Expression and significant roles of the long non-coding RNA CASC19/miR-491-5p/HMGA2 axis in the development of gastric cancer

BACKGROUND Gastric cancer(GC)is a common malignant tumor,long non-coding RNA and microRNA(miRNA)are important regulators that affect tumor proliferation,metastasis and chemotherapy resistance,and thus participate in tumor progression.CASC19 is a new bio-marker which can promote tumor invasion and metastasis.However,the mechanism by which CASC19 affects the progression of GC through miRNA is not clear.AIM To explore the role of the CASC19/miR-491-5p/HMGA2 regulatory axis in GC.METHODS To explore the expression and prognosis of CASC19 in GC through clinical samples,and investigate the effects of inhibiting CASC19 on the proliferation,migration,invasion and other functions of GC cells through cell counting Kit-8(CCK-8),ethynyldeoxyuridine,Wound healing assay,Transwell,Western blot and flow cytometry experiments.The effect of miR-491-5p and HMGA2 in GC were also proved.The regulatory relationship between CASC19 and miR-491-5p,miR-491-5p and HMGA2 were validated through Dual-luciferase reporter gene assay and reverse transcription PCR.Then CCK-8,Transwell,Wound healing assay,flow cytometry and animal experiments verify the role of CASC19/miR-491-5p/HMGA2 regulatory axis.RESULTS The expression level of CASC19 is related to the T stage,N stage,and tumor size of patients.Knockdown of the expression of CASC19 can inhibit the ability of proliferation,migration,invasion and EMT conversion of GC cells,and knocking down the expression of CASC19 can promote the apoptosis of GC cells.Increasing the expression of miR-491-5p can inhibit the proliferation of GC cells,miR-491-5p mimics can inhibit EMT conversion,and promote the apoptosis of GC cells,while decreasing the expression of miR-491-5p can promote the proliferation and EMT conversion and inhibit the apoptosis of GC cells.The expression of HMGA2 in GC tissues is higher than that in adjacent tissues.At the same time,the expression level of HMGA2 is related to the N and T stages of the patients.Reducing the level of HMGA2 can promote cell apoptosis and inhibit the proliferation of GC cells.Cell experiments and animal experiments have proved that CASC19 can regulates the expression of HMGA2 through miR-491-5p,thereby affecting the biological functions of GC.CONCLUSION CASC19 regulates the expression of HMGA2 through miR-491-5p to affect the development of GC.This axis may serve as a potential biomarker and therapeutic target of GC.

Long noncoding RNAs HAND2-AS1 ultrasound microbubbles suppress hepatocellular carcinoma progression by regulating the miR-873-5p/tissue inhibitor of matrix metalloproteinase-2 axis

BACKGROUND Increasing data indicated that long noncoding RNAs(lncRNAs)were directly or indirectly involved in the occurrence and development of tumors,including hepatocellular carcinoma(HCC).Recent studies had found that the expression of lncRNA HAND2-AS1 was downregulated in HCC tissues,but its role in HCC progression is unclear.Ultrasound targeted microbubble destruction mediated gene transfection is a new method to overexpress genes.AIM To study the role of ultrasound microbubbles(UTMBs)mediated HAND2-AS1 in the progression of HCC,in order to provide a new reference for the treatment of HCC.METHODS In vitro,we transfected HAND2-AS1 siRNA into HepG2 cells by UTMBs,and detected cell proliferation,apoptosis,invasion and epithelial-mesenchymal transition(EMT)by cell counting kit-8 assay,flow cytometry,Transwell invasion assay and Western blotting,respectively.In addition,we transfected miR-837-5p mimic into UTMBs treated cells and observed the changes of cell behavior.Next,the UTMBs treated HepG2 cells were transfected together with miR-837-5p mimic and tissue inhibitor of matrix metalloproteinase-2(TIMP2)overexpression vector,and we detected cell proliferation,apoptosis,invasion and EMT.In vivo,we established a mouse model of subcutaneous transplantation of HepG2 cells and observed the effect of HAND2-AS1 silencing on tumor formation ability.RESULTS We found that UTMBs carrying HAND2-AS1 restricted cell proliferation,invasion,and EMT,encouraged apoptosis,and HAND2-AS1 silencing eliminated the effect of UTMBs.Additionally,miR-873-5p targets the gene HAND2-AS1,which also targets the 3’UTR of TIMP2.And miR-873-5p mimic counteracted the impact of HAND2-AS1.Further,miR-873-5p mimic solely or in combination with pcDNA-TIMP2 had been transformed into HepG2 cells exposed to UTMBs.We discovered that TIMP2 reversed the effect of miR-873-5p mimic caused by the blocked signalling cascade for matrix metalloproteinase(MMP)2/MMP9.In vivo results showed that HAND2-AS1 silencing significantly inhibited tumor formation in mice.CONCLUSION LncRNA HAND2-AS1 promotes TIMP2 expression by targeting miR-873-5p to inhibit HepG2 cell growth and delay HCC progression.

