LINC00511靶向miR-497-5p调控胃癌细胞增殖、迁移和侵袭及机制研究

目的:探讨LINC00511对胃癌细胞增殖、迁移和侵袭的影响及其作用机制。方法:将pcDNA、pcDNA-LINC00511、si-NC、si-LINC00511、miR-NC、miR-497-5p分别转染至MGC-803细胞中,分别记为pcDNA组、pcDNA-LINC00511组、si-NC组、si-LINC00511组、miR-NC组、miR-497-5p组;将si-LINC00511质粒分别与anti-miR-NC、anti-miR-497-5p共转染至MGC-803细胞中,分别记为si-LINC00511+anti-miR-NC组、si-LINC00511+anti-miR-497-5p组。实时荧光定量PCR（RT-qPCR）检测miR-497-5p和LINC00511表达水平;蛋白质印迹（Western Blot）法检测细胞周期素D1（cyclin D1,CyclinD1）、p21、基质金属蛋白酶2（matrix metalloproteinase 2,MMP2）、基质金属蛋白酶9（matrix metalloproteinase 9,MMP9）蛋白表达水平;四甲基偶氮唑盐比色法(MTT)检测细胞活性;Transwell检测细胞迁移和侵袭;双荧光素酶报告基因实验检测LINC00511和miR-497-5p的靶向关系。结果:与正常胃黏膜上皮细胞GES-1相比,胃癌细胞MGC-803、MKN-45、AGS中miR-497-5p表达水平显著降低,LINC00511表达水平显著升高。LINC00511靶向调控miR-497-5p的表达。抑制LINC00511表达和miR-497-5p过表达可降低细胞活性和迁移、侵袭数量,降低CyclinD1、MMP2、MMP9蛋白表达水平,提高p21蛋白表达水平。干扰miR-497-5p表达逆转了抑制LINC00511表达对胃癌MGC-803细胞增殖、迁移和侵袭的抑制作用。结论:抑制LINC00511表达可抑制胃癌细胞增殖、迁移和侵袭,其机制可能与miR-497-5p表达有关,将为胃癌的治疗提供新思路和新靶点。     

LINC00460靶向miR-380-3p对皮肤鳞状细胞癌细胞增殖、迁移、侵袭和凋亡的影响

目的:探讨LINC00460对皮肤鳞状细胞癌（CSCC）细胞增殖、迁移、侵袭和凋亡的影响及可能机制。方法:实时荧光定量PCR（RT-qPCR）分析人类永生化表皮细胞（HaCaT）和CSCC细胞（SCC13、A431和HSC-5）中LINC00460和miR-380-3p的表达水平。将LINC00460小干扰RNA（si-LINC00460）、miR-380-3p模拟物（miR-380-3p mimics）、si-LINC00460+miR-380-3p抑制物（anti-miR-380-3p）分别转染A431细胞,细胞计数试剂盒（CCK-8）检测细胞活力,流式细胞术分析细胞凋亡,Transwell实验分析细胞迁移和侵袭能力,蛋白质印记（Western blot）检测细胞周期素D1（CyclinD1）、基质金属蛋白酶2（MMP2）、基质金属蛋白酶9（MMP9）、上皮细胞钙黏蛋白（E-Cadherin）、神经钙黏蛋白（N-Cadherin）、波形蛋白（Vimentin）的表达。双荧光素酶报告基因实验、RT-qPCR确定LINC00460对miR-380-3p的靶向调控作用。结果:与HaCaT比较,CSCC细胞中LINC00460表达显著增加,miR-380-3p表达显著降低（P＜0.05）。下调LINC00460表达后A431细胞增殖活力、迁移和侵袭细胞数以及CyclinD1、MMP2、MMP9、N-Cadherin和Vimentin蛋白表达显著降低（P＜0.05）,凋亡率、E-Cadherin蛋白表达显著升高（P＜0.05）。上调miR-380-3p表达后A431细胞增殖活力、迁移和侵袭细胞数以及CyclinD1、MMP2和MMP9表达显著降低（P＜0.05）,凋亡率显著升高（P＜0.05）。与下调LINC00460比较,同时下调LINC00460和miR-380-3p后A431细胞增殖活力、迁移和侵袭细胞数以及CyclinD1、MMP2、MMP9、N-Cadherin和Vimentin蛋白表达显著升高（P＜0.05）,凋亡率、E-Cadherin蛋白表达显著降低（P＜0.05）。LINC00460靶向负调控miR-380-3p表达。结论:CSCC细胞中LINC00460表达增加,下调LINC00460能够降低CSCC细胞的增殖、迁移和侵袭能力,诱导细胞凋亡,其机制与靶向调控miR-380-3p表达有关。     

