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long non-coding rna urothelial cancer-associated 1 promotes bladder cancer cell migration and invasion by way of the hsa-miR-145-ZEB1/2-FSCN1 pathway

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CANCER SCIENCE 2016年第1期107卷 18-27页

作者： Xue, Mei Pang, Huan Li, Xu Li, Huijin Pan, Jingjing Chen, Wei Xi An Jiao Tong Univ Affiliated Hosp 1 Ctr Translat Med Xian 710061 Shaanxi Peoples R China Xi An Jiao Tong Univ Affiliated Hosp 1 Clin Lab 277 West Yanta Rd Xian 710061 Peoples R China

Numerous studies suggest that several long non-coding rnas (lncrnas) play critical roles in bladder cancer development and progression. long non-coding rna urothelial cancer-associated 1 (lncrna-UCA1) is highly expressed in bladder cancer tissues and cells, and it has been shown to play an important role in regulating aggressive phenotypes of bladder cancer cells. However, little is known about the molecular mechanism of lncrna-UCA1-mediated bladder cancer cell migration and invasion. Here, we show that overexpression of lncrna-UCA1 could induce EMT and increase the migratory and invasive abilities of bladder cancer cells. Mechanistically, lncrna-UCA1 induced EMT of bladder cancer cells by upregulating the expression levels of zinc finger E-box binding homeobox 1 and 2 (ZEB1 and ZEB2), and regulated bladder cancer cell migration and invasion by tumor suppressive hsa-miR-145 and its target gene the actin-binding protein fascin homologue 1 (FSCN1). Furthermore, we also observed a positive correlation between lncrna-UCA1 and ZEB1/2 expression, and a negative correlation between lncrna-UCA1 and hsa-miR-145 expression in bladder cancer specimens. Importantly, we found that lncrna-UCA1 repressed hsa-miR-145 expression to upregulate ZEB1/2, whereas the suppression of hsa-miR-145 could upregulate lncrna-UCA1 expression in bladder cancer cells. Moreover, the binding site for hsa-miR-145 within exons 2 and 3 of lncrna-UCA1 contributed to the reciprocal negative regulation of lncrna-UCA1 and hsa-miR-145. Taken together, our results identified that lncrna-UCA1 enhances bladder cancer cell migration and invasion in part through the hsa-miR-145/ZEB1/2/FSCN1 pathway. Therefore, lncrna-UCA1 might act as a promising therapeutic target for the invasion and metastasis of bladder cancer.

关键词： Bladder cancer epithelial to mesenchymal transition Hsa-miR-145 long non-coding rna UCA1

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long non-coding rna MVIH indicates a poor prognosis for non-small cell lung cancer and promotes cell proliferation and invasion

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TUMOR BIOLOGY 2014年第8期35卷 7587-7594页

作者： Nie, Feng-qi Zhu, Quan Xu, Tong-peng Zou, Yan-fen Xie, Min Sun, Ming Xia, Rui Lu, Kai-hua Nanjing Med Univ Affiliated Hosp 1 Dept Oncol Nanjing Jiangsu Peoples R China Nanjing Med Univ Affiliated Hosp 1 Dept Cardiothorac Surg Nanjing Jiangsu Peoples R China Nanjing Med Univ Affiliated Hosp 1 Dept Obstet & Gynecol Nanjing Jiangsu Peoples R China Nanjing Med Univ Dept Biochem & Mol Biol Nanjing Jiangsu Peoples R China

long non-coding rnas (lncrnas) have emerged as major players in governing fundamental biological processes, and many of which are misregulated in multiple cancers and likely to play a functional role in tumorigenesis. Therefore, identification of cancer-associated lncrnas and investigation of their biological functions and molecular mechanisms are important for understanding the development and progression of cancer. lncrna associated with microvascular invasion in HCC (lncrna MVIH) was found to be generally upregulated in HCC. Moreover, MVIH overexpression could serve as an independent risk factor to predict poor RFS and promote tumor growth and metastasis via activating angiogenesis. However, its biological role and clinical significance in non-small cell lung cancer (NSCLC) development and progression is unknown. In this study, we found that lncrna MVIH levels were increased in NSCLC tissues compared with adjacent normal tissues. Its expression level was significantly correlated with TNM stages, tumor size, and lymph node metastasis. Moreover, patients with high levels of MVIH expression had a relatively poor prognosis. Furthermore, knockdown of MVIH expression by sirna could inhibit cell proliferation and invasion, while ectopic expression of MVIH promoted cell proliferation and invasion in NSCLC cells partly via regulating MMP2 and MMP9 protein expression. Our findings present that increased lncrna MVIH could be identified as a poor prognostic biomarker in NSCLC and regulate cell proliferation and invasion.