LncRNA AFAP1-AS1 exhibits oncogenic characteristics and promotes gemcitabine-resistance of cervical cancer cells through miR-7-5p/EGFR axis

Background:Drug resistance is the main factor contributing to cancer recurrence and poor prognosis.Exploration of drug resistance-related mechanisms and effective therapeutic targets are the aim of molecular targeted therapy.In our study,the role of long non-coding RNA(lncRNA)AFAP1-AS1 in gemcitabine resistance and related mechanisms were explored in cervical cancer cells.Methods:Gemcitabine-resistant cervical cancer cell lines HT-3-Gem and SW756-Gem were constructed using the gemcitabine concentration gradient method.The overall survival rates and recurrence-free survival rates were evaluated by Kaplan-Meier analysis.The interaction was verified through a Dual-luciferase reporter gene assay and a Biotinylated RNA pull-down assay.Cell proliferation ability was assessed through methyl-thiazolyl-tetrazolium(MTT),soft agar,and colony formation experiments.Cell cycle and apoptosis were detected byflow cytometry.Results:Up-regulation of AFAP1-AS1 in cervical cancer predicted a poor prognosis.Besides,patients in the gemcitabine-resistance group had higher levels of AFAP1-AS1 than the gemcitabine-sensitive group.AFAP1-AS1 promoted tumor growth and induced gemcitabine tolerance of cervical cancer cells.In addition,AFAP1-AS1 mediated epidermal growth factor receptor(EGFR)expression by serving as a molecular sponge for microRNA-7a-5p(miR-7-5p).This present study also proved that the knockdown of EGFR or overexpression of miR-7a-5p abolished the accelerative role of AFAP1-AS1 overexpression in cancer progression and gemcitabine tolerance.Conclusions:In general,the AFAP1-AS1/miR-7-5p/EGFR axis was tightly related to the progression and gemcitabine tolerance of cervical cancer,providing potential targets for the management of cervical cancer.

Long non-coding RNA highly up-regulated in liver cancer promotes exosome secretion

BACKGROUND Highly upregulated in liver cancer (HULC) is a long non-coding RNA (lncRNA) which has recently been identified as a key regulator in hepatocellular carcinoma (HCC) progression. However, its role in the secretion of exosomes from HCC cells remains unknown. AIM To explore the mechanism by which HULC promotes the secretion of exosomes from HCC cells. METHODS Serum and liver tissue samples were collected from 30 patients with HCC who had not received chemotherapy, radiotherapy, or immunotherapy before surgery. HULC expression in serum exosomes and liver cancer tissues of patients was measured, and compared with the data obtained from healthy controls and tumor adjacent tissues. The effect of HULC upregulation in HCC cell lines and the relationship between HULC and other RNAs were studied using qPCR and dualluciferase reporter assays. Nanoparticle tracking analysis was performed to detect the quantity of exosomes.RESULTS HULC expression in serum exosomes of patients with HCC was higher than that in serum exosomes of healthy controls, and HULC levels were higher in liver cancer tissues than in tumor adjacent tissues. The expression of HULC in serum exosomes and liver cancer tissues correlated with the tumor-node-metastasis (TNM) classification, and HULC expression in tissues correlated with that in serum exosomes. Upregulation of HULC promoted HCC cell growth and invasion and repressed apoptosis. Notably, it also facilitated the secretion of exosomes from HCC cells. Moreover, qPCR assays showed that HULC repressed microRNA-372-3p (miR-372-3p) expression. We also identified Rab11a as a downstream target of miR-372-3p. Dual-luciferase reporter assays suggested that miR-372-3p could directly bind both HULC and Rab11a. CONCLUSION Our findings illustrate the importance of the HULC/miR-372-3p/Rab11a axis in HCC and provide new insights into the molecular mechanism regulating the secretion of exosomes from HCC cells.

