检索结果-内蒙古大学图书馆

long noncoding rna AWPPH promotes hepatocellular carcinoma progression through YBX1 and serves as a prognostic biomarker

引用

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE 2017年第7期1863卷 1805-1816页

作者： Zhao, Xiaodong Liu, Yanbo Yu, Shuo Hebei Med Univ Hosp 2 Dept Oncol Surg 215 Peace West Rd Shijiazhuang 050000 Peoples R China Feixiang Cent Hosp Dept Surg 1 Handan 057550 Peoples R China

long noncoding rnas (Incrnas) have been shown to play important roles in various cancers. However, the clinical significances and biological roles of Incrnas in hepatocellular carcinoma (HCC) remain largely unknown. In this study, using online-available data sets and quantitative real-time PCR, we identified a novel lncrna termed lncrna-AWPPH, which is highly expressed in HCC tissues. Its upregulation is correlated with encapsulation incomplete, microvascular invasion, advanced TNM stage and BCLC stage. Cox proportional hazards regression analysis revealed that high lncrna-AWPPH expression is an independent prognostic factor for poor recurrence-free and overall survival. Functional experiments showed that overexpression of lncrna-AWPPH promotes HCC cell proliferation and migration in vitro, and tumor growth and metastasis in vivo. Conversely, depletion of lncrna-AWPPH has opposite effects on HCC. Mechanistically, Incrna-AWPPH interacts with YBX1, promotes YBX1-mediated activation of SNAIL1 translation, and upregulates SNAILI expression. Furthermore, Incrna-AWPPH promotes YBX1-mediated activation of PIK3CA transcription, upregulates PIK3CA expression, and activates PI3K/AKT pathway. Depletion of YBX1 abolishes the effects of lncrna-AWPPH on SNAILI and PIK3CA, and also the biological roles of lncrna-AWPPH on HCC cells. In conclusion, this study identifies a novel Incrna termed lncrna-AWPPH which is highly expressed in HCC, indicates poor prognosis of HCC patients, and promotes HCC cell proliferation, migration, and in vivo tumor growth and metastasis via a novel regulatory mechanism of interacting with YBX1.

关键词： long noncoding rna Hepatocellular carcinoma Proliferation Metastasis YBX1

来源：评论

学校读者我要写书评

暂无评论

long noncoding rna myocardial infarction-associated transcript regulated the pancreatic stellate cell activation to promote the fibrosis process of chronic pancreatitis

引用

JOUrnaL OF CELLULAR BIOCHEMISTRY 2019年第6期120卷 9547-9555页

作者： Liu, Hao Yu, Kaihuan Ma, Peng Xiong, Liangkun Wang, Maoming Wang, Weixing Wuhan Univ Dept Hepatobiliary Surg Renmin Hosp East Hosp Wuhan Hubei Peoples R China Wuhan Univ Renmin Hosp Dept Hepatobiliary Surg 99 ZhangZhiDong St Wuhan 430060 Hubei Peoples R China

Backgroundlong noncoding rnas (lncrnas) play crucial roles in fibrosis process. In our previous rna-seq study, we found that lncrna myocardial infarction-associated transcript (MIAT) was differentially expressed in pancreatic tissues of chronic pancreatitis (CP) patients. However, the function of MIAT in CP remains unknown. This study was aimed to investigate the function and underlying mechanism of MIAT in pancreatic fibrosis. Materials and MethodsThe expression levels of MIAT, miR-216a-3p, cyclooxygenase 2 (COX-2), -smooth muscle actin (-SMA), and collagen I were estimated by Western blot analysis and qualitative reverse transcription polymerase chain reaction. The relationships between miR-216a-3p,MIAT, and COX-2 were confirmed by luciferase reporter assay. The proliferation of human pancreatic stellate cells (HPaSteCs) was detected by cell counting kit-8 assay. ResultsWe found that MIAT, along with the levels of fibrosis-related proteins -SMA and collagen I, as well as COX-2 were upregulated, while miR-216a-3p was downregulated in transforming growth factor (TGF)-1-stimulated HPaSteCs. Mechanistically, MIAT acted as a molecular sponge for miR-216a-3p. Furthermore, we identified COX-2 as a direct target of miR-126a-3p. Additionally, MIAT overturned the inhibitory effect of miR-216a-3p overexpression and COX-2 knockdown on the activation and proliferation of HPaSteCs. ConclusionOur study provided mechanistic insights into a critical role for MIAT as a mirna sponge in CP.

