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long noncoding rna HOXD-AS1 induces epithelial-mesenchymal transition in breast cancer by acting as a competing endogenous rna of miR-421

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JOUrnaL OF CELLULAR BIOCHEMISTRY 2019年第6期120卷 10633-10642页

作者： Li, Yinyan Han, Xu Li, Qiaobei Wang, Chunyan Lou, Zhe Wang, Xuemei China Med Univ Dept Ultrason Diag Affiliated Hosp 1 155 Nanjing St Shenyang 110001 Liaoning Peoples R China China Med Univ Dept Tradit Chinese Med Affiliated Hosp 1 Shenyang Liaoning Peoples R China

Breast cancer (BCa) is the most common malignant tumor in females. long noncoding rnas (lncrnas) are deregulated in many types of human cancers, including BCa. The purpose of the present study was to examine the expression profile and biological role of HOXD cluster antisense rna 1 (HOXD-AS1) in BCa. Our results revealed that HOXD-AS1 was upregulated in BCa tissues and cell lines, and high HOXD-AS1 expression was correlated with aggressive clinicopathological characteristics of BCa patients. Further gain-of-function and loss-of-function analysis showed that HOXD-AS1 overexpression promoted, whereas HOXD-AS1 knockdown inhibited BCa cell proliferation, cell cycle progression, migration, and invasion, indicating that HOXD-AS1 may function as a novel oncogene in BCa. Mechanistically, HOXD-AS1 could activate epithelial-mesenchymal transition (EMT) in BCa cells. We further proved that HOXD-AS1 might serve as a competing endogenous rna of miR-421 in BCa cells, and miR-421 was downregulated and negatively correlated with HOXD-AS1 expression in BCa tissues. Besides, we confirmed that SOX4, a master regulator of EMT, was a direct target gene of miR-421. Further, rescue experiments suggested that miR-421 overexpression partly abrogated the oncogenic role of HOXD-AS1 in BCa cells. Therefore, we shed light on that HOXD-AS1/miR-421/SOX4 axis may be considered as a novel therapeutic target for the treatment of BCa patients.

关键词： breast cancer competing endogenous rna epithelial-mesenchymal transition HOXD-AS1 long noncoding rna microrna-421

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long noncoding rna CLAN promotes lymphangiogenesis in the colorectal carcinoma

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VIRCHOWS ARCHIV 2022年第6期481卷 847-852页

作者： Guo, Qingxi Chen, Qianxing Li, Xiabin Wen, Xue Cai, Jingbo Yang, Zixi Sun, Xingwang Yin, Tao Southwest Med Univ Coll Clin Med Luzhou Sichuan Peoples R China Southwest Med Univ Affiliated Hosp Dept Pathol 25 Taiping St Luzhou Sichuan Peoples R China Zigong Fourth Peoples Hosp Dept Pathol Zigong Sichuan Peoples R China

Metastasis is the main cause of colorectal cancer (CRC)-related death and lymph node plays a vital role in this process. long noncoding rnas (lncrnas) are emerging as an important factor of biological progress in cancers. However, lncrnas related to CRC metastasis was rarely reported. CLAN expression data of tumor tissues and normal tissues were obtained from GEPIA database and 23 paired tumor and normal samples of patients. CLAN expression of 85 patients was carried out with rna extracted from FFPE samples and quantified with qRT-PCR. Patients' clinical features were collected from department of Pathology of the Affiliated Hospital of Southwest Medical University. Immunohistochemistry staining was used to detect the metastasis-related proteins. CLAN was highly expressed in tumor tissues. And the expression level was not correlated with age, gender, differentiation, and location of CRC patients. Also, CLAN expression did not correlated with budding, LVI, and TILs. However, CLAN expression was strongly associated with lymph node metastasis and higher TNM stage. CLAN changed the lymphatic vessel density by promoting lymphangiogenesis but CLAN did not affect the blood vessel density. CLAN was a unique lncrna that promoted lymphangiogenesis to accelerate CRC metastasis. CLAN might play a unique role in tumor early dissemination through lymphatic vessel.