LINC01006靶向miR-331-3p调控多发性骨髓瘤细胞的增殖、凋亡和转移的机制研究

目的:探讨LINC01006靶向miR-331-3p在多发性骨髓瘤(multiple myeloma, MM)进展中的功能。方法:RT-qPCR检测39例MM患者和22例正常对照者骨髓标本来源的浆细胞中LINC01006和miR-331-3p的表达。分别转染si-LINC01006、si-NC、miR-331-3p mimics、miR-NC、si-LINC01006+anti-miR-NC、si-LINC01006+anti-miR-331-3p至MM细胞U266,通过CCK-8、流式细胞术和Transwell法评估U266细胞抑制率、凋亡率和转移数。DIANA Tools网站预测LINC01006与miR-331-3p的相互作用，并通过双荧光素酶报告基因法进一步验证。结果:MM患者骨髓标本来源的浆细胞中LINC01006表达升高，miR-331-3p表达降低。转染si-LINC01006可增加细胞抑制率和凋亡率(P<0.05),减少细胞转移数(P<0.05),并上调miR-331-3p表达(P<0.05)。转染miR-331-3p mimics可增加细胞抑制率和凋...     

LINC01503通过miR-342-3p/IGF2R轴促进上皮性卵巢癌的进展

目的：探讨LINC01503 在上皮性卵巢癌（EOC）中的表达水平和生物学功能及其可能的作用机制。方法：收集2015年5月至2016 年5月间在河北医科大学第四医院妇瘤科手术切除并经病理学确诊的85 例EOC患者的肿瘤组织和输卵管组织。常规培养人EOC 细胞A2780、SKOV3、OVCAR3 和OV90 及正常人卵巢上皮细胞IOSE80，将si-LINC01503、si-NC 及miR-342-3p mimic、miR mimic NC分别转染至SKOV3和A2780 细胞，分别作为si-LINC01503 组、si-NC 组、miR-342-3p mimic 组和miR mimic NC组。qPCR 法检测EOC组织和细胞中LINC01503 的表达水平，Kaplan-Meier 法分析LINC01503 表达水平与患者生存的关系。双荧光素酶报告基因实验验证LINC01503/miR-342-3p/IGF2R轴相关分子间的靶向关系。平板克隆、划痕愈合和Transwell 实验分别检测敲低LINC01503 及转染miR-342-3p mimic 对A2780 和SKOV3细胞增殖、迁移和侵袭能力的影响。WB法检测EOC细胞中LINC01503/miR-342-3p 通路对IGF2R蛋白表达的影响。构建A2780 细胞裸鼠移植瘤模型，观察敲低LINC01503 对移植瘤生长的影响。结果：EOC组织和细胞中LINC01503 表达水平分别显著高于输卵管组织和IOSE80 细胞（均P<0.01），LINC01503高表达组患者术后PFS 和OS 均显著短于LINC01503 低表达组患者（均P<0.01）。敲低LINC01503、转染miR-342-3p mimic 均可抑制EOC 细胞的增殖、迁移和侵袭能力（均P<0.01）。敲低LINC01503 可下调IGF2R的表达（P<0.01），这一现象可通过转染miR-342-3p inhibitor 挽救。敲低LINC01503 可抑制A2780 细胞裸鼠移植瘤的生长（P<0.01）。结论：在EOC 组织和细胞中呈高表达的LINC01503，与患者的不良预后密切相关，LINC01503可能通过吸附miR-342-3p影响IGF2R表达进而促进EOC的进展。     

