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Long non-coding RNA GATA6-AS1 is mediated by N6-methyladenosine methylation and inhibits the proliferation and metastasis of gastric cancer
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作者 Jun-Jie Shen Min-Chang Li +1 位作者 Shao-Qi Tian Wen-Ming Chen 《World Journal of Gastrointestinal Oncology》 SCIE 2024年第3期1019-1028,共10页
BACKGROUND Through experimental research on the biological function of GATA6-AS1,it was confirmed that GATA6-AS1 can inhibit the proliferation,invasion,and migration of gastric cancer cells,suggesting that GATA6-AS1 p... BACKGROUND Through experimental research on the biological function of GATA6-AS1,it was confirmed that GATA6-AS1 can inhibit the proliferation,invasion,and migration of gastric cancer cells,suggesting that GATA6-AS1 plays a role as an anti-oncogene in the occurrence and development of gastric cancer.Further experi-ments confirmed that the overexpression of fat mass and obesity-associated protein(FTO)inhibited the expression of GATA6-AS1,thereby promoting the occurrence and development of gastric cancer.AIM To investigate the effects of GATA6-AS1 on the proliferation,invasion and migration of gastric cancer cells and its mechanism of action.METHODS We used bioinformatics methods to analyze the Cancer Genome Atlas(https://portal.gdc.cancer.gov/.The Cancer Genome Atlas)and download expression data for GATA6-AS1 in gastric cancer tissue and normal tissue.We also constructed a GATA6-AS1 lentivirus overexpression vector which was transfected into gastric cancer cells to investigate its effects on proliferation,migration and invasion,and thereby clarify the expression of GATA6-AS1 in gastric cancer and its biological role in the genesis and development of gastric cancer.Next,we used a database(http://starbase.sysu.edu.cn/starbase2/)to analysis GATA6-AS1 whether by m6A methylation modify regulation and predict the methyltransferases that may methylate GATA6-AS1.Furthermore,RNA immunoprecipitation experiments confirmed that GATA6-AS1 was able to bind to the m6A methylation modification enzyme.These data allowed us to clarify the ability of m6A methylase to influence the action of GATA6-AS1 and its role in the occurrence and development of gastric cancer.RESULTS Low expression levels of GATA6-AS1 were detected in gastric cancer.We also determined the effects of GATA6-AS1 overexpression on the biological function of gastric cancer cells.GATA6-AS1 had strong binding ability with the m6A demethylase FTO,which was expressed at high levels in gastric cancer and negatively correlated with the expression of GATA6-AS1.Following transfection with siRNA to knock down the expression of FTO,the expression levels of GATA6-AS1 were up-regulated.Finally,the proliferation,migration and invasion of gastric cancer cells were all inhibited following the knockdown of FTO expression.CONCLUSION During the occurrence and development of gastric cancer,the overexpression of FTO may inhibit the expression of GATA6-AS1,thus promoting the proliferation and metastasis of gastric cancer. 展开更多
关键词 long non-coding rna GATA6-as1 N6-methyladenine modification Fat mass and obesity-associated protein Gastric cancer
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Long noncoding RNAs HAND2-AS1 ultrasound microbubbles suppress hepatocellular carcinoma progression by regulating the miR-873-5p/tissue inhibitor of matrix metalloproteinase-2 axis
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作者 Qiang Zou Hao-Wen Wang +2 位作者 Xi-Liang Di Yuan Li Hui Gao 《World Journal of Gastrointestinal Oncology》 SCIE 2024年第4期1547-1563,共17页
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 t... 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. 展开更多
关键词 Hepatocellular carcinoma Ultrasound microbubbles long noncoding rna HAND2-as1 miR-873-5p Tissue inhibitor of matrix metalloproteinase-2
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Basic Study Long non-coding RNA TP73-AS1 promotes pancreatic cancer growth and metastasis through miRNA-128-3p/GOLM1 axis 被引量:3
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作者 Bin Wang Xing Sun +2 位作者 Ke-Jian Huang Li-Sheng Zhou Zheng-Jun Qiu 《World Journal of Gastroenterology》 SCIE CAS 2021年第17期1993-2014,共22页
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 canc... 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. 展开更多
关键词 Pancreatic cancer long non-coding rna TP73-as1 miR-128-3p GOLM1