关键词： Colorectal carcinoma Metastasis long noncoding rna Lymphangiogenesis

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long noncoding rna EPIC1 interacts with YAP1 to regulate the cell cycle and promote the growth of pancreatic cancer cells

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2020年第4期522卷 978-985页

作者： Xia, Peng Liu, Pan Fu, Qiang Liu, Chuanjiang Luo, Qiankun Zhang, Xu Cheng, Liyou Qin, Tao Zhang, Hongwei Zhengzhou Univ Henan Prov Peoples Hosp Peoples Hosp Dept Hepatobiliary Pancreat Surg 7 Weiwu Rd Zhengzhou 450000 Henan Peoples R China Henan Prov Peoples Hosp Translat Res Inst Integrat Res Hub Zhengzhou Peoples R China

Pancreatic cancer (PC) is a fatal disease;most patients are asymptomatic before the disease enters the advanced stage, but molecular mechanisms of early PC that can be exploited for diagnosis are not clear. long noncoding rnas (lncrnas) play key roles in the progression of PC. In this study, we found that the expression of the lncrna EPIC1 (Lnc-EPIC1) is high in PC and closely related to tumor size, TNM staging and lymph node metastasis status. Silencing Lnc-EPIC1 by sirna targeting could significantly inhibit the cell growth and colony formation ability of PC cells and induced G1/S cell cycle arrest and apoptosis in PC cells. Lnc-EPIC1-specific sirnas could downregulate the expression of cyclins and CDKs, such as CDC20, CDK4 and Cyclin A1. Knocking out YAP1 with the CRISPR/Cas-9 gene editing method recapitulated the effects of the Lnc-EPIC1-specific sirnas on cell growth, colony formation ability and apoptosis in PC cells. In addition, the Lnc-EPIC1-specific sirnas did not further inhibit cell growth or promote apoptosis in YAP1-knockout (YAP1-KO) cells. rna immunoprecipitation (RIP) results showed that there was a direct interaction between Lnc-EPIC1 and YAP1. An Lnc-EPIC1-overexpressing lentiviral vector promoted the growth of PC cells. The results show that Lnc-EPIC1 interacts with YAP1 to promote the progression of PC. (C) 2019 Elsevier Inc. All rights reserved.

关键词： long noncoding rna EPIC1 YAP1 Pancreatic cancer Cell growth Apoptosis

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long noncoding rna turnover

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BIOCHIMIE 2015年 117卷 15-21页

作者： Yoon, Je-Hyun Kim, Jiyoung Gorospe, Myriam NIA LG IRP NIH Baltimore MD 21224 USA

Most rnas transcribed in mammalian cells lack protein-coding sequences. Among them is a vast family of long (>200 nt) noncoding (lnc)rnas. Lncrnas can modulate cellular protein expression patterns by influencing the transcription of many genes, the post-transcriptional fate of mrnas and ncrnas, and the turnover and localization of proteins. Given the broad impact of lncrnas on gene regulation, there is escalating interest in elucidating the mechanisms that govern the steady-state levels of lncrnas. In this review, we summarize our current knowledge of the factors and methanisms that modulate mammalian lncrna stability. (C) Published by Elsevier B.V.

关键词： Ribonucleoprotein complex rna-binding protein long noncoding rna

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long noncoding rna NEAT1 modulates cell proliferation and apoptosis by regulating miR-23a-3p/SMC1A in acute myeloid leukemia

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JOUrnaL OF CELLULAR PHYSIOLOGY 2019年第5期234卷 6161-6172页

作者： Zhao, Chen Wang, Shanshan Zhao, Yang Du, Feng Wang, Weiyao Lv, Peng Qi, Ling Jilin Med Univ Dept Clin Hematol Lab Jilin Jilin Peoples R China Jining Med Univ Dept Pathol Jining Peoples R China Jining Med Univ Inst Precis Med Jining Peoples R China 222 Hosp PLA Dept Infect Dis Jilin Jilin Peoples R China Jining Med Univ Dept Pathogen Biol Jining Peoples R China Jilin Med Univ Dept Pathophysiol 5 Jilin Ave Jilin 132013 Jilin Peoples R China