关键词： long non-coding rna MVIH Poor prognosis Proliferation Invasion

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long non-coding rna LY86-AS1 and HCG27_201 expression in type 2 diabetes mellitus

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MOLECULAR BIOLOGY REPORTS 2018年第6期45卷 2601-2608页

作者： Saeidi, Leyla Ghaedi, Hamid Sadatamini, Mirsaber Vahabpour, Rouhollah Rahimipour, Ali Shanaki, Mehrnoosh Mansoori, Zahra Kazerouni, Faranak Shahid Beheshti Univ Med Sci Sch Allied Med Sci Dept Med Lab Sci Tehran Iran Shahid Beheshti Univ Med Sci Fac Med Dept Med Genet Tehran Iran Shahid Beheshti Univ Med Sci Shohada Hosp Tehran Iran

long non-coding rnas (Lncrnas) are non-coding rnas. The potential roles of lncrnas in type 2 diabetes mellitus (T2DM) are not well-known. In this study, we aim to assess the expression levels of LY86-AS1 and HCG27_201 in T2DM patients and a healthy control group. We obtained whole blood and serum samples from 100 T2DM and 100 non-diabetic subjects. Peripheral blood mononuclear cells (PBMCs) were extracted from whole blood samples using Ficoll. Total rna was isolated from PBMCs obtained from patients with type 2 diabetes mellitus and healthy control individuals using TRIzol LS reagent (GeneAll Biotechnology Co., LTD.). Extracted rna was used to synthesize complementary DNA (cDNA) with a Reverse Transcription Kit (Takara). Real-time was performed with SYBR Green (Takara) and monitored by a Rotor-Gene (Qiagen) system. We performed quantitative PCR analysis of the LY86-AS1 and HCG27_201 lncrna expression levels in the 200 samples. Here we found that the expression of LY86-AS1 and HCG27_201 were down regulated in the T2DM group compared with the control group. We further identify that the expression of both lncrnas was negatively correlated with fasting blood sugar (FBS) levels. Receiver operating characteristic (ROC) analysis was used to assess the diagnostic value of LY86-AS1 and HCG27_201 as biomarkers for T2DM. ROC analysis demonstrated that LY86-AS1 with an area under the ROC curve (AUC) of 0.747 (P < 0.0001, sensitivity: 64.6, and specificity: 79.8) might be the potential novel diagnostic biomarkers for T2DM. Lower expression of our two studied long non-coding rnas LY86-AS1 and HCG27_201 in type 2 diabetes mellitus patients indicates their role in the pathogenesis of T2DM. Furthermore, LY86-AS1 could possibly be used as a diagnostic marker for T2DM.

关键词： long non-coding rna Lncrna LY86-AS1 HCG27_201 rs3132524 rs9502478 Diabetes Type-2 diabetes mellitus

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long non-coding rna SNHG15 promotes CDK14 expression via miR-486 to accelerate non-small cell lung cancer cells progression and metastasis

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JOUrnaL OF CELLULAR PHYSIOLOGY 2018年第9期233卷 7164-7172页

作者： Jin, Bing Jin, Hua Wu, Hai-Bo Xu, Jian-Jun Li, Bing Nanyang City Ctr Hosp Dept Chest Surg Nanyang Peoples R China Fudan Univ Dept Respirat Jinshan Hosp Shanghai Peoples R China Fudan Univ Handan Rd 220 Shanghai 200433 Peoples R China Fudan Univ Jinshan Hosp Cent Lab 1508 Longhang Rd Shanghai 201508 Peoples R China