关键词： chronic pancreatitis human pancreatic stellate cells long noncoding rna myocardial infarction-associated transcript

来源：评论

学校读者我要写书评

暂无评论

long noncoding rna SPRY4-IT1 promotes esophageal squamous cell carcinoma cell proliferation, invasion, and epithelial-mesenchymal transition

引用

TUMOR BIOLOGY 2016年第8期37卷 10871-10876页

作者： Cui, Fei Wu, Duoguang He, Xiaotian Wang, Wenjian Xi, Jingle Wang, Minghui Southern Med Univ Nanfang Hosp Dept Oncol Guangzhou 510515 Guangdong Peoples R China Sun Yat Sen Univ Sun Yat Sen Mem Hosp Dept Thorac Surg Guangdong Prov Key Lab Malignant Tumor Epigenet & Guangzhou 510120 Guangdong Peoples R China

The biology of esophageal squamous cell carcinoma (ESCC) remains poorly understood. long noncoding rnas (lncrnas) are found to be dysregulated in a variety of cancers, including ESCC. SPRY4-IT1 has been recently revealed as oncogenic regulator or tumor suppressors in different cancers;however, whether SPRY4-IT1 is involved in ESCC remains poorly understood. To investigate the role of SPRY4-IT1 in ESCC, we evaluated the SPRY4-IT1 expression levels in a series of ESCC patients and a panel of ESCC cell line using qRT-PCR. CCK8 and colony formation assay were performed to assess the effect of SPRY4-IT1sirna on cell proliferation, migration, and invasion of ESCC cell lines. SPRY4-IT1 expression was upregulated in ESCC tissues and the higher expression of SPRY4-IT1 was significantly correlated with tumor grade, depth of invasion, and lymph node metastasis. Moreover, silencing of SPRY4-IT1 expression inhibited ESCC cell proliferation, colony formation, migration, and invasion. Therefore, our study indicates that SPRY4-IT1 promotes proliferation and migration of ESCC cells and is a potential oncogene of ESCC.

关键词： SPRY4-IT1 long noncoding rna Esophageal squamous cell carcinoma EMT

来源：评论

学校读者我要写书评

暂无评论

long noncoding rna JAKMIP2-AS1 Promotes the Growth of Colorectal Cancer and Indicates Poor Prognosis

引用

ONCOTARGETS AND THERAPY 2021年 14卷 763-772页

作者： Ma, Tianyi Qiao, Tianyu Yuan, Ziming Wang, Guiyu Huang, Rui Wang, Meng Hu, Hanqing Zhu, Yihao Zou, Xiaoming Wang, Xishan Harbin Med Univ Dept Colorectal Surg Affiliated Hosp 2 Harbin 150001 Peoples R China Harbin Med Univ Dept Gen Surg Affiliated Hosp 2 Harbin 150001 Peoples R China Chinese Acad Med Sci Canc Inst & Hosp Peking Union Med Coll Dept Colorectal Surg Beijing 100021 Peoples R China

Background: The identification of cancer-associated long noncoding rnas and the investigation of their molecular and biological functions are important for understanding the molecular biology and progression of cancer. JAKIV1IP2-AS1 has not been reported in the literature, especially in the context of colorectal cancer. The aim of the present study was to examine the expression pattern of JAKMIP2-AS1 in colorectal cancer (CRC) and evaluate its biological role and clinical significance in tumor progression. Methods: JAKMIP2-AS1 expression was analyzed in 56 CRC tissues and nine CRC cell lines by quantitative reverse-transcription polymerase chain reaction (qRT-PCR). Overexpression and rna interference (rnai) approaches were used to investigate the biological functions of JAKMIP2-AS1. The effect of JAKMIP2-AS1 on proliferation was evaluated by CCK-8, colony formation, and EdU assays. Subcutaneous injection of cells was used to study proliferation in BALB/c nude male mice. Proliferation-related protein levels were examined by immunohistochemical analysis. Differences between groups were tested for significance using Student's t-test (two-tailed). Results: JAKMIP2-AS1 was highly expressed in both CRC samples and cell lines compared with the corresponding normal counterparts. The upregulation of JAKMIP2-AS1 expression promoted the proliferation of colorectal cancer cells. Moreover, patients with high levels of JAKMIP2-AS1 expression had a relatively poor prognosis. Inhibition of JAKMIP2-AS1 by rnai decreased the proliferation of CRC cells in vitro and impeded cell growth in vivo. Ki67 and PCNA levels were affected by JAKMIP2-AS1 knockdown or overexpression in vivo. Conclusion: Our findings indicate that JAKMIP2-AS1 is significantly upregulated in CRC tissues and regulates CRC cell proliferation. Thus, JAKMIP2-AS1 may represent a new marker of poor prognosis and is a potential therapeutic target for CRC intervention.