Long noncoding RNA RP4 functions as a competing endogenous RNA through miR-7-5p sponge activity in colorectal cancer

AIM To investigate the role of long noncoding RNA(lnc RNA) RP4 in colorectal cancer.METHODS Lentivirus-mediated lnc RNA RP4 overexpression and knockdown were performed in the colorectal cancer cell line SW480. Cell proliferation, tumor growth, and early apoptosis were evaluated by a cell counting kit-8 assay, an in vivo xenograft tumor model, and annexin V/propidium iodide staining, respectively. Analysis of the lnc RNA RP4 mechanism involved assessment of the association of its expression with mi R-7-5 p and the SH3 GLB1 gene. Western blot analysis was also performed to assess the effect of lnc RNA RP4 on the autophagy-mediated cell death pathway and phosphatidylinositol-3-kinase(PI3 K)/Akt signaling.RESULTS Cell proliferation, tumor growth, and early apoptosis in SW480 cells were negatively regulated by lnc RNA RP4. Functional experiments indicated that lnc RNA RP4 directly upregulated SH3 GLB1 expression by acting as a competing endogenous RNA(ce RNA) for mi R-7-5 p. This interaction led to activation of the autophagy-mediated cell death pathway and de-repression of PI3 K and Akt phosphorylation in colorectal cancer cells in vivo.CONCLUSION Our results demonstrated that lnc RNA RP4 is a ce RNA that plays an important role in the pathogenesis of colorectal cancer, and could be a potential therapeutic target for colorectal cancer treatment.

Analytical models for the penetration of semi-infinite targets by rigid,deformable and erosive long rods

A theoretical study is presented herein on the pen- etration of a semi-infinite target by a spherical-headed long rod for Yp 〉 S, where Yp is the penetrator strength and S is the static target resistance. For Yp 〉 S, depending upon initial impact velocity, there exist three types of penetration, namely, penetration by a rigid long rod, penetration by a deforming non-erosive long rod and penetration by an erosive long rod. If the impact velocity of the penetrator is higher than the hydrodynamic velocity （VH）, it will penetrate the target in an erosive mode; if the impact velocity lies between the hydrodynamic velocity （VH） and the rigid body velocity （VR）, it will penetrate the target in a deformable mode; if the impact velocity is less than the rigid body velocity （VR）, it will penetrate the target in a rigid mode. The critical conditions for the transition among these three penetration modes are proposed. It is demonstrated that the present model predictions correlate well with the experimental observations in terms of depth of penetration （DOP） and the critical transition conditions.

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.

Basic Study Long non-coding RNA TP73-AS1 promotes pancreatic cancer growth and metastasis through miRNA-128-3p/GOLM1 axis