lncRNA LINC00909靶向miR-548-3p对结直肠癌细胞放射敏感性的研究

目的 探讨lncRNA LINC00909是否通过靶向miR-548-3p而影响结直肠癌细胞放射敏感性。方法 采用qRT-PCR检测结直肠癌组织、癌旁组织中LINC00909、miR-584-3p的表达量;体外培养结直肠癌细胞SW480、SW620,分别将si-NC、si-LINC00909、miR-NC、miR-584-3p mimics、si-LINC00909与anti-miR-NC、si-LINC00909与anti-miR-584-3p转染至SW480、SW620细胞,用4 Gy照射细胞;克隆形成实验检测细胞存活分数及放射增敏比;MTT检测细胞增殖;Transwell小室实验检测细胞迁移及侵袭;双荧光素酶报告实验验证LINC00909、miR-584-3p的靶向关系。裸鼠皮下移植瘤实验检测干扰LINC00909表达或抑制miR-584-3p表达对照射后移植瘤重量的影响。结果 结直肠癌组织中LINC00909的表达水平显著升高(P<0.05),miR-584-3p的表达水平显著降低(P<0.05);干扰LINC00909表达或miR-584-3p过表达后细胞存活分数明显降低(P<0.05),放射增敏比分别为2.017、1.762,并可抑制增殖、迁移及侵袭(P<0.05);双荧光素酶报告实验证实LINC00909可靶向结合miR-584-3p;干扰LINC00909表达后移植瘤重量显著降低(P<0.05)。共转染anti-miR-584-3p后移植瘤重量显著升高(P<0.05)。结论 干扰LINC00909表达可通过上调miR-548-3p的表达而减弱结直肠癌细胞增殖、迁移及侵袭能力从而增强细胞放射敏感性。     

长基因间非编码RNA 1980靶向微小RNA-335-5p及对胃癌细胞迁移侵袭的影响

目的探讨长基因间非编码RNA 1980(LINC01980)对微小RNA-335-5p(miR-335-5p)的靶向调控作用及胃癌细胞迁移侵袭的影响。方法采用实时荧光定量PCR(qPCR)检测人胃黏膜上皮细胞GES-1及胃癌细胞(AGS、HGC-27、MKN-45和MGC80-3)的LINC01980和miR-335-5p水平,双荧光素酶报告基因实验验证LINC01980与miR-335-5p的相互关系;将MGC80-3细胞分为4组:对照组(未转染)、LINC01980干扰(si-LINC01980)组(转染si-LINC01980+miR-335-5p无关序列miR-NC)、miR-335-5p抑制物inhibitor(miR-inhibitor)组(转染无关序列si-NC+miR-335-5p inhibitor)和共转染组(转染si-LINC01980+miR-335-5p inhibitor)。MTT、划痕实验和Transwell小室实验分别检测细胞增殖活力、迁移和侵袭能力。结果与GES-1细胞相比,胃癌细胞的LINC01980水平升高,而miR-335-5p水平降低(P<0.05)。野生型LINC01980序列与miR-335-5p模拟物共转染细胞的荧光素酶活性降低且MGC80-3细胞转染si-LINC01980后的miR-335-5p水平升高(P<0.05)。对照组、si-LINC01980组、miR-inhibitor组和共转染组的细胞活力分别为1.508±0.101、0.944±0.077、1.856±0.117和1.404±0.082,划痕愈合率分别为(65.552±3.701)%、(19.920±2.571)%、(88.133±1.264)%和(75.433±7.313)%,穿膜细胞数分别为(80.349±8.763)、(31.151±1.338)、(114.064±2.983)和(78.920±7.811)个,与对照组相比,si-LINC01980组的细胞活力、划痕愈合率和穿膜细胞数均降低(P<0.05),miR-inhibitor组均升高(P<0.05),而共转染组的无明显变化(P>0.05)。结论干扰LINC01980可能通过增强miR-335-5p表达来抑制胃癌的进展,LINC01980/miR-335-5p轴有望成为胃癌治疗的潜在靶点。     