关键词： colorectal cancer long noncoding rna proliferation prognosis

来源：评论

学校读者我要写书评

暂无评论

long noncoding rna, CCDC26, controls myeloid leukemia cell growth through regulation of KIT expression

引用

MOLECULAR CANCER 2015年第1期14卷 1-16页

作者： Hirano, Tetsuo Yoshikawa, Ryoko Harada, Hironori Harada, Yuka Ishida, Atsuhiko Yamazaki, Takeshi Hiroshima Univ Domain Life Sci Grad Sch Integrated Arts & Sci Higashihiroshima Hiroshima 7398521 Japan Juntendo Univ Dept Hematol Sch Med Bunkyo Ku Tokyo 1138421 Japan

Background: Accumulating evidence suggests that some long noncoding rnas (lncrnas) are involved in certain diseases, such as cancer. The lncrna, CCDC26, is related to childhood acute myeloid leukemia (AML) because its copy number is altered in AML patients. Results: We found that CCDC26 transcripts were abundant in the nuclear fraction of K562 human myeloid leukemia cells. To examine the function of CCDC26, gene knockdown (KD) was performed using short hairpin rnas (shrnas), and four KD clones, in which CCDC26 expression was suppressed to 1% of its normal level, were isolated. This down-regulation included suppression of CCDC26 intron-containing transcripts (the CCDC26 precursor mrna), indicating that transcriptional gene suppression (TGS), not post-transcriptional suppression, was occurring. The shrna targeting one of the two CCDC26 splice variants also suppressed the other splice variant, which is further evidence for TGS. Growth rates of KD clones were reduced compared with non-KD control cells in media containing normal or high serum concentrations. In contrast, enhanced growth rates in media containing much lower serum concentrations and increased survival periods after serum withdrawal were observed for KD clones. DNA microarray and quantitative polymerase chain reaction screening for differentially expressed genes between KD clones and non-KD control cells revealed significant up-regulation of the tyrosine kinase receptor, KIT, hyperactive mutations of which are often found in AML. Treatment of KD clones with ISCK03, a KIT-specific inhibitor, eliminated the increased survival of KD clones in the absence of serum. Conclusions: We suggest that CCDC26 controls growth of myeloid leukemia cells through regulation of KIT expression. A KIT inhibitor might be an effective treatment against the forms of AML in which CCDC26 is altered.

关键词： long noncoding rna Myeloid leukemia cells Cell survival Receptor tyrosine kinase shrna-induced transcriptional gene suppression Stem cell factor Serum depletion

来源：评论

学校读者我要写书评

暂无评论

long noncoding rna HOXA-AS2 regulates the expression of SCN3A by sponging miR-106a in breast cancer

引用

JOUrnaL OF CELLULAR BIOCHEMISTRY 2019年第9期120卷 14465-14475页

作者： Wu, Jie Li, Maolan Zhang, Yijian Shanghai Jiao Tong Univ Sch Naval Architecture Ocean & Civil Engn Key Lab Hydrodynam Minist Educ 800 Dongchuan Rd Shanghai 200240 Peoples R China Shanghai Res Ctr Biliary Tract Dis Shanghai Peoples R China Shanghai Key Lab Biliary Tract Dis Res Shanghai Peoples R China

Breast cancer is the most commonly diagnosed cancer that affects women worldwide. This study aimed to investigate the competing endogenous rnas (cernas) mechanism in breast cancer. Microarray data were downloaded from the University of California Santa Cruz (UCSC) Xena database. The limma package was used to screen the differentially expressed messenger rnas (DEMs) and differentially expressed long noncoding rnas (DELs). Subsequently, functional analysis was performed using DAVID tool. After constructing the protein-protein interaction (PPI) network, we identified the major gene modules using the Cytoscape software. Univariate survival analysis in the survival package was performed. Finally, the cerna regulatory network was constructed to identify the critical genes. A total of 1380 DEMs and 345 DELs were identified in breast cancer samples compared with normal samples. Functional enrichment analysis showed that DEMs were mainly involved in cell division, and cell cycle. We screened four major gene modules and identified the hub nodes in these functional modules. Several DEMs (including FABP7, C4BPA, and LAMB3) and three long noncoding rnas (lncrnas) (LINC00092, ***1, and COLCA1) exhibited significant correlation with patients' survival outcomes. In the cerna network, the lncrna HOXA-AS2 regulated the expression level of SCN3A by interacting with hsa-miR-106a-5p. Thus, our study investigated the cerna mechanism in breast cancer. The results showed that lncrna HOXA-AS2 might modulate the expression of SCN3A by sponging miR-106a in breast cancer.

