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Genome-Wide Screening Identifies Prognostic Long Noncoding Rnas in Hepatocellular Carcinoma

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Hindawi BioMed Research International Volume 2021, Article ID 6640652, 16 pages https://doi.org/10.1155/2021/6640652 Research Article Genome-Wide Screening Identifies Prognostic Long Noncoding RNAs in Hepatocellular Carcinoma Yujie Feng, Xiao Hu, Kai Ma, Bingyuan Zhang , and Chuandong Sun Department of Hepatobiliary and Pancreatic Surgery, The Affiliated Hospital of Qingdao University, Qingdao, Shandong Province 266003, China Correspondence should be addressed to Bingyuan Zhang; [email protected] and Chuandong Sun; [email protected] Received 19 October 2020; Revised 18 April 2021; Accepted 23 April 2021; Published 21 May 2021 Academic Editor: Min Tang Copyright © 2021 Yujie Feng et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Hepatocellular carcinoma (HCC) is a common malignancy with a poor prognosis. Therefore, there is an urgent call for the investigation of novel biomarkers in HCC. In the present study, we identified 6 upregulated lncRNAs in HCC, including LINC01134, RHPN1-AS1, NRAV, CMB9-22P13.1, MKLN1-AS, and MAPKAPK5-AS1. Higher expression of these lncRNAs was correlated to a more advanced cancer stage and a poorer prognosis in HCC patients. Enrichment analysis revealed that these lncRNAs played a crucial role in HCC progression, possibly through a series of cancer-related biological processes, such as cell cycle, DNA replication, histone acetyltransferase complex, fatty acid oxidation, and lipid modification. Moreover, competing endogenous RNA (ceRNA) network analysis revealed that these lncRNAs could bind to certain miRNAs to promote HCC progression. Loss-of-function assays indicated that silencing of RHPN1-AS1 significantly suppressed HCC proliferation and migration. Though further validations are still needed, these identified lncRNAs could serve as valuable potential biomarkers for HCC prognosis. 1. Introduction link to the regulation of HCC growth and metastasis. Specif- ically, lncRNA XIST regulates HCC tumor growth and Hepatocellular carcinoma (HCC) has ranked as the second migration by sponging miR-497-5p [9]. DANCR retained leading cause of cancer-related deaths worldwide [1], as more HCC stemness by suppressing CTNNB1 expression [11]. than 782,000 HCC-associated deaths are predicted to occur The LINC01138 drives carcinogenesis in HCC via activating annually [2]. Previous studies have demonstrated that the arginine methyltransferase 5 [10]. Meanwhile, several upregulation of oncogenes and downregulation of tumor lncRNAs have been demonstrated as potential prognostic suppressors were related to HCC tumorigenesis. For exam- biomarkers in HCC. For example, overexpression of lncRNA ple, ID1 enhanced tumor growth in HCC patients [3], while ENST00000429227.1, LINC00511, SNHG16, and AK001796 FABP4 inhibited tumor growth and invasion [4]. However, were associated with worse prognosis in HCC patients [12] . there is still an urgent call to explore new biomarkers in A further appreciation of the molecular functions and HCC, as novel therapeutic targets are needed for establishing expression patterns of lncRNAs could help reveal novel bio- future molecular therapies, in the hope of improving progno- markers for HCC. ses of HCC patients. In this study, using gene expression data of HCC patients Noncoding RNAs (ncRNAs) have emerged as a very and healthy controls, we screened possible prognostic promising resource for the identification of prognostic bio- lncRNAs in HCC. Additionally, we utilized bioinformatic markers. ncRNAs longer than 200 bps are regarded as long approaches to explore the potential functions of such noncoding RNAs (lncRNAs) [5]. Growing evidence has con- lncRNAs and constructed competing endogenous RNA firmed the association between HCC and lncRNAs [6]. For (ceRNA) networks to further demonstrate potential mecha- example, XIST [7–9] and LINC01138 [10] were reported to nisms concerning those identified lncRNAs in HCC P er- ff 0.001 < 3 2 1 0 −1 −2 −3 RAD54L MCM10 value CENPK E2F8 CDC25C P CELSR3 RP11−218F10.3 CTD−2349P21.9 AC010761.8 RP5−967N21.11 and WBP2NL The gene list of di RP11−127B20.3 0 RP4−620E11.8 : CTGLF10P RP11−225B17.2 >2 LINC01268 cant association with overall ∣ IGJ fi OLFM1 AXIN1 ADH4 FC BioMed Research International RPL14P3 ∣ SPEF1 ATRIP RP11−932O9.10 RP11−197P3.5 erentially expressed lncRNAs, and DNASE1L3 erential expression analysis, and pro- ff CLEC3B log 2 XCR1 ff OMG STAG3 ZNF131 cally, GEPIA normalized gene expression PSMC3IP