吴茱萸碱对神经母细胞瘤SK-N-SH细胞增殖、迁移及侵袭的影响

目的：探讨吴茱萸碱（Evo）是否通过调控lncRNA LINC00858 表达调控神经母细胞瘤SK-N-SH 细胞的增殖、迁移及侵袭。方法：在体外以3、6、12 μmol/L Evo 处理人神经母细胞瘤SK-N-SH 细胞，利用RNA干扰技术分别将si-NC、si-LINC00858转染至SK-N-SH 细胞，将pcDNA、pcDNA-LINC00858 转染至SK-N-SH 细胞并经12 μmol/L Evo 处理，实验分为对照组、Evo 低剂量组、Evo 中剂量组、Evo 高剂量组、si-NC 组、si-LINC00858 组、Evo+pcDNA 组、Evo+pcDNA-LINC00858 组。采用qPCR法检测各组细胞LINC00858 的表达量，MTT、Transwell 实验分别检测细胞的增殖、迁移、侵袭能力，WB 法检测细胞中cyclinD1、MMP-2、 MMP-9和p21 蛋白的表达。结果：与对照组相比，Evo低、中、高剂量组SK-N-SH 细胞中LINC00858 表达均显著降低（均P<0.05），细胞增殖抑制率显著升高、迁移及侵袭细胞数显著减少（均P<0.01），cyclinD1、MMP-2、MMP-9 蛋白表达降低、p21 蛋白表达升高（均P<0.01）。与si-NC 组相比，si-LINC00858 组细胞的增殖抑制率、迁移和侵袭细胞数及相关蛋白表达变化同Evo 低、中、高剂量组。与Evo+pcDNA 组相比，Evo+pcDNA-LINC00858 组细胞的增殖抑制率显著降低、迁移及侵袭细胞数均显著增多（均P<0.01），cyclinD1、MMP-2、MMP-9蛋白表达升高、p21蛋白表达降低（均P<0.05）。结论：Evo 通过下调LINC00858 表达抑制神经母细胞瘤SK-N-SH细胞的增殖、迁移及侵袭。     

LINC01018 通过 miR-297 调控胃癌 HGC-27 细胞的增殖、凋亡及放射 敏感性

目的：探讨长基因间非编码 RNA（long intergene non-coding RNA,LINC）01018 是否通过抑制 miR-297 调控胃癌 HGC-27细胞的增殖、凋亡及放射敏感性。方法：收集于青海省第五人民医院接受手术的胃癌患者（21例）及化疗抵抗胃癌患者 （19例）的癌组织和癌旁组织,以qPCR检测胃癌组织、化疗抵抗胃癌组织和胃癌HGC-27细胞中LINC01018、miR-297的表达。双 荧光素酶报告基因实验验证 LINC01018 与 miR-297 之间的靶向关系。在 HGC-27 细胞中转染 LINC01018 过表达质粒 pcDNA[1]LINC01018或miR-297抑制剂,或共转染pcDNA-LINC01018和miR-297模拟物,以qPCR检测验证细胞转染效果。MTT和克隆 形成实验检测转染后HGC-27细胞的增殖活力与克隆形成能力,流式细胞术检测转染后HGC-27细胞的凋亡率,克隆形成实验检 测各组转染后HGC-27细胞的放射敏感性,WB实验检测细胞中Ki67、cleaved-caspase3、pro-caspase3蛋白的表达。结果：与癌旁 组织或胃正常黏膜上皮细胞GES-1相比,胃癌组织、化疗抵抗胃癌组织和胃癌HGC-27细胞中LINC01018呈低表达、miR-297呈 高表达（均P<0.01）。LINC01018与miR-297存在靶向结合关系,LINC01018负向调控miR-297的表达。过表达LINC01018或敲 减miR-297可抑制HGC-27细胞的增殖活力与克隆形成能力、降低细胞存活率,促进细胞的凋亡、下调Ki67和pro-caspase3蛋白表 达水平、上调cleaved-caspase3蛋白表达水平、提高HGC-27细胞的放射敏感性（均P<0.01）。共转染pcDNA-LINC01018和miR[1]297模拟物可逆转过表达LINC01018对HGC-27细胞的所有上述作用,尤其可逆转其对HGC-27细胞的放射增敏作用（P<0.05或P<0.01）。结论：LINC01018通过下调miR-297表达抑制胃癌HGC-27细胞增殖而促进凋亡和增强细胞的放射敏感性,该作用与 Ki67和caspase3的表达变化有关。     

