b-3p were associated with poor prognosis in patients with lung adenocarcinoma (P=0.005,8). Overexpression of miR-30b-3p could inhibit the proliferation and the invasion of lung adenocarcinoma cells (P<0.05). Double luciferase assay proved that miR-30b-3p could target and bind to COX6B1 (P<0.05). Western blot analysis showed that the overexpression of miR-30b-3p could downregulate the expression of COX6B1 in A549 cells (P<0.05). EdU cell proliferation assay and Transwell invasion assay showed that the overexpression of miR-30b-3p could reverse the promoting effect of upregulation of COX6B1 on proliferation and invasion in lung adenocarcinoma cells (P<0.05).CONCLUSIONS:miR-30b-3p acts as a tumor suppressor gene in lung adenocarcinoma, and it can inhibit the proliferation and invasion of lung adenocarcinoma by targeting the expression of COX6B1.

Objective:To explore the effect of health education based on theory of planned behavior combined with stepped care model on negative emotion, psychological flexibility and quality of life in patients with lung cancer undergoing chemotherapy.Methods:From October 2020 to December 2021, 108 chemotherapy patients who underwent lung cancer surgery in Affiliated Hospital of Weifang Medical College and had anxiety or depression that scores was greater than 7 in any dimension of the Hospital Anxiety and Depression Scale (HADS) were selected as the study subjects. The study subjects were divided into observation group ( n=46) and control group ( n=48) by random digits table method. Routine care was implemented in the control group. The observation group implemented health education based on the theory of planned behavior combined with stepped care model intervention. The HADS scale was used every 4 weeks to assess negative emotion in both groups. In observation, patients with negative emotion relief stop the next stage of nursing intervention, and patients without relief continue the next stage of higher intensity nursing intervention. Results:Before the intervention, there were no significant difference in the scores of negative emotion, psychological flexibility and quality of life between the two groups ( P>0.05). After intervention, the scores of all dimensions of negative emotion and the total score in the observation group were significantly lower than those in the control group, and the differences had statistical significance ( t=4.86, 3.19 and 4.53, all P<0.05). After the intervention the scores of psychological flexibility and quality of life dimensions and the total score in the observation group were higher than those in the control group, the differences had statistical significance (t values were -6.01--2.89, all P<0.05). After the intervention, there was no significant difference in the remission rate of negative emotions between the clinical observation stage of the observation group and the concurrent control group ( P>0.05). The remission rates of guided self-help, problem-solving therapy, psychological or drug therapy and total negative emotions in the observation group were 38.46%(15/39), 33.33%(8/24), 6/16 and 78.26%(36/46), respectively, which were higher than those in the control group, and the differences had statistical significance ( χ2 values were 7.04 - 13.80, all P<0.05). Conclusions:Health education based on the theory of planned behavior combined with stepped care model can effectively alleviate the negative emotions of lung cancer patients undergoing chemotherapy and improve psychological flexibility and quality of life.

科研能力是学术型病理学硕士研究生的必备能力,也是判断研究生培养质量的重要标准之一.学术型病理学硕士研究生作为科学研究的主力军,已成为国家科技发展的重要后备力量,受到了国家及各高校的高度重视.要想提高学术型病理学硕士研究生的科研能力,培养严谨的科研精神,激发他们的创新活力,就必须针对目前培养过程中存在的问题进行分析,并构建一套行之有效问题解决方案,充分发掘研究生的科研潜力,提高研究生的素质,从而不断为国家培养高素质的科研人才.

The roles of microRNAs (miRNAs) in the occurrence, metastasis, and prognosis of lung adenocarcinoma (LUAD) have been drawing extensive attention from researchers. The aim of this study is to identify the effects of miR-4732-5p on the migration, invasion, and metastasis of LUAD. In this study, we found that the expression of miR-4732-5p was decreased in LUAD based on the data derived from The Cancer Genome Atlas (TCGA) database, tissues, and cell lines. LUAD patients with a low expression of miR-4732-5p exhibited a lower survival rate. Meanwhile, miR-4732-5p could directly target xenotropic and polytropic retrovirus receptor 1 (XPR1), and elevated XPR1 was observed in LUAD mRNA microarrays, Gene Expression Omnibus (GEO), and The Human Protein Atlas (HPA) database. Overexpression of miR-4732-5p significantly inhibits the migration, invasion, and metastasis of LUAD in vitro and in vivo, which can be reversed by overexpression of XPR1. We also found that the PI3K/Akt/GSK3β/Snail pathway induced by EGF induced EMT could be inhibited by miR-4732-5p overexpression and XPR1 knockdown. The migration and invasion of LUAD could be converted by cytoskeletal rearrangements, and the polymerization of EGF induced F-actin in A549 cells could be inhibited by elevated miR-4732-5p. Our results suggest that miR-4732-5p exerts anti-tumor effects on the invasion and metastasis of LUAD by regulating XPR1 in vivo and in vitro, indicating that the miR-4732-5p/XPR1 axis may be a potential target for LUAD therapeutic intervention.