erentially expressed genes ranked by the LRP11 fi HEATR5A ff CCZ1B LCN6 Overall survival RP11−709D24.8 Log2 Hazard ratio C2orf66 BFSP1 erentially expressed lncRNAs in HCC and nontumor DDAH2 ff SPATA2 EZH2 MKI67 PARPBP EME1 0 0.5 1 1.5 2 2.5 3 3.5 4 SGOL1 RNFT2 SLC25A19 AP000695.4 CAD ently expressed lncRNAs in HCCGEPIA was downloaded dataset from the newly (http://gepia.cancer-pku.cn/). developed GEPIA interactiveRNA is sequencing web expression a server datanormal of for samples 9,736 from tumors the analyzing TCGA and and the a 8,587 the GTEx projects standard using report processing [13]. Speci pipeline, according to a previous values. lncRNAs with by transcript perpackage to million conduct (TPM), di employed the R limma 2.2. Data Preparation and Processing. vided a list of di XPO5 were considered as di DHX57 BRCA1 MYO19 (a) (b) NUP205 les of the 100 di GPSM2 fi C5orf45 BRD8 RP5−1074L1.4 SNHG20 ZWINT MCM6 CHEK1 CHAF1B 01234 LMNB1 MCM3 NASP CENPH Log2 Hazard ratio STMN1 Disease-free survival KIF2C PTTG1 CCNB1 KPNA2 WDR4 STX1A RBM28 PHF19 NRM UBE2S FAM216A PCNT POLR3F PRR3 NR2C1 TRIM45 RP13−516M14.1 RAD51C NUP85 SRP68 UTP18 EFTUD2 UTP6 C12orf43 Gene symbol CTB−147N14.6 RP11−286H15.1 RP11−295D4.1 RHPN1−AS1 SNRPEP2 LINC01134 NRAV NAP1L1P1 CMB9−22P13.1 MKLN1−AS RP5−864K19.4 CTC−297N7.9 MAPKAPK5−AS1 MIR210HG AP001469.9 RHOT2 TBRG4 From April 2016 to March 2020, 6 MED7 RPL39P3 Non-tumor HCC HIST1H1B SCRT1 WI2−89031B12.1 Tissue Tissue liated Hospital of Qingdao University. The ethics 1: LINC01134, RHPN1-AS1, NRAV, CMB9-22P13.1, MKLN1-AS, and MAPKAPK5-AS1 were associated with both disease-free ffi 2. Materials and Methods 2.1. Clinical Samples. paired HCC andthe adjacent normal A tissuescommittee were of collected at thisenrollment hospital of approved patients. this Allinformed study consent. patients before or the their parents signed development and progression. Loss-of-functionperformed assays to were investigate potential functionsin of HCC. key We lncRNAs believemarkers in that HCC this and study inspire could further researches. provide valuable Figure survival and overall survival time in HCC. (a) The expression pro 2 tissues. (b) The two forest plots of disease-free survival and overall survival for the 15 genes with signi survival. The gene symbols with red color are associated with both disease-free survival and overall survival. BioMed Research International 3 Disease-free survival Disease-free survival Disease-free survival 1.0 1.0 1.0 0.8 0.8 0.8 Logrank P = 0.0034 Logrank P = 0.0014 Logrank P = 0.0014 0.6 0.6 0.6 0.4 0.4 0.4 Percent survival 0.2 Percent survival 0.2 Percent survival 0.2 0.0 0.0 0.0 0 20 40 60 80 100 120 0 20 40 60 80 100 120 0 20 40 60 80 100 120 Months Months Months Low LINC01134 Low RHPN1−AS1 Low NRAV High LINC01134 High RHPN1−AS1 High NRAV Disease-free survival Disease-free survival Disease-free survival 1.0 1.0 1.0 0.8 0.8 0.8 0.6 Logrank P = 0.002 0.6 Logrank P = 0.01 0.6 Logrank P = 0.037 0.4 0.4 0.4 Percent survival 0.2 Percent survival 0.2 Percent survival 0.2 0.0 0.0 0.0 0 20 40 60 80 100 120 0 20 40 60 80 100 120 0 20 40 60 80 100 120 Months Months Months Low CMB9−22P13.1 Low MKLN1−AS Low MAPKAPK5−AS1 High CMB9−22P13.1 High MKLN1−AS High MAPKAPK5−AS1 (a) Figure 2: Continued. 4 BioMed Research International Overall survival Overall survival Overall survival 1.0 1.0 1.0 0.8 0.8 0.8 0.6 0.6 0.6 0.4 0.4 0.4 Percent survival 0.2 Percent survival 0.2 Percent survival 0.2 0.0 Logrank P = 7.9e−06 0.0 Logrank P = 3.5e−06 0.0 Logrank P = 7.1e−06 0 20 40 60 80 100 120 0 20 40 60 80 100 120 0 20 40 60 80 100 120 Months Months Months Low LINC01134 Low RHPN1−AS1 Low NRAV High LINC01134 High RHPN1−AS1 High NRAV Overall survival Overall survival Overall survival 1.0 1.0 1.0 0.8 0.8 0.8 0.6 0.6 0.6 0.4 0.4 0.4 Percent survival 0.2 Percent survival 0.2 Percent survival 0.2 Logrank P = 2.4e−05 Logrank P = 3.9e−05 Logrank P = 3.6e−05 0.0 0.0 0.0 0 20 40 60 80 100 120 0 20 40 60 80 100 120 0 20 40 60 80 100 120 Months Months Months Low CMB9−22P13.1 Low MKLN1−AS Low MAPKAPK5−AS1 High CMB9−22P13.1 High MKLN1−AS High MAPKAPK5−AS1 (b) Figure 2: LINC01134, RHPN1-AS1, NRAV, CMB9-22P13.1, MKLN1-AS, and MAPKAPK5-AS1 were related to disease-free and overall survival time in HCC. The Kaplan-Meier (KM) curves of disease-free survival (a) and overall survival (b) for six prognostic lncRNAs in HCC. the top 100 lncRNAs ranked by the P values were selected for HCC. The hypergeometric test was employed to determine downstream analysis. Moreover, those lncRNAs associated the statistical significance. with survival time in HCC were also downloaded from the GEPIA website [13].