long non-coding rnas (lncrnas) have been validated to play important role in multiple cancers, including non-small cell lung cancer (NSCLC). In present study, our team investigate the biologic role of SNHG15 in the NSCLC tumorigenesis. Lncrna SNHG15 was significantly upregulated in NSCLC tissue samples and cells, and its overexpression was associated with poor prognosis of NSCLC patients. In vitro, loss-of-functional cellular experiments showed that SNHG15 silencing significantly inhibited the proliferation, promoted the apoptosis, and induced the cycle arrest at G0//G1 phase. In vivo, xenograft assay showed that SNHG15 silencing suppressed tumor growth of NSCLC cells. Besides, SNHG15 silencing decreased CDK14 protein expression both in vivo and vitro. Bioinformatics tools and luciferase reporter assay confirmed that miR-486 both targeted the 3-UTR of SNHG15 and CDK14 and was negatively correlated with their expression levels. In summary, our study conclude that the ectopic overexpression of SNHG15 contribute to the NSCLC tumorigenesis by regulating CDK14 protein via sponging miR-486, providing a novel insight for NSCLC pathogenesis and potential therapeutic strategy for NSCLC patients.

关键词： CDK14 long non-coding rna miR-486 non-small cell lung cancer SNHG15

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long non-coding rna LINC00526 represses glioma progression via forming a double negative feedback loop with AXL

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JOUrnaL OF CELLULAR AND MOLECULAR MEDICINE 2019年第8期23卷 5518-5531页

作者： Yan, Jian Xu, Chunhua Li, Youping Tang, Bin Xie, Shenhao Hong, Tao Zeng, Erming Nanchang Univ Affiliated Hosp 1 Dept Neurosurg 17 Yongwai Zheng St Nanchang 330006 Jiangxi Peoples R China

Glioma is the most common primary intracranial carcinoma with extremely poor prognosis. The significances of long non-coding rna (lncrna) involved in glioma have been started revealed. However, the expression, roles and molecular mechanisms of most lncrnas in glioma are still unknown. In this study, we identified a novel lncrna LINC00526, which is significantly low expressed in glioma. Low expression of LINC00526 is correlated with aggravation and poor survival in glioma. Functional assays revealed that ectopic expression of LINC00526 inhibits glioma cell proliferation, migration, and invasion. LINC00526 silencing promotes glioma cell proliferation, migration and invasion. Mechanistically, we found that LINC00526 directly interacts with EZH2, represses the binding of EZH2 to AXL promoter, attenuates the transcriptional activating roles of EZH2 on AXL, and therefore represses AXL expression. Via repressing AXL, LINC00526 further represses PI3K/Akt/NF-kappa B signalling. Intriguingly, we identified that NFKB1 and NFKB2 directly binds LINC00526 promoter and represses LINC00526 transcription. We further found that via activating NF-kappa B signalling, AXL represses LINC00526 transcription. Therefore, LINC00526/EZH2/AXL/PI3K/Akt/NF-kappa B form a feedback loop in glioma. Analysis of the TCGA data revealed that the expression of LINC00526 is inversely correlated with that of AXL in glioma tissues. In addition, functional rescue assays revealed that the tumour suppressive roles of LINC00526 are dependent on the negative regulation of AXL. Collectively, our data identified LINC00526 as a tumour suppressor in glioma via forming a double negative feedback loop with AXL. Our data also suggested LINC00526 as a potential prognostic biomarker and therapeutic candidate for glioma.

关键词： AXL feedback loop glioma long non-coding rna progression

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long non-coding rna in lung cancer

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CLINICA CHIMICA ACTA 2020年第0期504卷 190-200页

作者： Chen, Zhenyao Lei, Tianyao Chen, Xin Gu, Jingyao Huang, Jiali Lu, Binbin Wang, Zhaoxia Nanjing Med Univ Affiliated Hosp 2 Canc Med Ctr 121 Jiangjiayuan Rd Nanjing 210011 Jiangsu Peoples R China

Lung cancer is the leading cause of cancer-related death worldwide. Owing to the difficulty in early diagnosis and the lack of effective treatment strategies, the 5-year survival rates for lung cancer remain very low. With the development of whole genome and transcriptome sequencing technology, long non-coding rna (lncrna) has attracted increasing attention. Lncrnas regulate gene expression at the epigenetic, transcriptional and posttranscriptional levels and are widely involved in a variety of diseases, including tumorigenesis. In lung cancer studies, multiple differentially expressed lncrnas have been identified;several lncrnas were identified as oncogenic lncrnas with tumor-driving effects, while other lncrnas play a role in tumor inhibition and are called tumor-suppressive lncrnas. These tumor-suppressive lncrnas are involved in multiple physiological processes such as cell proliferation, apoptosis, and metastasis and thus participate in tumor progression. In this review, we discussed the oncogenic and tumor-suppressive lncrnas in lung cancer, as well as their biological functions and regulatory mechanisms. Furthermore, we found the potential significance of lncrnas in clinical diagnosis and treatment.