在新医科大力发展的背景下,教师在讲授肿瘤病理学专业知识的同时,如何挖掘肿瘤病理学的思政元素,将知识传授与价值引领结合起来,如何达到既能开展课程思政,又能培养德才兼备的医学人才是教学过程中应该思考的问题.要结合临床病例将思政教育融入肿瘤病理学课程,帮助医学研究生提高人文素养.

Background Many studies have shown that microRNAs (miRNAs) play an essential role in gene regulation and tumor development. This study aimed to explore the expression of miR-379-5p and its mechanisms of affecting proliferation, migration, and invasion in breast cancer (BC). Methods MiRNAs and mRNAs expression data of BC and normal breast tissue samples were downloaded from the TCGA and GEO databases. qRT-PCR was used to detect the expression of miR-379-5p in human normal breast epithelial cell lines and human BC cell lines. The proliferation ability of transfected cells was detected by colony formation and EdU assays. The mobility and invasion ability of transfected cells was measured by wound healing and transwell assays. The relative protein expression of transfected cells was detected by western blot. Dual luciferase reporter assay was performed to identify the targeted binding of miR-379-5p and KIF4A. Results MiR-379-5p was lowly expressed in BC tissue samples and BC cell lines. The target genes of miR-379-5p were involved in many cancer-related signaling pathways. PPI analysis and the cytoHubba algorithm of Cytoscape identified 10 genes as the hub genes. Survival analysis showed that only KIF4A expression in 10 hub genes was significantly associated with the prognosis of BC patients and was significantly upregulated in BC. Overexpression of miR-379-5p inhibited proliferation, migration, and invasion in the BC cell line MDA-MB-231, which could be reversed by KIF4A. Conclusions MiR-379-5p inhibits proliferation, migration, and invasion of BC by targeting KIF4A.

Cachexia is a common complication in patients with lung cancer. It aggravates the toxic and side effects of chemotherapy, hinders the treatment plan, weakens the responsiveness of chemotherapy, reduces the quality of life, increases complications and mortality, and seriously endangers the physical and mental health of patients with lung cancer. The causes and pathogenesis of tumor cachexia are extremely complex, which makes its treatment difficult and complex. Controlling cachexia in lung cancer patients requires many means such as anti-tumor therapy, inhibition of inflammatory response, nutritional support, physical exercise, and relief of symptoms to exert the synergistic effect of multimodal therapy against multiple mechanisms of tumor cachexia. To date, there has been a consensus within the discipline that no single therapy can control the development of cachexia. Some therapies have made some progress, but they need to be implemented in combination with multimodal therapy after fully assessing the individual characteristics of lung cancer patients. This article reviews the application of drug therapy and nutritional support in lung cancer patients, and looks forward to the research direction of cachexia control in lung cancer patients.
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Abstract Background:In recent years, some studies have found that long non-coding RNA Small nucleolar RNA host gene 17 (lncRNA SNHG17) is abnormally expressed in a variety of cancers. However, the prognostic and clinical value of lncRNA SNHG17 expression in cancer is still unclear. This meta-analysis aims to comprehensively elaborate the prognostic value of SNHG17 in cancer.Methods:PubMed, Web of Science, Embase and Cochrane Library were absolutely searched. Hazards ratios (HRs) or odd ratios (ORs) with 95% confidence intervals (CIs) were pooled to estimate the prognostic value of SNHG17 in cancers, including overall survival (OS), progression-free survival (PFS), disease-free survival (DFS), recurrence-free survival (RFS), age, gender, tumor size, differentiation, metastasis, clinical stage, and lymph node metastasis (LNM). In addition, we further searched for the expression and prognosis of SNHG17 in various cancer through TCGA dataset.Results:13 studies containing 1492 cancer patients was finally Selected into this study. The results showed that patients with high SNHG17 expression tended to have shorter OS (HR = 1.78, 95%CI = 1.50-2.10, P < 0.01), DFS (HR = 1.36, 95%CI = 1.06-1.74, P < 0.05), RFS (R = 2.49,95%CI = 1.13-5.49, P < 0.01), and PFS (R = 2.02, 95%CI = 1.24–3.28, P < 0.05). Additionally, increased lncRNA SNHG17 expression was significantly related to worse differentiation (HR = 1.41, 95%CI = 0.82-2.45, P < 0.01), advanced clinical stage (HR = 3.25, 95%CI = 1.77-5.97, P < 0.01), earlier metastasis (HR = 2.33, 95%CI = 1.30-4.19, P < 0.01) and earlier lymph node metastasis (HR = 2.94, 95%CI = 2.15-4.02, P < 0.01). No publication bias was found in all studies and the results were robust. The TCGA dataset further validated that SNHG17 is highly expressed in a variety of cancers and is strongly correlated with OS and DFS.Conclusion:The high expression of lncRNA SNHG17 may predict poor prognosis and advanced clinical stage, which means that SNHG17 may be a possible prognostic biomarker of cancer.