基因间长链非编码RNA00963通过靶向miRNA-511-3p调控胰腺癌细胞增殖、迁移和侵袭的分子机制研究

目的 探讨基因间长链非编码RNA00963(LINC00963)对胰腺癌细胞增殖、迁移和侵袭的影响及分子机制.方法 常规培养正常胰腺上皮细胞hTERT-HPNE和胰腺癌细胞系Capan-1、SW1990、PaTu8988,将Capan-1细胞分为NC组、si-NC组、si-LINC00963组、pcDNA-NC组、pcDNA-LINC00963组、miRNA-NC组、miRNA-511-3p组、anti-miRNA-NC组、anti-miRNA-511-3p组、si-LINC00963+anti-miRNA-NC组、si-LINC00963+anti-miRNA-511-3p组.采用实时荧光定量聚合酶链反应检测LINC00963和miRNA-511-3p的表达水平,蛋白质印迹(Western blot)法检测细胞周期蛋白D1(cyclin D1)、基质金属蛋白酶(MMP)2、MMP9的表达水平,细胞计数试剂盒8(CCK-8)检测细胞增殖,Transwell实验检测细胞迁移和侵袭,双荧光素酶报告实验检测LINC00963和miRNA-511-3p的靶向调控关系.结果 与正常胰腺上皮细胞hTERT-HPNE比较,胰腺癌细胞系Capan-1、SW1990、Pa-Tu8988中LINC00963相对表达量均升高,miRNA-511-3p相对表达量均降低(P<0.05).与si-NC组比较,si-LINC00963组中cyclin D1、MMP2、MMP9相对表达量均降低,细胞活性降低,细胞迁移和侵袭数目均减少(P<0.05);与miRNA-NC组比较,miRNA-511-3p组中cyclin D1、MMP2、MMP9相对表达量均明显降低,细胞活性明显降低,细胞迁移和侵袭数目均明显减少(P<0.01).miRNA-511-3p与LINC00963野生型报告质粒共转染后Ca-pan-1细胞的荧光素酶活性明显低于miRNA-NC与LINC00963野生型报告质粒共转染后的细胞(P<0.01).与si-LINC00963+anti-miRNA-NC组比较,si-LINC00963+anti-miRNA-511-3p组中cyclin D1、MMP2、MMP9相对表达量均升高,细胞活性升高,细胞迁移和侵袭数目均增加(P<0.05).结论 低表达LINC00963可通过靶向上调miRNA-511-3p的表达抑制胰腺癌细胞增殖、迁移和侵袭.     

基因间长链非编码RNA152靶向微小RNA?103a?3p对非小细胞肺癌细胞增殖和侵袭迁移的影响

目的探讨基因间长链非编码RNA 152(LINC00152)靶向调控微小RNA-103a-3p(miR-103a-3p)表达及对非小细胞肺癌(NSCLC)细胞增殖和侵袭迁移的影响。方法采用实时定量PCR(QPCR)检测正常肺上皮细胞BEAS-2B及NSCLC细胞(ANIP-973、NCI-H157、A549和NCI-H1975)的LINC00152水平。选取LINC00152水平最高的细胞分别转染LINC00152特异性小干扰RNA(si-LINC00152组)或无关序列(si-NC组),另设未转染细胞为对照组。QPCR检测LINC00152水平,活细胞计数CCK-8法、Transwell小室和划痕实验测定细胞增殖、侵袭和迁移能力,Western blotting检测基质金属蛋白酶(MMP)-2、MMP-9和第10号染色体缺失的磷酸酶及张力蛋白同源基因(PTEN)的水平;荧光素酶报告实验验证LINC00152靶向结合miR-103a-3p的能力。结果NSCLC细胞的LINC00152水平均高于BEAS-2B细胞(P<0.05),尤其是NCI-H1975细胞的最高。si-LINC00152组的LINC00152水平为0.352±0.087,低于对照组的1.058±0.219和si-NC组的1.126±0.139(P<0.05)。与si-NC组和对照组相比,si-LINC00152组NCI-H1975细胞转染48、72 h的增殖活力下降(P<0.05);si-LINC00152组的划痕愈合率和穿膜细胞数分别为(27.386±2.428)%和(78.840±5.031)个,低于si-NC组的(77.675±4.803)%和(179.208±13.264)个及对照组的(76.371±5.385)%和(174.003±15.678)个(P<0.05);与si-NC组和对照组相比,si-LINC00152组的MMP-2和MMP-9水平均降低,而PTEN水平升高(P<0.05)。对照组和si-NC组上述指标的差异无统计学意义(P>0.05)。双荧光素酶报告分析证实,miR-103a-3p模拟物降低了野生型LINC00152的荧光素酶活性(P<0.05),但对突变型无影响(P>0.05)。结论LINC00152在NSCLC细胞中高表达并发挥促癌作用,与NSCLC的迁移侵袭密切相关,LINC00152与miR-103a-3p间的相互作用在NSCLC靶向治疗中有一定潜能。     

