Regulatory network analysis of LINC00472, a long noncoding RNA downregulated by DNA hypermethylation in colorectal cancer

Colorectal cancer (CRC), one of the common malignant cancers in the world, is caused by accumulated alterations of genetic and epigenetic factors over a long period of time. Along with that protein‐coding genes being identified as oncogenes or tumor suppressors in CRC, a number of lncRNAs have also been found to be associated with CRC. Considering the important regulatory role of lncRNAs, the first goal of this study was to identify CRC‐associated lncRNAs from a public database. One such lncRNA, LINC00472, was verified to be downregulated in CRC cell lines and cancer tissues compared with adjacent tissues. In addition, the down‐regulation of LINC00472 seemed to be caused by DNA hypermethylation at its promoter region. Furthermore, the expression of LINC00472 and DNA methylation of promoter were significantly correlated with clinicopathological features. And DNA hypermethylation of LINC00472 may serve as a better diagnostic biomarker than its expression for CRC. Finally, we predicted the functions of LINC00472 and constructed a regulatory network and found LINC00472 may be involved in cell cycle and cell proliferation processes. Our results may provide a clue to further research into the function and regulatory mechanism of LINC00472 in CRC.     

LINC01123 enhances osteosarcoma cell growth by activating the Hedgehog pathway via the miR-516b-5p/Gli1 axis

The lncRNA LINC01123 has been reported to act as an oncogene in many human cancers. Nevertheless, the function and underlying mechanism of LINC01123 in osteosarcoma (OS) remain unclear. This study aimed to explore the roles and mechanisms of LINC01123 in OS progression. In this study, the expression of LINC01123 was significantly upregulated in OS cell lines than in a human osteoblast cell line. Furthermore, in vitro and in vivo experiments confirmed that knockdown of LINC01123 suppressed cell progression. Mechanistically, LINC01123 acted as a competing endogenous RNA by sponging miR-516b-5p, thus, increasing Gli1 expression by directly targeting its 3ʹUTR. Taken together, LINC01123 enhances OS proliferation and metastasis via the miR-516b-5p/Gli1 axis. Therefore, LINC01123 may be a potential therapeutic target for OS treatment.     

lncRNA LINC01410通过miR-205-5p调控胶质瘤A172细胞的增殖、凋 亡和替莫唑胺敏感性

目的：探讨长链非编码RNA（lncRNA）LINC01410对胶质瘤A172细胞增殖、凋亡和替莫唑胺（temozolomide, TMZ）敏 感性的影响及其机制。方法: 用qPCR法检测胶质瘤细胞系H4、SHG-44、A172和正常星形胶质细胞HA1800中LINC01410表达 水平。将LINC01410 shRNA、shRNA control和miR-205-5p 抑制剂（inhibitor）、inhibitor control转染至A172细胞,MTT法、流式细 胞术分别检测400 μmol/L TMZ处理后,转染细胞的增殖活性和凋亡水平,WB法检测细胞中Bax、Bcl-2、cyclin D1、p27的表达。 在线生物信息学软件LncBase分析LINC01410的靶基因,双荧光素酶报告基因实验验证LINC01410与miR-205-5p的靶向关系。 结果: LINC01410在3种胶质瘤细胞中的表达水平均显著高于正常星形胶质细胞HA1800（均P<0.01）,以在A172细胞中的表达 水平最高（P<0.01）。转染LINC01410 shRNA和TMZ 处理后 ,A172 细胞的增殖能力下降、G1 期细胞比例和凋亡率均升高 （均 P<0.01）,细胞中 Bax、p27 表达水平升高而 Bcl-2、cyclin D1 表达水平下降（均P<0.01）。双荧光素酶报告基因实验证实 LINC01410 靶向结合 miR-205-5p,下调 LINC01410 促进 miR-205-5p 表达。转染 miR-205-5p 抑制剂可逆转下调 LINC01410 和 TMZ处理对A172细胞增殖、周期和凋亡的影响。结论: 下调lncRNA LINC01410可抑制胶质瘤A172细胞增殖、阻滞细胞周期、 诱导细胞凋亡且提高对TMZ敏感性,其发生机制似与LINC01410对miR-205-5p的靶向作用有关。     