关键词： breast cancer competing endogenous rna network differentially expressed genes long noncoding rna protein-protein interaction network

来源：评论

学校读者我要写书评

暂无评论

long noncoding rna LUCAT1 promotes malignancy of ovarian cancer through regulation of miR-612/HOXA13 pathway

引用

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2018年第3期503卷 2095-2100页

作者： Yu, He Xu, Yajie Zhang, Dongya Liu, Guangxin Zhoukou Cent Hosp Dept Gynaecol 26 Renmin Rd Zhoukou 466000 Peoples R China Zhengzhou Univ Affiliated Hosp 1 Dept Gynaecol Zhengzhou 450052 Henan Peoples R China

Emerging evidence shows that long noncoding rna (Incrna) is implicated in numerous kinds of malignant cancers, including ovarian cancer. In this study, we focused on the expression and function of long noncoding rna lung cancer associated transcript 1 (LUCAT1) in ovarian cancer progression. We indicated that LUCAT1 expression was significantly upregulated in ovarian cancer tissues. Moreover, LUCAT1 expression was positively associated with tumor metastasis and clinical stage. Elevated expression of LUCAT1 decreased the survival rate of patients with ovarian cancer. In addition, we revealed that repression of LUCAT1 significantly suppressed the proliferation, migration and invasion, whereas promoted apoptotic rate. Through online predictive tools and functional experiments, we demonstrated that LUCAT1 and HOXA13 were targets of miR-612. We showed that LUCAT1 and miR-612 suppressed each other in a reciprocal way. Moreover, LUCAT1 promoted HOXA13 expression through inhibition of miR-612, eventually leading to ovarian cancer development. In conclusion, our findings revealed a novel molecular mechanism that LUCAT1 imiR-612/HOXA13 pathway modulates ovarian cancer progression. (C) 2018 Elsevier Inc. All rights reserved.

关键词： Ovarian cancer long noncoding rna LUCAT1 miR-612 HOXAI3 Progression

来源：评论

学校读者我要写书评

暂无评论

long noncoding rna BCAR4 promotes osteosarcoma progression through activating GLI2-dependent gene transcription

引用

TUMOR BIOLOGY 2016年第10期37卷 13403-13412页

作者： Chen, Fenyong Mo, Jiadong Zhang, Li Fujian Med Univ Union Hosp Dept Orthopaed Fuzhou 350001 Peoples R China Fujian Univ Tradit Chinese Med Coll Orthopaed & Traumatol Fuzhou 350122 Peoples R China

Despite great advances have been made in the understanding of biology of osteosarcoma, the molecular mechanisms involved in osteosarcoma tumorigenesis and progression are still largely unknown. long noncoding rna (lncrna) is a new type of rna molecule, which plays pivotal roles in many tumors. lncrna BCAR4 has been identified as an oncogenetic lncrna involved in the progression of breast cancer. However, the functions and clinical significances of BCAR4 in osteosarcoma are unknown now. In this study, we found that BCAR4 was significantly upregulated in osteosarcoma tissues. Increased expression of BCAR4 was significantly correlated with large tumor size, advanced Enneking stage, lung metastasis, and poor prognosis. Functional experiments demonstrated that knockdown of BCAR4 inhibits the proliferation and migration of osteosarcoma cell in vitro. Consistently, knockdown of BCAR4 inhibits osteosarcoma tumorigenesis and lung metastasis in vivo. Chromatin isolation by rna purification assay showed that BCAR4 physically associates with the promoters of GLI2 target genes. The depletion of BCAR4 inhibits the expression of GLI2 target genes and GLI2 reporter luciferase activity in a dose-dependent manner. The expression of BCAR4 and GLI2 target genes is significantly correlated in osteosarcoma tissues. Depletion of DLI2 abolished the effects of BCAR4 on osteosarcoma. Taken together, these findings demonstrated that BCAR4 promotes osteosarcoma progression via activating GLI2-dependent gene transcription and serves as a potential prognostic biomarker and a therapeutic target of osteosarcoma.