BACKGROUND Previous studies have suggested that long non-coding RNAs(lncRNA)TP73-AS1 is significantly upregulated in several cancers.However,the biological role and clinical significance of TP73-AS1 in pancreatic cancer(PC)remain unclear.AIM To investigate the role of TP73-AS1 in the growth and metastasis of PC.METHODS The expression of lncRNA TP73-AS1,miR-128-3p,and GOLM1 in PC tissues and cells was detected by quantitative real-time polymerase chain reaction.The bioinformatics prediction software ENCORI was used to predict the putative binding sites of miR-128-3p.The regulatory roles of TP73-AS1 and miR-128-3p in cell proliferation,migration,and invasion abilities were verified by Cell Counting Kit-8,wound-healing,and transwell assays,as well as flow cytometry and Western blot analysis.The interactions among TP73-AS1,miR-128-3p,and GOLM1 were explored by bioinformatics prediction,luciferase assay,and Western blot.RESULTS The expression of TP73-AS1 and miRNA-128-3p was dysregulated in PC tissues and cells.High TP73-AS1 expression was correlated with a poor prognosis.TP73-AS1 silencing inhibited PC cell proliferation,migration,and invasion in vitro as well as suppressed tumor growth in vivo.Mechanistically,TP73-AS1 was validated to promote PC progression through GOLM1 upregulation by competitively binding to miR-128-3p.CONCLUSION Our results demonstrated that TP73-AS1 promotes PC progression by regulating the miR-128-3p/GOLM1 axis,which might provide a potential treatment strategy for patients with PC.

Synthesis of M1-3xAl2O4:Eu2+x/Dy3+ 2x(M^2+= Sr^2+, Ca^2+ and Ba^2+) phosphors with long-lasting phosphorescence properties via co-precipitation method

The long afterglow fluorescent material of M1-3xAl2O4:Eu2+ x/Dy3+2x(M2+= Sr2+, Ca2+ and Ba2+) phosphors are successfully synthesized by calcining precursor obtained via co-precipitation method at 1300oC for 4 h with reducing atmosphere (20% H2 and 80% N2). The phase evolution, morphology and afterglow fluorescent properties are systematically studied by the various instruments of XRD, FE-SEM, PLE/PL spectroscopy and fluorescence decay analysis. The PL spectra shows that the Sr1-3xAl2O4:Eu2+x/Dy3+ 2x phosphors display vivid green emission at s519 nm (4f65d1!4f7 transition of Eu2+) with monitoring of the maximum excitation wavelength at s334 nm (8S7=2!6IJ transition of Eu2+), among which the optimal concentration of Eu2+ and Dy3+ is 15 at.% and 30 at.%, respectively. The color coordinates and temperature of Sr1-3xAl2O4:Eu2+ x/Dy3+ 2x phosphors are approximately at (s0.27, s0.57) and s6700 K, respectively. On the above basis, the M0:55Al2O4:Eu2+ 0:15/Dy3+ 0:3 (M2+= Ca2+ and Ba2+) phosphors is obtained by the same method. The PL spectra of these phosphors shows the strongest blue emission at s440 nm and cyan emission at s499 nm under s334 nm wavelength excitation, respectively, which are blue shifted comparing to Sr1??3xAl2O4:Eu2+ x/Dy3+ 2x phosphors. The color coordinates and temperatures of M0:55Al2O4:Eu2+ 0:15/Dy3+ 0:3 (M2+= Ca2+ and Ba2+) phosphors are approximately at (s0.18, s0.09), s2000 K and (s0.18, s0.42), s11600 K, respectively. In this work, long afterglow materials of green, blue and cyan aluminates phosphors with excellent properties have been prepared, in order to obtain wide application in the field of night automatic lighting and display.

Long noncoding RNA TNFRSF10A-AS1 promotes colorectal cancer through upregulation of HuR

BACKGROUND Recent studies have emphasized the emerging importance of long noncoding RNAs(lncRNAs)in colorectal cancer(CRC).However,the functions and regulatory mechanisms of numerous lncRNAs in CRC have not been fully elucidated.AIM To explore the functional role and underlying molecular mechanisms of lncRNA TNFRSF10A-AS1 in CRC.METHODS TNFRSF10A-AS1 expression was measured by quantitative real-time polymerase chain reaction in CRC,and the relationship between TNFRSF10A-AS1 levels and the clinicopathological features of CRC patients was analyzed.The effect of TNFRSF10A-AS1 expression on CRC proliferation and metastasis was examined in vitro and in vivo.Mechanistically,we investigated how TNFRSF10A-AS1 is involved in CRC as a competitive endogenous RNA.RESULTS TNFRSF10A-AS1 was expressed at a high level in CRC and the upregulation of TNFRSF10A-AS1 was associated with advanced T grade and tumor size in CRC patients.A functional investigation revealed that TNFRSF10A-AS1 enhanced the proliferation,migration ability and invasion ability of colon cancer cells in vitro and in vivo.A mechanistic analysis demonstrated that TNFRSF10A-AS1 acted as a miR-3121-3p molecular sponge to regulate HuR expression,ultimately promoting colorectal tumorigenesis and progression.CONCLUSION TNFRSF10A-AS1 exerts a tumor-promoting function through the miR-3121-3p/HuR axis in CRC,indicating that it may be a novel target for CRC therapy.