关键词： long non-coding rna Lung cancer Diagnosis Therapy

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long non-coding rna GPR65-1 is up-regulated in gastric cancer and promotes tumor growth through the PTEN-AKT-slug signaling pathway

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CELL CYCLE 2018年第6期17卷 759-765页

作者： Li, Yansen Shen, Zhanlong Wang, Bo Ye, Chunxiang Lai, Zhiyong Jiang, Hongpeng Wang, Zhu Jiang, Kewei Ye, Yingjiang Wang, Shan Peking Univ Peoples Hosp Dept Gastroenterol Surg Beijing Peoples R China Peking Univ Peoples Hosp Lab Surg Oncol Beijing Peoples R China Peking Univ Peoples Hosp Beijing Key Lab Colorectal Canc Diag & Treatment Beijing Peoples R China

Increasing evidence has shown that abnormal expression of lncrnas is involved in various biological behaviors and major cellular pathways of human cancers. However, the role of lncrnas in the progression of gastric cancer has not been adequately investigated. Therefore, in this study, we investigated the expression levels of linc-GPR65-1 using Quantitative real-time PCR (qRT-PCR) and found that linc-GPR65-1 was significantly up-regulated in 50 gastric cancer tissues compared to the corresponding normal tissues. In addition, increased linc-GPR65-1 expression was associated with TNM stage (P = 0.037), tumor size (P = 0.024), distal metastasis (P = 0.023), and poor prognosis of gastric cancer patients. Moreover, functional assays indicated that decreased linc-GPR65-1 expression inhibited the aggressive phenotypes of gastric cancer cells, and enhanced linc-GPR65-1 expression resulted in the opposite phenomenon. Then, a cancer signaling phosphoantibody microarray was conducted to explore the potential mechanisms of linc-GPR65-1 in regulating gastric cancer progression and observed that linc-GPR65-1 could regulate the PTEN-AKT-slug signaling pathway. These data showed that linc-GPR65-1, regulating the PTEN-AKT-slug signaling pathway, might act as a tumor promoter and serve as a novel target for gastric cancer prevention and therapy.

关键词： long non-coding rna linc-GPR65-1 gastric cancer PTEN AKT

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long non-coding rna (lncrna) and epithelial-mesenchymal transition (EMT) in colorectal cancer: a systematic review

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CANCER BIOLOGY & THERAPY 2020年第9期21卷 769-781页

作者： O'Brien, Stephen J. Bishop, Campbell Hallion, Jacob Fiechter, Casey Scheurlen, Katharina Paas, Mason Burton, James Galandiuk, Susan Univ Louisville Dept Surg Price Inst Surg Res Louisville KY 40292 USA

Background Colorectal cancer (CRC) is a leading cause of cancer-related death. Epithelial-mesenchymal transition (EMT) is a major process in tumor metastasis development. This systematic review aims to describe the role of long non-coding rna (lncrna) in EMT in CRC. Methods The electronic databases, PubMed, Cochrane, and EMBASE, were searched from January1990 to June 2019 to identify studies examining lncrna and their role in mediating EMT in CRC. Studies examining clinical specimens and/or in vitro experiments were included. Results In 61 identified studies, 54 lncrnas were increased in CRC compared to normal colorectal epithelium. Increased lncrna expression was frequently associated with worse survival. Many lncrnas mediate their effect through competitive endogenous rna or transcription factor regulation. The ZEB1, 2/E-cadherin, Wnt/beta-catenin signaling, and chromatin remodeling pathways are discussed in particular. Conclusions lncrnas are major regulators of EMT and predictor adverse outcome in CRC patients. Future research must focus on delineating lncrna function prior to potential clinical use.