The aim of this study was to determine the function of the NEAT1/miR-23a-3p/SMC1A axis in cell proliferation and apoptosis in acute myeloid leukemia (AML). Microarray analysis was used to screen differentially expressed lncrnas/mirnas/mrnas in primary AML cells. The expression of nuclear paraspeckle assembly transcript 1 (NEAT1), miR-23a-3p, and structural maintenance of chromosome 1 alpha (SMC1A) in primary AML cells and THP-1 cells were measured by quantitative real-time polymerase chain reaction (qRT-PCR). A Cell Counting Kit-8 (CCK-8) assay was used to analyze proliferation. Cell cycle progression and apoptosis were examined by flow cytometry. rna immunoprecipitation (RIP) and dual-luciferase assays were performed to determine the correlation between miR-23a-3p and NEAT1 or SMC1A. The qRT-PCR illustrated that NEAT1 and SMC1A expression was decreased but that miR-23a-3p expression was increased in primary AML cells and THP-1 cells compared with that in normal cells. The RIP assay and dual-luciferase assay revealed the targeting relationship between miR-23a-3p and NEAT1 or SMC1A. The CCK-8 assay showed that the overexpression of NEAT1 and SMC1A or repression of miR-23a-3p inhibited cell proliferation. Flow cytometry showed that the upregulation of NEAT1 and SMC1A or repression of miR-23a-3p promoted apoptosis and affected the cell cycle. NEAT1 repressed the expression of miR-23a-3p, and therefore promoted SMC1A, which in turn suppressed myeloid leukemia cell proliferation and enhanced apoptosis.

关键词： acute myeloid leukemia long noncoding rna miR-23a-3p NEAT1 SMC1A

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long noncoding rna FGFR3-AS1 promotes osteosarcoma growth through regulating its natural antisense transcript FGFR3

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MOLECULAR BIOLOGY REPORTS 2016年第5期43卷 427-436页

作者： Sun, Jiabing Wang, Xuming Fu, Chunjiang Wang, Xiaoyu Zou, Jilong Hua, Hanbing Bi, Zhenggang Harbin Med Univ Dept Orthoped Affiliated Hosp 1 23 Youzheng St Harbin 150001 Heilongjiang Peoples R China

long noncoding rnas (lncrnas), a new class of rnas with no protein-coding potential, have been reported to have crucial roles in the regulation of a variety of tumors. However, the functions and molecular mechanisms of lncrnas to osteosarcoma are still largely unknown. The purpose of this study is to examine the expression, functions and molecular mechanisms of a new lncrna FGFR3 antisense transcript 1 (FGFR3-AS1) in osteosarcoma. The expression of FGFR3-AS1 was examined by real-time quantitative PCR. The regulation of FGFR3 by FGFR3-AS1 was examined by rnase protection assay, real-time quantitative PCR, western blotting, and luciferase reporter assay. The effects of FGFR3-AS1 on osteosarcoma cell proliferation and cell cycle were determined by Cell Counting Kit-8, Ethynyl deoxyuridine incorporation assay and flow cytometry. FGFR3-AS1 was upregulated in osteosarcoma. Increased FGFR3-AS1 expression correlates with large tumor size, advanced Enneking stage, metastasis and poor survival. Through antisense pairing with FGFR3 3'UTR, FGFR3-AS1 increases FGFR3 mrna stability and upregulates FGFR3 expression. The expression of FGFR3-AS1 and FGFR3 is positively correlated in osteosarcoma tissues. Knockdown of FGFR3-AS1 inhibits the proliferation and cell cycle progression of osteosarcoma cells in vitro. Moreover, knockdown of FGFR3-AS1 inhibits xenograft tumor growth of osteosarcoma cells in vivo. These data demonstrate the mechanisms of how antisense noncoding rna regulate the expression of sense genes, and show the pivotal functions of FGFR3-AS1 in osteosarcoma.

关键词： Osteosarcoma long noncoding rna Antisense transcript Proliferation

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long noncoding rna MNX1-AS1 contributes to lung cancer progression through the miR-527/BRF2 pathway

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JOUrnaL OF CELLULAR PHYSIOLOGY 2019年第8期234卷 13843-13850页

作者： Liu, Haibo Han, Leng Liu, Zhengjia Gao, Nan Jilin Univ Dept Emergency Part 2 Hosp 1 Changchun Jilin Peoples R China Jilin Univ Dept Hematol & Oncol China Japan Union Hosp Changchun Jilin Peoples R China Jilin Univ Dept Thorac Surg China Japan Union Hosp 126 XianTai Rd Changchun 130033 Jilin Peoples R China