抑制LINC00958表达调控miR-422a促进结直肠癌细胞凋亡及放射敏感性的机制

目的 探讨lncRNA LINC00958对结直肠癌细胞凋亡及放射敏感性的影响以及其作用机制。方法 将pcDNA、pcDNA-LINC00958、si-NC、si-LINC00958、miR-NC和miR-422a质粒分别转染到SW480细胞中,并分别记为pcDNA组、pcDNA-LINC00958组、si-NC组、si-LINC00958组、miR-NC组和miR-422a组;将anti-miR-NC和anti-miR-422a质粒分别与si-LINC00958共转染到SW480细胞中,并分别记为si-LINC00958+anti-miR-NC组和si-LINC00958+anti-miR-422a组;分别将miR-NC和miR-422a分别转染到WT-LINC00958和MUT-LINC00958组细胞中,检测荧光活性;转染均用脂质体法。采用qRT-PCR检测miR-422a和LINC00958的表达;Western blot检测蛋白表达;流式细胞术检测细胞凋亡;细胞克隆形成实验检测对结直肠癌细胞放射敏感性的影响;双荧光素酶报告基因检测实验检测荧光活性。结果 结直肠癌细胞中LINC00958高表达,miR-422a低表达;抑制LINC00958表达和过表达miR-422a,可促进结直肠癌细胞凋亡,并增加细胞放射敏感性。LINC00958可靶向调节miR-422a表达;抑制miR-422a,逆转了抑制LINC00958表达对结直肠癌细胞的放射增敏和细胞凋亡促进的作用。结论 抑制LINC00958表达,增加结直肠癌细胞的放射敏感性,并促细胞凋亡,其机制可能与调控miR-422a有关,将为结直肠癌治疗提供新靶点和新思路。     

Inhibiting lncRNA LINC00958 expression promotes apoptosis of colorectal cancer cells and increases the radiosensitivity throuth targeting miR-422a

Objective To investigate the effect of lncRNA LINC00958 on the apoptosis and radiosensitivity of colorectal cancer cells and its underlying mechanism. Methods The pcDNA, pcDNA-LINC00958, si-NC, si-LINC00958, miR-NC, and miR-422a plasmids were transfected into SW480 cells and assigned into the pcDNA group, pcDNA-LINC00958 group, si-NC group, si-LINC00958 group, miR-NC group, miR-422a group, respectively. Anti-miR-NC and anti-miR-422a plasmids were co-transfected into SW480 cells with si-LINC00958, and assigned into the si-LINC00958+anti-miR-NC group and si-LINC00958+anti-miR-422a group. miR-NC and miR-422a were transfected into the WT-LINC00958 and MUT-LINC00958 cells, respectively. The fluorescence activity was detected. Cell transfection was performed by liposome method. The expression levels of miR-422a and LINC00958 were measured by qRT-PCR. The expression levels of proteins were detected by Western Blot. Cell apoptosis was assessed by flow cytometry. The radiosensitivity of colorectal cancer cells was evaluated by cell clone formation assay. The fluorescence activity was detected by dual luciferase reporter assay. Results High expression of LINC00958 and low expression of miR-422a were observed in colorectal cancer cells. Inhibition of LINC00958 expression and overexpression of miR-422a could promote cell apoptosis and increase cell radiosensitivity of colorectal cancer cells. LINC00958 could target the regulation of miR-422a expression. Inhibition of miR-422a reversed the effect of inhibiting the expression of LINC00958 on increasing the radiosensitization and promoting cell apoptosis of colorectal cancer cells. Conclusions Inhibition of LINC00958 expression increases the radiosensitivity and promotes the apoptosis of colorectal cancer cells. The mechanism may be related to the regulation of miR-422a, which will provide new targets and new ideas for the treatment of colorectal cancer.     