关键词： long non-coding rna colorectal cancer systematic review epithelial-mesenchymal transition metastasis

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long non-coding rna SNHG16 affects cell proliferation and predicts a poor prognosis in patients with colorectal cancer via sponging miR-200a-3p

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BIOSCIENCE REPORTS 2019年第5期39卷 BSR20182498.-BSR20182498.页

作者： Li, Yanling Lu, Ying Chen, Yanglong Huazhong Univ Sci & Technol Tongji Med Coll Union Hosp Dept Gastroenterol Wuhan 430022 Hubei Peoples R China Huazhong Univ Sci & Technol Tongji Med Coll Union Hosp Dept Emergency Med Wuhan 430022 Hubei Peoples R China

Previous study has explored that SNHG16, a long non-coding rna (lncrna), mediated cell growth and proliferation. Yet, the role of SNHG16 in human colorectal cancer (CRC) still remains to be explored. Therefore, we conducted the present study to explore the functions of SNHG16 in CRC. In the present study, SNHG16 was significantly up-regulated in CRC tissues and cell lines. Gain-and loss-of-function of SNHG16 further presented that SNHG16 promoted the progression of CRC cells, including proliferation, migration, and invasion. Further, in vivo study also revealed that overexpression of SNHG16 could promote tumor growth. Bioinformatics analysis and luciferase reporter assay showed that SNHG16 was a direct target of miR-200a-3p. MiR-200a-3p was inversely correlated with SNHG16 expression in CRC tissues. In brief, the above results elucidate the important role of SNHG16 in CRC tumorigenesis, suggesting that SNHG16 might be quite vital for the diagnosis and development of CRC.

关键词： colorectal cancer long non-coding rna miR-200a-3p SNHG16

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long non-coding rna NAPIL6 promotes tumor progression and predicts poor prognosis in prostate cancer by targeting Inhibin-β A

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ONCOTARGETS AND THERAPY 2018年 11卷 4965-4977页

作者： Zheng, Yuxiao Gao, Yiren Li, Xiao Si, Shuhui Xu, Haoxiang Qi, Feng Wang, Jun Cheng, Gong Hua, Lixin Yang, Haiwei Jiangsu Canc Hosp Dept Urol Surg Nanjing 210009 Jiangsu Peoples R China Jiangsu Inst Canc Res Nanjing 210009 Jiangsu Peoples R China Nanjing Med Univ Affiliated Canc Hosp Nanjing 210009 Jiangsu Peoples R China Nanjing Med Univ Dept Urol Affiliated Hosp 1 300 Guangzhou Rd Nanjing 210029 Jiangsu Peoples R China Nanjing Med Univ Res Div Clin Pharmacol Affiliated Hosp 1 Nanjing 210029 Jiangsu Peoples R China

Background/purpose: long non-coding rnas (lnernas) have emerged as key molecules in initiation and progression of prostate cancer (PCa). In this study, we aimed to explore the role of lncrna NAP1L6 in the development and progression of PCa. Materials and methods: We identified that lncrna NAP1L6 was over-expressed both in PCa tissues and cell lines by gene expression array profiling. The expression level of NAP1L6 in 75 PCa tissues and adjacent tissues was detected by RT-PCR. Next, the correlations between NAP1L6 expression and clinical features of patients with PCa were analyzed by paired i-test or chi-squared test, and its association with patient prognosis was assessed by the Kaplan-Meier method. The effects of NAP1L6 on PC-3 and 22RV1 cells were evaluated by Cell Counting Kit-8 (CCK-8), migration, invasion, and colony formation assays. Further analysis of the results of the microarray was performed to find downstream gene of NAP1L6. Cell function experiments were performed in order to explore the relationship between NAP1L6 and Inhibin-beta A (INHBA) and the specific mechanism by which INHBA affects the development of PCa. Results: Using microarray analysis, we identified 412 lncrnas and 1245 m rnas to be significantly differentially expressed in three PCa samples when compared with adjacent nontumor tissues (ANTT) (fold-change >= 2.0 or <= 0.5, P<0.05, false discovery rate (FDR) <0.05). NAP1L6 expression was upregulated in PCa tissues and cell lines (both P<0.05) compared with ANTT. Besides, high expression level of NAPIL6 promotes PCa cell proliferation, migration, and invasion (all P<0.05), and is significantly associated with larger tumor diameter, distant metastasis, and shorter survival time (all P<0.05). We found that NAP1L6 promoted the expression of INHBA (P<0.05), and knockdown of NAP1L6 led to the reduction of PCa cell migration, invasion, and proliferation by regulating the expression of INHBA (all P<0.05). Conclusion: lncrna NR6A1 might play an onco

关键词： long non-coding rna NR6A1 INHBA prostate cancer prognosis

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