关键词： long noncoding rna Osteosarcoma Proliferation Metastasis GLI2 pathway

来源：评论

学校读者我要写书评

暂无评论

long noncoding rna Ftx regulates the protein expression profile in HCT116 human colon cancer cells

引用

PROTEOME SCIENCE 2022年第1期20卷 1-12页

作者： Jia, Ruzhen Song, Lulu Fei, Zhiqiang Qin, Chengyong Zhao, Qi Shandong Univ Shandong Prov Hosp Cheeloo Coll Med Dept Gastroenterol 44 Wenhua West Rd Jinan 250021 Shandong Peoples R China Shandong First Med Univ Shandong Prov Hosp Dept Gastroenterol Jinan 250021 Shandong Peoples R China Shandong Second Prov Gen Hosp Dept Gastroenterol Jinan 250022 Shandong Peoples R China

Background The long noncoding rna (lncrna) five prime to Xist (Ftx) is involved in distant metastasis in colorectal cancer (CRC). This study aimed to investigate Ftx alteration-induced proteomic changes in the highly metastatic CRC cell line HCT116. Methods Tandem mass tag (TMT)-based proteomics analysis was performed to detect the differential protein expression in Ftx-overexpressing and Ftx-silenced HCT116 cells. The differentially expressed proteins were classified and characterized by bioinformatics analyses, including gene ontology (GO) annotation, GO/Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway/protein domain enrichment analyses, as well as hierarchical clustering. A total of 5471 proteins were quantified, and the proteins with |fold change|>= 1.2 and p < 0.05 were identified as differentially expressed proteins in response to Ftx overexpression or silencing. Results The bioinformatics analyses revealed that the differentially expressed proteins were involved in a wide range of GO terms and KEGG signaling pathways and contained multiple protein domains. These terms, pathways, and protein domains were associated with tumorigenesis and metastasis in CRC. Conclusions Our results indicate that the alteration of Ftx expression induces proteomic changes in highly metastatic HCT116 cells, suggesting that Ftx and its downstream molecules and signaling pathways could be potential diagnostic biomarkers and therapeutic targets for metastatic CRC.

关键词： long noncoding rna Colorectal cancer Proteome Metastasis

来源：评论

学校读者我要写书评

暂无评论

long noncoding rna NHEG1 Drives β-Catenin Transactivation and Neuroblastoma Progression through Interacting with DDX5

引用

MOLECULAR THERAPY 2020年第3期28卷 946-962页

作者： Zhao, Xiang Li, Dan Yang, Feng Lian, Heng Wang, Jianqun Wang, Xiaojing Fang, Erhu Song, Huajie Hu, Anpei Guo, Yanhua Liu, Yang Li, Hongjun Chen, Yajun Huang, Kai Zheng, Liduan Tong, Qiangsong Huazhong Univ Sci & Technol Union Hosp Tongji Med Coll Dept Pediat Surg 1277 Jiefang Ave Wuhan 430022 Hubei Peoples R China Huazhong Univ Sci & Technol Union Hosp Tongji Med Coll Clin Ctr Human Genom Res 1277 Jiefang Ave Wuhan 430022 Hubei Peoples R China Huazhong Univ Sci & Technol Union Hosp Tongji Med Coll Dept Pathol 1277 Jiefang Ave Wuhan 430022 Hubei Peoples R China

Recent studies suggest that long noncoding rnas (lncrnas) play essential roles in tumor progression. However, the functional roles and underlying mechanisms of lncrnas in neuroblastoma (NB), the most common malignant solid tumor in pediatric population, still remain elusive. Herein, through integrating analysis of a public rna sequencing dataset, neuroblastoma highly expressed 1 (NHEG1) was identified as a risk-associated lncrna, contributing to an unfavorable outcome of NB. Depletion of NHEG1 led to facilitated differentiation and decreased growth and aggressiveness of NB cells. Mechanistically, NHEG1 bound to and stabilized DEAD-box helicase 5 (DDX5) protein through repressing proteasomemediated degradation, resulting in beta-catenin transactivation that altered target gene expression associated with NB progression. We further determined a lymphoid enhancer binding factor 1 (LEF1)/transcription factor 7-like 2 (TCF7L2)/NHEG1/DDX5/beta-catenin axis with a positive feedback loop and demonstrated that NHEG1 harbored oncogenic properties via its interplay with DDX5. Administration of small interfering rnas against NHEG1 or DDX5 reduced tumor growth and prolonged survival of nude mice bearing xenografts. High NHEG1 or DDX5 expression was associated with poor survival of NB patients. These results indicate that lncrna NHEG1 exhibits oncogenic activity that affects NB progression via stabilizing the DDX5 protein, which might serve as a potential therapeutic target for NB.

关键词： DEAD-box helicase 5 beta-catenin long noncoding rna neuroblastoma neuroblastoma highly expressed 1 tumor progression tumorigenesis

来源：评论

学校读者我要写书评

暂无评论

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案：

请选择收藏分类：

通借通还

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：