Lung cancer belongs to a leading popular and malignant cancer around the world. However, the root mechanism underlying lung cancer progression remains unclear. Recently, long noncoding rna (lncrna) has been identified as important for tumorigenesis. Lncrna MNX1-AS1 is proven to regulate colon adenocarcinoma, cervical cancer, glioblastoma, and ovarian cancer. Whether MNX1-AS1 participates in lung cancer needs investigation. In our research, we found that MNX1-AS1 was dramatically upregulated in lung cancer. MNX1-AS1 upregulation indicated poor prognosis in lung cancer patients. Functionally, MNX1-AS1 promoted lung cancer progression through regulating proliferation, migration, and invasion. Mechanistically, MNX1-AS1 was found to locate in the cytoplasm and interact with miR-527. Through inhibiting miR-527 availability, MNX1-AS1 facilitated BRF2 expression. Restoration of BRF2 rescued defects of proliferation, migration, and invasion caused by MNX1-AS1 knockdown. Taken together, our study found a novel signaling pathway, namely MNX1-AS1/miR-527/BRF2 axis, involved in lung cancer progression.

关键词： BRF2 long noncoding rna lung cancer miR-527 MNX1-AS1

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long noncoding rna NEAT1 Upregulates Survivin and Facilitates Gallbladder Cancer Progression by Sponging microrna-335

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ONCOTARGETS AND THERAPY 2020年 13卷 2357-2367页

作者： Yang, Facai Tang, Zhaohui Duan, Anqi Yi, Bin Shen, Ningjia Bo, Zhiyuan Yin, Lei Zhu, Bin Qiu, Yinghe Li, Jingdong North Sichuan Med Coll Dept Gen Surg Affiliated Hosp 63 Wenhua Rd Nanchong 637000 Peoples R China Shanghai Jiao Tong Univ Xinhua Hosp Dept Gen Surg Sch Med Shanghai 200092 Peoples R China Naval Mil Med Univ Shanghai Eastern Hepatobiliary Surg Hosp Dept Biliary 2 225 Changhai Rd Shanghai 200438 Peoples R China

Background: Gallbladder cancer (GBC) is the most common cancer of the biliary tract, but molecularly targeted therapies are not available for GBC. Loss of microrna (miR)-335 expression may be a useful predictor of clinical outcomes and the reversal of its loss of expression may be a useful treatment strategy for GBC. In this study, we investigated whether a long noncoding rna, nuclear paraspeckle assembly transcript 1 (NEAT1) sponges miR-335 in GBC cells. Materials and Methods: Quantitative reverse transcription-polymerase chain reaction (qRT-PCR), Western blotting, and immunohistochemistry were used to determine the expression of miR-335;NEAT1;survivin;and Ki67 in GBC cell lines (GBC-SD and SGC-996) and tissue samples from patients (n = 25). Cell Counting Kit-8, colony-formation, and Transwell migration and invasion assays were performed to measure cell proliferation, migration, and invasion. Bioinformatic analysis and dual-luciferase reporter assays were utilized to analyze correlativity. Results: miR-335 overexpression resulted in inhibition of GBC cell proliferation and invasion. In addition, knockdown of NEAT1 resulted in downregulation of survivin expression. As NEAT1 competitively "sponges" miR-335, NEAT1 knockdown resulted in inhibited GBC cell proliferation and invasion in vitro and GBC tumor growth in vivo. Furthermore, NEAT1 was found to be upregulated in GBC samples, and its expression was inversely correlated with miR-335 levels, but positively correlated with survivin levels. Conclusion: These findings indicate that NEAT1 promotes survivin expression by functioning as a competitive endogenous rna for miR-335 in GBC cells;thus, we have identified a potential biomarker and target for GBC diagnosis and therapy.

