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NR2C2介导的长链非编码RNA LINC00675靶向miR-665调控肝癌细胞生物学行为的机制研究
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作者 汪建初 李曙波 +5 位作者 陆礼柏 陈益晨 马嘉盛 罗宗将 路远 浦涧 《右江医学》 2022年第2期124-130,共7页
目的探讨研究长链非编码RNA LINC00675对肝癌细胞生物学行为的影响及其分子机制。方法通过qRT-PCR检测LINC00675在肝癌组织以及细胞中表达量,并检测LINC00675在肝癌细胞HepG3与Huh7细胞质及细胞核中的表达分布。通过在HepG3与Huh7中稳... 目的探讨研究长链非编码RNA LINC00675对肝癌细胞生物学行为的影响及其分子机制。方法通过qRT-PCR检测LINC00675在肝癌组织以及细胞中表达量,并检测LINC00675在肝癌细胞HepG3与Huh7细胞质及细胞核中的表达分布。通过在HepG3与Huh7中稳定转染慢病毒过表达LINC00675建立细胞模型。通过CCK-8与流式细胞学检测LINC00675对肝癌细胞增殖、凋亡行为的影响,并通过检测细胞模型中葡萄糖摄取量以及乳酸产量变化监测细胞Warburg效应的变化,运用带有AGO2抗体的RNA免疫沉淀技术评估LINC00675与mRNA的潜在结合能力。使用LncBase Predicted v.2 DIANA工具预测LINC00675下游mRNA靶基因。运用RNA pull-down技术检测LINC00675与miR-665结合的可能性。运用荧光素酶实验验证LINC00675与miR-665的靶向结合,共转染实验验证miR-665介导了LINC00675对肝癌生物学行为的影响。通过使用JASPAR数据库预测LINC00675上游调控基因。通过构建NR2C2过表达以及敲低细胞模型,并使用qRT-PCR实验检测细胞模型中的LINC00675表达量的变化。运用荧光素酶实验验证LINC00675启动子与NR2C2的靶向结合位点。结果LINC00675在肝癌细胞系中低表达,且主要表达于细胞质中。过表达LINC00675抑制肝癌细胞的增殖能力与Warburg效应,并促进肝癌细胞凋亡。NR2C2介导的LINC00675在肝癌细胞中靶向结合miR-665,负向调控miR-665的表达,并通过结合miR-665来调控肝癌细胞的生物学行为。结论NR2C2介导的LINC00675通过靶向结合miR-665调控肝癌细胞的增殖和凋亡的生物学行为。 展开更多
关键词 linc00675 miR-665 NR2C2 肝癌 增殖 凋亡 Warburg效应
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Linc00675 is a novel marker of short survival and recurrence in patients with pancreatic ductal adenocarcinoma 被引量:6
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作者 Dou-Dou Li Zhi-Qiang Fu +6 位作者 Qing Lin Yu Zhou Quan-Bo Zhou Zhi-Hua Li Lang-Ping Tan Ru-Fu Chen Yi-Min Liu 《World Journal of Gastroenterology》 SCIE CAS 2015年第31期9348-9357,共10页
AIM: To detect linc00675 expression in pancreatic ductal adenocarcinoma(PDAC),to analyze the relationship between the expression level of linc00675 and the clinical pathological characteristics,to explore the biologic... AIM: To detect linc00675 expression in pancreatic ductal adenocarcinoma(PDAC),to analyze the relationship between the expression level of linc00675 and the clinical pathological characteristics,to explore the biological functions of linc00675,and to determine whether linc00675 has independent prognostic value in PDAC.METHODS: We studied linc00675 expression among eight histologically confirmed PDAC tissue samples and four chronic pancreatitis tissue samples through microarray screening. RT-q PCR was conducted to further investigate linc00675 expression in PDAC cell lines as well as archived tissues from a large cohort of PDAC patients. The correlations between the level of lnc00675 and clinicopathological characteristics and survival in patients with pancreatic cancer were evaluated using Correlation analysis. Univariate andmultivariate analyses were conducted to predict whether lnc00675 expression is an independent prognostic and recurrence factor in patients with pancreatic cancer. After downregulating the expression of linc00675 through si RNA,MTT assay,flow cytometry,transwell assay and Western blot were used to explore the biological function of linc00675 in proliferation,invasion,and