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LncRNA AFAP1-AS1 exhibits oncogenic characteristics and promotes gemcitabine-resistance of cervical cancer cells through miR-7-5p/EGFR axis
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作者 CHAOQUN WANG TING ZHANG CHAOHE ZHANG 《Oncology Research》 SCIE 2024年第12期1867-1879,共13页
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 ... 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. 展开更多
关键词 long non-coding rna(lncrna)AFAP1-as1 miR-7-5p Epidermal growth factor receptor(EGFR) Gemcitabine-resistance Cervical cancer
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长链非编码RNA SOCS2-AS1通过Hippo-YAP信号通路调控胃癌细胞增殖和侵袭迁移的机制研究
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作者 吕文瑶 李琳 许崇安 《中国临床药理学杂志》 CAS CSCD 北大核心 2023年第24期3618-3622,共5页
目的 探讨长链非编码RNA(lncRNA)SOCS2-AS1对胃癌细胞增殖及侵袭迁移的影响。方法 收集40例胃癌组织及其40例癌旁组织作为实验标本,用实时荧光定量聚合酶链反应(RT-qPCR)检测胃癌组织及癌旁组织中SOCS2-AS1表达水平。将人胃癌SGC-7901... 目的 探讨长链非编码RNA(lncRNA)SOCS2-AS1对胃癌细胞增殖及侵袭迁移的影响。方法 收集40例胃癌组织及其40例癌旁组织作为实验标本,用实时荧光定量聚合酶链反应(RT-qPCR)检测胃癌组织及癌旁组织中SOCS2-AS1表达水平。将人胃癌SGC-7901细胞分为Vector组(转染vector)、pcDNA-SOCS2-AS1组(转染pcDNA-SOCS2-AS1)、NC-siRNA组(转染NC-siRNA)、SOCS2-AS1-siRNA组(转染SOCS2-AS1-siRNA)、pcDNA-SOCS2-AS1+vector组(转染pcDNA-SOCS2-AS1+vector)和pcDNA-SOCS2-AS1+pcDNA-YAP1组(转染pcDNA-SOCS2-AS1+pcDNA-YAP1)。用RT-qPCR检测细胞中SOCS2-AS1表达水平,用蛋白质印迹法检测胃癌细胞中Hippo-YAP通路相关蛋白LATS1和YAP1的表达水平,用EDU染色方法检测胃癌细胞增殖能力,用Transwell实验检测细胞迁移和侵袭能力。结果 SOCS2-AS1在胃癌组织、癌旁组织、正常胃上皮细胞GES-1和胃癌细胞SGC-7901中的相对表达水平分别为1.00±0.18、0.38±0.09、1.03±0.21和0.42±0.11,胃癌组织、胃癌细胞SGC-7901与癌旁组织、正常胃上皮细胞GES-1比较,差异均有统计学意义(均P<0.05)。Vector组、pcDNA-SOCS2-AS1组、NC-siRNA组和SOCS2-AS1-siRNA组的细胞增殖率分别为(36.23±2.53)%、(18.15±1.04)%、(35.83±2.15)%和(56.11±6.57)%;侵袭细胞数分别为168.15±19.11、54.36±6.27、124.47±14.53和238.62±21.34;迁移细胞数分别为194.22±16.33、91.61±8.47、148.14±16.25和279.31±24.68;LATS1蛋白的相对表达水平为0.93±0.08、2.86±0.21、0.96±0.09和0.31±0.03;YAP1蛋白的相对表达水平为0.95±0.11、0.28±0.04、0.92±0.12和3.16±0.28。pcDNA-SOCS2-AS1组上述指标与Vector组比较,SOCS2-AS1-siRNA组上述指标与NC-siRNA组比较,差异均有统计学意义(均P<0.05)。pcDNA-SOCS2-AS1+vector组与pcDNA-SOCS2-AS1+pcDNA-YAP1组的细胞增殖率分别为(33.62±5.73)%和(88.46±9.17)%;侵袭细胞数分别为53.61±6.44和131.73±15.29;迁移细胞数分别为68.35±7.63和159.81±16.47,差异均有统计学意义(均P<0.05)。结论 LncRNA SOCS2-AS1通过激活Hippo-YAP信号通路从而抑制胃癌细胞增殖、侵袭及迁移。 展开更多
关键词 长链非编码rna socs2-as1 胃癌 Hippo-Yes相关蛋白信号通路 增殖 侵袭
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Expressions of Long Non-Coding RNAs in Carcinogenesis of Cervix: A Review
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作者 Shrestha Reshies Min-Min Yu 《Open Journal of Obstetrics and Gynecology》 2018年第2期130-145,共16页
Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides mostly transcribed by RNA which do not encode proteins. Previously, lncRNAs were considered transcriptional byproducts called “junk DNA” wit... Long non-coding RNAs (lncRNAs) are transcripts longer than 200 nucleotides mostly transcribed by RNA which do not encode proteins. Previously, lncRNAs were considered transcriptional byproducts called “junk DNA” with no biological functions. There are many studies conducted on lncRNAs showing they are actively involved in regulation of epigenetic, transcriptional, and post-transcriptional events. Expressions of lncRNAs are more different in many malignant tumors than in benign tumors and normal tissue. Aberration of lncRNAs is responsible to promote or suppress tumorigenesis and cancer progression. Under different circumstances, lncRNAs exhibit their roles in carcinogenesis such as MALAT1 is responsible for intervening mRNA instability, HOTAIR, MALAT1, ANRIL, PVT1 links with miRNA and histonemodifying complexes, MEG3 associates with miRNA, CCAT2, MEG3, GAS5, UCA1 allies with c-Myc or P53 causing suppression of tumor or oncogenesis. Abnormal expressions of lncRNAs are noticed in gynecological cancers, such as cervical cancer, ovarian cancer, and endometrial cancer. Identification of cervical cancer associated lncRNAs is necessary to understand the molecular biogenesis of cancers. In this review, we summarized the foundation and function of the lncRNAs in terms of tumor progression, invasion, prognosis, apoptosis, metastasis, and chemo-resistance. This review will provide references to determine the clinical applications of lncRNAs as ideal diagnostic biomarkers or therapeutic targets in cervical cancers. 展开更多
关键词 lncrnas long non-coding rnaS CERVICAL Cancer HPV HOTAIR MALAT-1 GAS5 MEG3 PVT1 HULC ANRIL CCHE1 CCAT2 UCA1
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