Potential role of long noncoding RNA RP5-881L22.5 as a novel biomarker and therapeutic target of colorectal cancer

BACKGROUND The incidence of colorectal cancer in humans is high,and it is in the top five for cancer-related morbidity and mortality.It is one of the main threats to human health.The function of long noncoding RNAs in tumor occurrence and development has gradually gained attention in recent years.In increasing numbers of studies,researchers have demonstrated that it plays an important role in the pathogenesis of colorectal cancer.AIM To find out if long noncoding RNA RP5-881L22.5 played a role in the pathogenesis of colorectal cancer in relation to the tumor microenvironment.METHODS We analyzed the transcriptome data and clinical data in The Cancer Genome Atlas-colon adenocarcinoma.The CIRBERSORT algorithm was applied to evaluate these tumor-infiltrating immune cells in The Cancer Genome Atlas-colon adenocarcinoma cancer tissue samples.Using the“estimate”package in R,we assessed the tumor immune microenvironment.The expression level of RP5-881L22.5 in tumor tissue and adjacent normal tissue samples from 4 pairs of colorectal cancer patients was determined by quantitative reverse transcription PCR.Colorectal cancer cells were tested for invasiveness using a transwell invasion assay after RP5-881L22.5 expression was knocked down.RESULTS The expression of lncRNA RP5-881L22.5 was related to the clinical characteristics of the tumors,and it was negatively related to the infiltration level of immune cells in the tumor microenvironment and the expression of T cell inhibitory receptors.A major function of its coexpressed mRNA was to regulate tumor immunity,such as the immune response.When quantitative reverse transcription PCR was performed on tumor tissues from 4 pairs of colorectal cancer patients,the results showed that RP5-881L22.5 was highly expressed.Subsequently,knocking down the expression of RP5-881L22.5,the invasiveness of colorectal cancer cell lines was reduced,and the apoptosis rate was increased.CONCLUSION RP5-881L22.5 plays a crucial role in the microenvironment of tumors as well as in the pathogenesis of colorectal cancer.The relationship between RP5-881L22.5 and the tumor immune microenvironment deserves further study.

Non-stationary Buffeting Response Analysis of Long Span Suspension Bridge Under Strong Wind Loading

The non-stationary buffeting response of long span suspension bridge in time domain under strong wind loading is computed. Modeling method for generating non-stationary fluctuating winds with probabilistic model for non-stationary strong wind fields is first presented. Non-stationary wind forces induced by strong winds on bridge deck and tower are then given a brief introduction. Finally,Non-stationary buffeting response of Pulite Bridge in China,a long span suspension bridge,is computed by using ANSYS software under four working conditions with different combination of time-varying mean wind and time-varying variance. The case study further confirms that it is necessity of considering non-stationary buffeting response for long span suspension bridge under strong wind loading,rather than only stationary buffeting response.