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    9765 Clairemont Mesa Blvd, Suite C San Diego, CA 92124 Tel: 858.875.1900 Fax: 858.622.0609 PRAK (MAPKAPK5) Antibody (T182) Peptide Affinity Purified Rabbit Polyclonal Antibody (Pab) Catalog # AP7216a Specification PRAK (MAPKAPK5) Antibody (T182) - Product Information Application WB,E Primary Accession Q8IW41 Reactivity Human Host Rabbit Clonality Polyclonal Isotype Rabbit Ig Clone Names RB13233 Calculated MW 54220 Antigen Region 160-189 PRAK (MAPKAPK5) Antibody (T182) - Additional Information Gene ID 8550 Other Names MAP kinase-activated protein kinase 5, Western blot analysis of MAPKAPK5 Antibody MAPK-activated protein kinase 5, MAPKAP (T182) (Cat.#AP7216a) in Hela cell line lysates kinase 5, MAPKAP-K5, MAPKAPK-5, MK-5, (35ug/lane). MAPKAPK5 (arrow) was detected MK5, p38-regulated/activated protein kinase, using the purified Pab. PRAK, MAPKAPK5, PRAK Target/Specificity This PRAK(MAPKAPK5) antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 160-189 amino acids from human PRAK(MAPKAPK5). Dilution WB~~1:1000 Format Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. Storage Maintain refrigerated at 2-8°C for up to 6 Western blot analysis of MAPKAPK5 (arrow) months. For long term storage store at -20°C using rabbit polyclonal MAPKAPK5 Antibody in small aliquots to prevent freeze-thaw (T182) (Cat.#AP7216a). 293 cell lysates (2 cycles. ug/lane) either nontransfected (Lane 1) or transiently transfected (Lane 2) with the Precautions MAPKAPK5 gene. PRAK (MAPKAPK5) Antibody (T182) is for research use only and not for use in diagnostic or therapeutic procedures.
  • Inhibitors of MBNL1-CUG RNA Binding with Distinct Cellular Effects Jason W

    Inhibitors of MBNL1-CUG RNA Binding with Distinct Cellular Effects Jason W

    Published online 20 April 2014 Nucleic Acids Research, 2014, Vol. 42, No. 10 6591–6602 doi: 10.1093/nar/gku275 Lomofungin and dilomofungin: inhibitors of MBNL1-CUG RNA binding with distinct cellular effects Jason W. Hoskins1, Leslie O. Ofori2, Catherine Z. Chen3,AmitKumar4, Krzysztof Sobczak1, Masayuki Nakamori1, Noel Southall3, Samarjit Patnaik3, Juan J. Marugan3, Wei Zheng3, Christopher P. Austin3, Matthew D. Disney4, Benjamin L. Miller5 and Charles A. Thornton1,* 1Department of Neurology, University of Rochester, Rochester, NY 14642, USA, 2Department of Chemistry, University of Rochester, Rochester, NY 14642, USA, 3Division of Pre-clinical Innovation, National Center for Advancing Translational Sciences, National Institutes of Health, Bethesda, MD 20892, USA, 4Department of Chemistry, Scripps Florida, Jupiter, FL 33458, USA and 5Department of Dermatology, University of Rochester, Rochester, NY 14642, USA Received May 8, 2013; Revised March 21, 2014; Accepted March 24, 2014 ABSTRACT INTRODUCTION Myotonic dystrophy type 1 (DM1) is a dominantly Myotonic dystrophy type 1 (DM1) is the prototypical ge- inherited neuromuscular disorder resulting from ex- netic disease resulting from a toxic gain-of-function by mu- pression of RNA containing an expanded CUG repeat tant RNA (1). RNA toxicity has been implicated in several (CUGexp). The pathogenic RNA is retained in nuclear other disorders that share a distinctive set of genetic fea- foci. Poly-(CUG) binding proteins in the Muscleblind- tures: the causal mutations are large polymorphic expan- sions of simple tandem repeats that are genetically unsta- like (MBNL) family are sequestered in foci, caus- ble and located in non-coding regions of the genome (2–9). ing misregulated alternative splicing of specific pre- The underlying disease mechanisms are heterogeneous and exp mRNAs.