cell cycle progression of pancreatic cancer cells. The relative molecular expression levels of epithelial-mesenchymal transition were determined by reverse transcription-polymerase chain reaction(RT-PCR) and Western blot.RESULTS: The expression of Linc00675 in PDAC tissue samples was shown to be 672 times that in chronic pancreatitis tissue samples by microarray screening(P = 3.69 × 10-5). This finding was confirmed in tumor tissues from 90 patients with PDAC compared with adjacent normal tissue samples by quantitative RTPCR. We found that linc00675 overexpression positively correlated with lymph node metastasis(P = 0.005),perineural invasion(P = 0.006),and poor survival(P < 0.001). Univariate and multivariate analyses showed that linc00675 expression served as an independent predictor of overall survival(P = 0.009). Additionally,receiver operating characteristic curve analysis showed that high linc00675 might serve as a predictor of tumor progression within 6 mo to a year after surgery. In vitro functional analysis demonstrated that knockdown of linc00675 attenuated pancreatic cancer cell proliferation and invasion as well as induced S phase arrest. Suppression of linc00675 in pancreatic cancer cells resulted can reverse the progress of epithelialmesenchymal transition.CONCLUSION: Linc00675 may function as an oncogene during PDAC development,and its expression is an independent predictor of unfavorable prognosis in patients with PDAC. 展开更多
关键词 linc00675 Long noncoding RNAS Pro-gnosis BIOMARKER
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linc00675在肺癌组织和细胞中的表达及其抑制肺癌细胞迁移和侵袭的机制
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作者 赵凌燕 梁宗安 +1 位作者 曾茄 熊小敏 《现代肿瘤医学》 CAS 北大核心 2021年第1期16-21,共6页
目的:探讨linc00675在肺癌组织和细胞中的表达以及其对肺癌细胞迁移、侵袭的影响。方法:采用qRT-PCR检测linc00675在35例肺癌组织和癌旁组织及肺癌细胞株SPCA1、A549、NCI-H446和人肺正常上皮细胞BEAS-2B中的表达。利用细胞转染实验对... 目的:探讨linc00675在肺癌组织和细胞中的表达以及其对肺癌细胞迁移、侵袭的影响。方法:采用qRT-PCR检测linc00675在35例肺癌组织和癌旁组织及肺癌细胞株SPCA1、A549、NCI-H446和人肺正常上皮细胞BEAS-2B中的表达。利用细胞转染实验对肺癌细胞SPCA1进行LV-linc00675和siRNA-linc00675及相关阴性对照的转染,采用qRT-PCR检测linc00675的表达水平。采用Transwell实验检测过表达及干扰linc00675表达对SPCA1细胞迁移和侵袭能力的影响。通过Western blot实验检测细胞上皮标志蛋白E-钙黏蛋白(E-cadherin)、间质标志蛋白N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)的表达水平。结果:linc00675在肺癌组织中的表达显著低于癌旁组织,在肺癌细胞株中的表达显著低于人肺正常上皮细胞。转染LV-linc00675可显著增加linc00675在肺癌细胞中的表达,转染siRNA-linc00675可显著降低linc00675在肺癌细胞中的表达。Transwell实验结果显示,过表达linc00675可显著抑制肺癌细胞的迁移和侵袭能力,干扰linc00675表达可显著增强肺癌细胞的迁移和侵袭能力。Western blot实验结果显示,过表达linc00675可显著抑制SPCA1细胞上皮间质转化(EMT)的发生,干扰linc00675表达后SPCA1细胞发生了明显的EMT。结论:linc00675在肺癌细胞中发挥抑癌作用,linc00675可能通过抑制肺癌细胞EMT的发生从而减弱其迁移和侵袭能力,提示linc00675可能成为肺癌治疗的新靶点。 展开更多
关键词 linc00675 肺癌 迁移 侵袭
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LINC00675在恶性肿瘤中的研究现状
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作者 王江斌 龚训 张全 《中文科技期刊数据库(全文版)医药卫生》 2021年第10期0001-0005,共5页
研究发现 LINC00675 在晚期肝癌,食管癌,结肠癌,直肠癌,胰腺癌,前列腺癌,肾癌, 和神经胶质瘤中表达失衡。各种分子生物学效应危及恶性肿瘤的繁殖,迁移和侵蚀。该文详细描述总结了 LINC00675 在近年来各种癌症疾病中的研究结果。
关键词 lncRNA linc00675 恶性肿瘤
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