杨慎批点《文心雕龙》考

杨慎是明中期重要文人,在明代文坛有很大的影响力。作为《文心雕龙》明代的首个批点本,杨慎批点本反映出杨慎本人乃至明代文学风向之转变,并开启了明代《文心雕龙》评点的潮流,这对明朝中后期的诸多文学流派借鉴、继踵六朝之风均产生了较为深远的影响。前人对批点本成书时间并无深入研究,忽略了杨慎其他著作中对批点本的征引及杨慎生平经历中存在的确定撰作时间的线索。考证可知,杨慎批点《文心雕龙》在嘉靖四年,这展现了杨慎与张含文学交往的一个侧面,印证了杨慎文学研究重心自先秦两汉至六朝的转变,以及其强调“情”的价值、将风雅传统与六朝绮靡风格进行弥合的尝试。

前癃通胶囊对人前列腺组织bcl-2、bax表达的影响

目的:检测前癃通对前列腺组织bcl-2、bax表达的影响。方法:(1)免疫组化法检测前癃通对体外培养BPH患者前列腺组织bcl-2、bax蛋白表达的影响。(2)RT-PCR法检测前癃通对体外培养BPH患者前列腺组织块细胞bcl-2mRNA、baxmRNA基因表达的影响。结果:前癃通高、中剂量组对前列腺组织bcl-2蛋白、bcl-2mRNA基因的表达有不同程度的抑制作用,对bax蛋白、baxmRNA基因的表达有不同程度的增强作用。结论:前癃通对前列腺组织能抑制bcl-2的基因表达,增强bax的基因表达,从而抑制前列腺增生。

Identification of key long noncoding RNAs and their biological functions in hepatocellular carcinoma

Long noncoding RNAs(lncRNAs)are vital regulators in tumorigenesis and metastasis.However,the pathological role of lncRNAs in hepatocellular carcinoma(HCC)is still unclear.In this study,we filtered out three lncRNAs from The Cancer Genome Atlas(TCGA)data that were screened for basic expression and clinical research.We selected lncRNA-NEAT1 for further study to explore its function in HCC progression and its regulatory mechanism.We identified three differentially expressed lncRNAs(DElncRNAs)in tumor and adjacent normal tissues from the TCGA library using data mining methods:lncRNA-NEAT1,lncRNA-MAGI2-AS3 and lncRNA-HCG11.Their basic expression levels were detected by qPCR.Then,we selected lncRNA-NEAT1 as a potentially important lncRNA to verity its biological function and mechanism in HCC cell lines.lncRNA-NEAT1,lncRNA-MAGI2-AS3 and lncRNA-HCG11 were overexpressed in liver cancer tissues and cell lines.We found that silencing NEAT1 in vitro can inhibit the proliferation of HuH-7 and Li-7 cells,inhibit cell migration,and induce apoptosis as well as significantly increase the level of miR-16-5p.We also confirmed that miR-16-5p has a significant correlation with Bcl-2.When NEAT1 is silenced,the expression of Bcl-2 decreases.Inhibiting miR-16-5p can restore Bcl-2 to its original level.We conclude that miR-16-5p1/lncRNA NEAT1 plays a crucial role in regulating the delivery of Bcl-2 in HCC.Overall,the miR-16-5p/lncRNA-NEAT1/Bcl-2 signaling axis may be a promising target for HCC treatment.

DNAH17-AS1 promotes pancreatic carcinoma by increasing PPME1 expression via inhibition of miR-432-5p

BACKGROUND The incidence and mortality rates of pancreatic carcinoma(PC)are rapidly increasing worldwide.Long noncoding RNAs(lncRNAs)play critical roles during PC initiation and progression.Since the lncRNA DNAH17-AS1 is highly expressed in PC,the regulation of DNAH17-AS1 in PC was investigated in this study.AIM To investigate the expression and molecular action of lncRNA DNAH17-AS1 in PC cells.METHODS The PC expression data for the lncRNA DNAH17-AS1 was downloaded from The Cancer Genome Atlas database and used to examine its profile.Western blot and reverse transcription-quantitative PCR were employed to assess protein and mRNA expression.A subcellular fractionation assay was used to determine the location of DNAH17-AS1 in cells.In addition,the regulatory effects of DNAH17-AS1 on miR-432-5p,PPME1,and tumor activity were investigated using luciferase reporter assay,MTT viability analysis,flow cytometry,and transwell migration analysis.RESULTS DNAH17-AS1 was upregulated in PC cells and was associated with aggressive tumor behavior and poor prognosis for patients.Silencing DNAH17-AS1 promoted the apoptosis and reduced the viability,invasion,and migration of PC cells.In addition,DNAH17-AS1 served as a PC oncogene by downregulating miR-432-5p which normally directly targeted PPME1 to downregulate its expression.CONLUSION DNAH17-AS1 functions in PC as a tumor promoter by regulating the miR-432-5p/PPME1 axis.This finding may provide new insights for PC prognosis and therapy.