Background Long non-coding RNAs (LncRNAs) has been confirmed to play a crucial role in the development and progression of various cancer types. Here we evaluated the expression profiles of LncRNAs in Lung adenocarcinoma (LUAD) tissues and identified a novel LncRNA, termed LncRNA-AC009948.5. However, the role and potential molecular mechanisms of this novel LncRNA in LUAD carcinogenesis is unknown. Methods Regarding the public databases and based on integrating bioinformatics analyses, we determined whether LncRNA-AC009948.5 exerts its oncogenic functions via sponging miR-186-5p in LUAD. Furthermore, we determined whether NCAPG2 was a downstream target of miR-186-5p. Moreover, the expression level and biological function of LncRNA-AC009948.5 in LUAD were determined by qRT-PCR, cell apoptosis, Edu, transwell, wound healing and western blot assays. Besides, xenograft mice were established for validation. We explored the expression of LncRNA-AC009948.5 and its roles in the prognosis of LUAD. Results LncRNA expression microarray data indicate that LncRNA-AC009948.5 is upregulated in LUAD samples. The present study confirmed the upregulation of LncRNA-AC009948.5 in LUAD tissues and cells. Encreased expression of LncRNA-AC009948.5 was correlated with tumor size, lymph nodes, distant metastasis and histological grade, and poor prognosis.LncRNA-AC009948.5 knockdown significantly inhibited cell proliferation, migration, and invasion in vitro , as well as tumorigenesis and metastasis in vivo . Conversely, LncRNA-AC009948.5 upregulated had opposite effects. Mechanistically, we elucidated that LncRNA-AC009948.5 could directly bind to miR-186-5p and subsequently suppress expression of the target gene of NCAPG2. Conclusions LncRNA-AC009948.5 promotes lung adenocarcinoma cells metastasis via the miR-186-5p/NCAPG2 axis and activation of the EMT process. Which may serve as potential targets for the treatment of LUAD in the future.

Abstract Background: Glioma is one of the most common intracranial malignancies. As competing for endogenous RNA (ceRNA), long chain non-coding RNA (lncRNA) can affect the binding of microRNA (miRNA) to mRNA and thus affect the occurrence and development of glioma, which has been suggested as a key role in the development of human cancers. This study was to investigate the effects of TCGA on the development of glioma.Results: Here, we screened the differential genes by differential analyses on the matrix data for glioma in TCGA and GEO databases and selected the potential prognostic markers among them. Surprisingly, LEF1-AS1 was identified capable of influencing the survival of glioma patients. The results derived from the proportional risk (Cox) regression model showed a significant association between LEF1-AS1 overexpression and poorer prognosis (HR = 1.518, P < 0.001). The ROC model validated the feasibility of LEF1-AS1 (AUC = 0.702). MiR-128-3p, the target gene for LEF1-AS1, was screened using the Bioinformatics Online website and found down-regulated with increasing glioma grade in glioma tissues. Then the target gene for miR-128-3p, CSRP2, was obtained through miRTarBase, TargetScan, and miRDB. The survival curve of CSRP2 showed that CSRP2 with low expression corresponded to a better prognosis in glioma patients. The level of CSRP2 was positively correlated with the infiltration ones of CD4+ T and CD8+ T cells in glioma tissues. In addition, the CellMiner database predicted three drugs (Elesclomol, Entinostat, and Staurosporine) with high sensitivity to CSRP2 expression, and their molecular structures were retrieved using the PubChem22 database.Conclusions: In summary, the LEF1-AS1/miR-128-3p/CSRP2 axis may play a vital role in the development of glioma and provide guiding significance for the early diagnosis and treatment for it.