长链非编码RNA LINC01018在非小细胞肺癌中的表达与意义

目的:探讨长链非编码RNA LINC01018在非小细胞肺癌(non-small cell lung cancer,NSCLC)组织中的表达水平和临床意义,以及LINC01018对NSCLC细胞增殖的影响.方法:用qRT-PCR检测60例NSCLC组织和癌旁肺组织中LINC01018的表达,分析LINC01018表达与非小细胞肺癌临床特征的相关性.通过转染pcDNA-LINC01018上调 LINC01018的表达水平,采用qRT-PCR方法检测重组质粒在细胞中的表达水平.CCK8检测NSCLC细胞增殖能力的变化,Western blot法检测LINC01018对RAC1蛋白的影响.结果:相比癌旁肺组织,在NSCLC组织中LINC01018的表达出现显著下调.肺癌组织中LINC01018的表达水平与患者性别、肿瘤大小、分化程度及淋巴转移和远端转移明显相关(P<0.05).LINC01018的过表达能降低肺癌细胞的增殖能力并下调RAC1的表达.结论:LINC01018表达随着女性患者、肿瘤直径大、分期晚及分化差而显著下调.LINC01018可通过影响RAC1,抑制NSCLC细胞的增殖.     

罗哌卡因抑制人肝癌细胞系Hep3B增殖、迁移和侵袭

目的 研究罗哌卡因对人肝癌细胞系Hep3B生物学行为的影响,并探讨其分子机制.方法 设置对照组、罗哌卡因组、si-NC组、si-LINC00853组、pcDNA-NC组、pcDNA-LINC00853组、(罗哌卡因+pcDNA-NC)组、(罗哌卡因+pcDNA-LINC00853)组.采用细胞计数试剂盒(CCK-8法)...     

LINC01232 serves as a novel biomarker and promotes tumour progression by sponging miR-204-5p and upregulating RAB22A in clear cell renal cell carcinoma

BackgroundLong non-coding RNAs (lncRNAs) are involved in the progression of various cancers, including clear cell renal cell carcinoma (ccRCC). This study aimed to investigate the expression and prognostic value of long intergenic non-protein coding RNA (LINC) 01232 in ccRCC and preliminary explore the molecular mechanism underlying the role of LINC01232 in ccRCC progression.MethodsTumour tissues and adjacent normal tissues of 122 patients with ccRCC were collected in this study. The levels of LINC01232, microRNA (miR)-204-5p and RAB22A were measured by quantitative real-time PCR. The proliferation, migration and invasion of ccRCC cells were detected by cell counting kit-8 assay and Transwell assay, respectively. The interaction among LINC01232, miR-204-5p and RAB22A was confirmed by bioinformatics analysis, dual-luciferase reporter assay and Pearson correlation analysis. The association of LINC01232 and miR-204-5p with ccRCC patient survival was verified by the Kaplan–Meier method and log-rank test. The prognostic value of LINC01232 in ccRCC was confirmed by Cox regression analysis.ResultsLINC01232 expression was increased in ccRCC tumour tissues and ccRCC cells and independently predicted the prognosis of ccRCC patients. In addition, LINC01232 silencing inhibited ccRCC cell proliferation, migration and invasion. Moreover, LINC01232 served as a sponge for miR-204-5p, and miR-204-5p reduction reversed the inhibitory effect of LINC01232 silencing on ccRCC cell function. Furthermore, LINC01232 could sponge miR-204-5p, causing the elevation of RAB22A in ccRCC, thereby promoting ccRCC cell function.ConclusionLINC01232 may be an independent prognostic biomarker in ccRCC and plays an oncogenic role in ccRCC progression by sponging miR-204-5p and upregulating RAB22A.     

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。     

lncRNA LINC00339通过下调miR-149-5p表达调控ox-LDL诱导的人脑微血管内皮细胞损伤

目的:探讨长链非编码RNA(lncRNA)LINC00339对氧化型低密度脂蛋白(ox-LDL)诱导的人脑微血管内皮细胞(HBMEC)损伤的影响及分子机制.方法:将HBMEC分为对照组(未经任何处理)、ox-LDL(50 mg/L)组、ox-LDL+si-NC组(转染si-NC+50 mg/L ox-LDL)、ox-L...     

Correction to “Novel long non-coding RNA LINC02532 promotes gastric cancer cell proliferation,migration, and invasion in vitro”

We have replaced the misapplied images and the revised Figure 3 is provided.     

Development and validation of a noninvasive 2-gene molecular assay for cutaneous melanoma

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