Differentially expressed long noncoding RNAs and regulatory mechanism of LINC02407 in human gastric adenocarcinoma

BACKGROUND Long noncoding RNAs(lncRNAs)have been identified to play important roles in the development and progression of various tumors,including gastric cancer(GC).However,the molecular role of lncRNAs in GC progression remains unclear.AIM To investigate the differential expression of lncRNAs in human GC and elucidate the function and regulatory mechanism of LINC02407.METHODS The Cancer Genome Atlas database was used to investigate the involvement of lncRNAs in GC.Quantitative real-time polymerase chain reaction was used to estimate the relative expression level of LINC02407 in GC tissues and cells.Functional experiments including CCK8 assay,apoptosis assay,wound healing assay,and transwell assay were used to investigate the effect of LINC02407 on GC cells.Some microRNAs were predicted and verified via bioinformatics analysis and the luciferase reporter system.Predictive analysis and Western blot assay were used to analyze the expression of related proteins.RESULTS Many differentially expressed lncRNAs were identified in GC,and some of them including LINC02407 can affect the survival.LINC02407 was upregulated in tumor tissues compared with adjacent tissues.HGC-27 cells showed the highest LINC02407 expression and HaCaT cells exhibited the lowest expression.Different experiment groups were constructed using LINC02407 overexpressing plasmids and related siRNAs.The results of functional experiments showed that LINC02407 can promote the proliferation,migration,and invasion of GC cells but inhibit apoptosis.Luciferase reporter assay showed that hsa-miR-6845-5p and hsa-miR-4455 was downstream regulated by LINC02407.Western blot analysis showed that adhesion G protein-coupled receptor D1(ADGRD1)was regulated by the LINC02407-miR-6845-5p/miR-4455-ADGRD1 pathways.CONCLUSION LINC02407 plays a role in GC through the LINC02407-miR-6845-5p/miR-4455-ADGRD1 pathways,and thus,it may be an important oncogene and has potential value in GC diagnosis and treatment.

Editorial Board 2011-2015

The World Journal of Gastrointestinal Oncology Editorial Board consists of 428 members,representing a team of worldwide experts in gastrointestinal oncology.They are from 40 countries,including Argentina(2),Australia(10),Belgium(5),Brazil(2),Canada(4),Chile(2),China(56),Czech Republic(1),Denmark(1),Finland(3),France(7),Germany(24),Greece(13),Hungary(2),India(9),Iran(2),Ireland(2),Israel(4),Italy(41),Japan(47),Kuwait(2),Mexico(1),Netherlands(7),New Zealand(2),Norway(1),Poland(3),Portugal(5),Romania(1),Saudi Arabia(1),Serbia(2),Singapore(4),South Korea(27),Spain(10),Sweden(5),Switzerland(2),Syria(1),Thailand(1),Turkey(6),United Kingdom(15),and United States(95).

Editorial Board 2011-2015

The World Journal of Gastrointestinal Oncology Editorial Board consists of 428 members,representing a team of worldwide experts in gastrointestinal oncology.They are from 40 countries,including Argentina(2),Australia(10),Belgium(5),Brazil(2),Canada(4),Chile(2),China(56),Czech Republic(1),Denmark(1),Finland(3),France(7),Germany(24),Greece(13),Hungary(2),India(9),Iran(2),Ireland(2),Israel(4),Italy(41),Japan(47)。

Editorial Board 2011-2015

The World Journal of Gastrointestinal Oncology Editorial Board consists of 428 members,representing a team of worldwide experts in gastrointestinal oncology.They are from 40 countries,including Argentina(2),Australia(10),Belgium(5),Brazil(2),Canada(4),Chile(2),China(56),Czech Republic(1),Denmark(1),Finland(3)。