关键词： long noncoding rna NEAT1 miR-335-5p competitive endogenous rna survivin gallbladder cancer

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long noncoding rna expression profile of infantile hemangioma identified by microarray analysis

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TUMOR BIOLOGY 2016年第12期37卷 15977-15987页

作者： Liu, Xiaowen Lv, Renrong Zhang, Linfeng Xu, Guangqi Bi, Jianhai Gao, Feng Zhang, Jian Xue, Feng Wang, Fagang Wu, Yiliang Fu, Cong Wang, Qiang Huo, Ran Shandong Univ Dept Burn & Plast Surg Shandong Prov Hosp Jinan Shandong Peoples R China Tengzhou Cent Peoples Hosp Dept Burn & Plast Surg Tengzhou Shandong Peoples R China

Infantile hemangioma (IH) is one of the most common vascular tumors of childhood. long noncoding rnas (lncrnas) play a critical role in angiogenesis, but their involvement in hemangioma remains unknown. This study aimed to assess the expression profiles of lncrnas in IH and adjacent normal tissue samples, exploring the biological functions of lncrnas as well as their involvement in IH pathogenesis. The lncrna expression profiles were determined by lncrna microarrays. A total of 1259 and 857 lncrnas were upregulated and downregulated in IH, respectively, at a fold change cutoff of 2.0 (p < 0.05);in addition, 1469 and 1184 messenger rnas (mrnas) were upregulated and downregulated, respectively (fold change cutoff of 2.0;p < 0.05). A total of 292 differentially expressed mrnas were targeted by the lncrnas with altered expression in hemangioma, including 228 and 64 upregulated and downregulated, respectively (cutoff of 2.0, p < 0.05). Gene ontology (GO) analyses revealed several angiogenesis-related pathways. An lncrna-mrna co-expression network for differentially expressed lncrnas revealed significant associations of the lncrnas MEG3, MEG8, FENDRR, and Linc00152 with their related mrnas. The validation results of nine differentially expressed lncrnas (MALAT1, MEG3, MEG8, p29066, p33867, FENDRR, Linc00152, p44557_v4, p8683) as well as two mrnas (FOXF1, EGFL7) indicated that the microarray data correlated well with the QPCR results. Interestingly, MALAT1 knockdown induced apoptosis and S-phase cell cycle arrest in human umbilical vein endothelial cells (HUVECs). Overall, this study revealed the lncrna expression profile of IH and that lncrnas likely regulate several genes with important roles in angiogenesis.

关键词： long noncoding rna MALAT1 Infantile hemangioma Angiogenesis Microarrays

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long noncoding rna CCAT1, which could be activated by c-Myc, promotes the progression of gastric carcinoma

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JOUrnaL OF CANCER RESEARCH AND CLINICAL ONCOLOGY 2013年第3期139卷 437-445页

作者： Yang, Feng Xue, Xuchao Bi, Jianwei Zheng, Luming Zhi, Kangkang Gu, Yan Fang, Guoen Shanghai Jiao Tong Univ Sch Med Shanghai Peoples Hosp 9 Dept Gen Surg Shanghai 200011 Peoples R China Second Mil Med Univ Changhai Hosp Dept Gen Surg Shanghai 200433 Peoples R China

long noncoding rnas (lncrnas) have been shown to have functional roles in cancer biology and are deregulated in many tumors. The specific aim of this study was to determine the role of a long noncoding rna CCAT1 in the progression of gastric carcinoma and discover which factors contribute to the deregulation of CCAT1. A computational screen of CCAT1 promoter was conducted to search for transcription-factor-binding sites. The association of c-Myc with the CCAT1 promoter in vivo was tested by chromatin immunoprecipitation assay. CCAT1 promoter activities were examined by luciferase reporter assay. The function of the c-Myc binding site in the CCAT1 promoter region was tested by a promoter assay with nucleotide substitutions in the putative E-box. The effect of CCAT1 on gastric carcinoma cell proliferation and migration was tested using in vitro cell proliferation and migration assays. CCAT1 levels were markedly increased in gastric carcinoma tissues compared with normal tissues. c-Myc directly binds to the E-box element in the promoter region of CCAT1, and when ectopically expressed increased promoter activity and expression of CCAT1. Nucleotide substitutions in the E-box element in the promoter region abrogated c-Myc-dependent promoter activation. The expression of CCAT1 and c-Myc shows strong association in gastric carcinomas. Moreover, abnormally expressed CCAT1 promotes cell proliferation and migration. These data suggest that c-Myc induction of CCAT1 holds an important role in gastric carcinoma and implicate the potential application of CCAT1 in the treatment of gastric carcinoma.

关键词： long noncoding rna CCAT1 c-Myc Gastric carcinoma

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