Radiosensitivity of lncrna linc00909 targeting mir-548-3p on colorectal cancer cells

Objective To investigate whether lncRNA LINC00909 affected the radiosensitivity of colorectal cancer cells by targeting miR-548-3p. Methods The expression levels of LINC00909 and miR-584-3p in colorectal cancer and adjacent tissues were detected by qRT-PCR. The colorectal cancer cells SW480 and SW620 were cultured in vitro, and transfected with si-NC, si-LINC00909, miR-NC, miR-584-3p mimics, si-LINC00909, and anti-miR-NC and si-LINC00909, and anti-miR-584-3p, respectively. The cells were irradiated with a dose of 4 Gy. The cell survival fraction and sensitization enhancement ratio (SER) were detected by clone formation assay. Cell proliferation was detected by MTT assay. Cell migration and invasion were assessed by Trans well chamber assay. The targeting relationship between LINC00909 and miR-584-3p was confirmed by dual luciferase reporter assay. The effect of interfering with the expression of LINC00909 or inhibiting the expression of miR-584-3p on the weight of the xenograft tumor after irradiation was evaluated by subcutaneous xenograft experiment in nude mice. Results The expression level of LINC00909 in colorectal cancer tissues was significantly up-regulated (P<0.05), whereas the expression level of miR-584-3p was significantly down-regulated (P<0.05). After interfering with the expression of LINC00909 or miR-584-3p overexpression, the cell survival fraction score was significantly reduced (P<0.05), the SERs were 2.017 and 1.762, and cell proliferation, migration and invasion were suppressed (all P<0.05). Dual luciferase reporter assay confirmed that LINC00909 could target and bind to miR-584-3p. After interfering with the expression of LINC00909, the weight of the transplanted tumor was significantly reduced (P<0.05), whereas the weight of the transplanted tumor was significantly increased after co-transfection with anti-miR-584-3p (P<0.05). Conclusion Interfering with the expression of LINC00909 can inhibit the proliferation, migration and invasion ability of colorectal cancer cells by up-regulating the expression of miR-548-3p, thereby enhancing the cell radiosensitivity.     

TFESB调控lncRNA LINC00858/miR-324-5p通路抑制宫颈癌细胞的增殖、迁移和侵袭

目的:探讨半枝莲总黄酮提取物(total fiavonoids extract from Scutellaria barbata D.Don,TFESB)调控长链非编码RNA(lncRNA) LINC00858/miR-324-5p通路对宫颈癌细胞增殖、迁移和侵袭的影响及其机制.方法:qRT-PCR检测20例宫颈癌组织...     

Long Noncoding RNA LINC02163 Accelerates Malignant Tumor Behaviors in Breast Cancer by Regulating the MicroRNA-511-3p/HMGA2 Axis

Long intergenic nonprotein-coding RNA 02163 (LINC02163) has been reported to be upregulated and work as an oncogene in gastric cancer. The aims of the present study were to determine the expression profile and clinical value of LINC02163 in breast cancer. Additionally, the detailed functions of LINC02163 in breast cancer were explored, and relevant molecular events were elucidated. In this study, LINC02163 was upregulated in breast cancer, and its expression level was closely associated with tumor size, lymph node metastasis, and TNM stage. Patients with breast cancer presenting high LINC02163 expression exhibited shorter overall survival than those presenting low LINC02163 expression. Knockdown of LINC02163 resulted in a decrease in breast cancer cell proliferation, migration, and invasion and an increase in cell apoptosis in vitro. In addition, silencing of LINC02163 impeded breast cancer tumor growth in vivo. Mechanistic investigation revealed that LINC02163 served as a competing endogenous RNA for microRNA-511-3p (miR-511-3p) and consequently upregulated the expression of the high-mobility group A2 (HMGA2), a downstream target of miR-511-3p. Intriguingly, miR-511-3p inhibition and HMGA2 restoration counteracted the effects of LINC02163 deficiency on the malignant properties of breast cancer cells. LINC02163 exerts cancer-promoting effects during the initiation and progression of breast cancer via regulation of the miR-511-3p/HMGA2 axis. Our findings add to our understanding of the roles of the LINC02163/miR-511-3p/HMGA2 pathway as a regulator of breast cancer pathogenesis and may be useful in the development of lncRNA-directed cancer diagnosis, prognosis, and therapy.