@article{b8b2b795d9af454ab634bf78550ec5b3,
title = "Profiling of LINE-1-related genes in hepatocellular carcinoma",
abstract = "Hepatocellular carcinoma (HCC) is a prime public health concern that accounts for most of the primary liver malignancies in humans. The most common etiological factor of HCC is hepatitis B virus (HBV). Despite recent advances in treatment strategies, there has been little success in improving the survival of HCC patients. To develop a novel therapeutic approach, evaluation of a working hypothesis based on different viewpoints might be important. Long interspersed element 1 (L1) retrotransposons have been suggested to play a role in HCC. However, the molecular machineries that can modulate L1 biology in HBV-related HCC have not been well-evaluated. Here, we summarize the profiles of expression and/or activation status of L1-related genes in HBV-related HCC, and HBV- and HCC-related genes that may impact L1-mediated tumorigenesis. L1 restriction factors appear to be suppressed by HBV infection. Since some of the L1 restriction factors also limit HBV, these factors may be exhausted in HBV-infected cells, which causes de-suppression of L1. Several HBV- and HCC-related genes that interact with L1 can affect oncogenic processes. Thus, L1 may be a novel prime therapeutic target for HBV-related HCC. Studies in this area will provide insights into HCC and other types of cancers.",
keywords = "DNA damage, Hepatitis B virus, Hepatocellular carcinoma, LINE-1, Retrotransposition, Tumorigenesis",
author = "Tomoyuki Honda and Rahman, {Md Arifur}",
note = "Funding Information: This study was supported in part by JSPS KAKENHI Grant Numbers 15K08496, 18H02664 and 18K19449, the Program on the Innovative Development and the Application of New Drugs for Hepatitis B from Japan Agency for Medical Research and Development (AMED), and grants from the Takeda Science Foundation, Kobayashi International Scholarship Foundation, The Shimizu Foundation for Immunology and Neuroscience Grant for 2015 and Akaeda Medical Research Foundation (T.H.). Funding Information: A1.uthoFrerCeonncti,riPb.;uFtiroiends,: MT.H.; L. aanbdreMcq.uAe.,R D. w.; Brortueixth, eJ.;pSahpeerrm. an, M.; Omata, M.; Heathcote, J.; Piratsivuth, T.; Kew, Funding:M.; OtThisegbstudyayo, J.wasA.; etsuppoal. HrtedepaintocpartellulabyrJSPSCarcKAKENHIinoma (HCCGrant). J. CliNumbersn. Gastr15K08496,oenterol. 2018H0266410, 44, 239and–24518K19449,. t2h.e PrToogrrraem, Lo.nAt.h; eSiIengneol,vRat.iLv.e; WDeavrdel,oEp.mMe.;nJteamnadl,thAe.AGplopbliacla tCioanncoefrNInewcidDernucgesafnodr HMeoprattailtiitsyBRfarotems aJanpda nTrAengednsc—y for Medical Research and Development (AMED), and grants from the Takeda Science Foundation, Kobayashi An Update. Cancer Epidemiol. Biomark. Prev. 2016, 25, 16–27. International Scholarship Foundation, The Shimizu Foundation for Immunology and Neuroscience Grant for 2015 and3. AkaedaHollingMedicaler, F.B.;ResearLiangch, T.FoundationJ. Hepatitis (TB .HV.).irus, 4th ed.; Fields Virology; Lippincott-Raven Publishers: Philadelphia, PA, USA, 2001. Conflicts of Interest: The authors declare no conflicts of interest. 4. Ghouri, Y.A.; Mian, I.; Rowe, J.H. Review of hepatocellular carcinoma: Epidemiology, etiology, and carcinogenesis. J. Carcinog. 2017, 16, 1. References 5. Ganem, D.; Prince, A.M. Hepatitis B Virus Infection—Natural History and Clinical Consequences. N. Engl. 1. FJ.eMreendc.i,2P0.0;4F,r 3ie5d0,,M11.1;8L–a1b1re2c9q.ue,D.;Bruix,J.;Sherman,M.;Omata,M.;Heathcote,J.;Piratsivuth,T.;Kew,M.; 6. OYatenggb,aJy.Do.,;J.KAim.;e, tWal..RH.;eCpoaetolhcoe,lluRl.a;rMCeatrtlceinr,oTm.Aa.(;HBCenCs)o.nJ.,CJ.lTin.;.GSaanstdreoresnotenr,olS..O20.1;0T,h4e4r,n2e3a9u–,2 T45.M.[.C;rKoismsR, eBf.]; [RPoubbeMrtse,dL] .R. Cirrhosis Is Present in Most Patients With Hepatitis B and Hepatocellular Carcinoma. Clin. 2. TGoarsrter,oeLn.Ate.r;oSl.ieHgeepl,atRo.lL. .2;0W11a,r d9,, 6E4.M–7.0; .Jemal, A. Global Cancer Incidence and Mortality Rates and Trends—An 7. UWpodrladte.HCeaanlctehr EOprigdeamniizola.tBioinom. aHrke.pParteivti.s20B1 6W, 2o5r,l1d6–H27e.a[lCthroOssrRgeafn]i[zPautiboMneFda]ct Sheet. Available online: 3. Hhtotpllsi:n//gwerw, wF..Bw.;hoL.iinant/gn,ewT.sJ-.roHoempa/tfiatcist-sBheVeitrsu/ds,et4atihl/heedp.a;tiFtiise-lbd(sacVciersosleodg yo;n L30ipDpeincecmotbt-eRra2v0e1n8).Publishers: 8. PLhi,iXla.d;Zelhpahoia,,J.P;AY,uUanS,AQ,.2;0X0i1a.,N.Detectionof HBV CovalentlyClosed CircularDNA.Viruses2017, 9,139. 9. Summers, J.; O{\textquoteright}Connell, ?.; Millman, I. Genome of hepatitis B virus: Restriction enzyme cleavage and structure of DNA extracted from Dane particles. Proc. Natl. Acad. Sci. USA 1975, 72, 4597–4601. Funding Information: contribute to the regulation of L1 activity. Further investigation will be required for clarifying this point. Intriguingly, we have demonstrated that another oncogenic virus, Kaposi{\textquoteright}s sarcoma-associated Funding: This study was supported in part by JSPS KAKENHI Grant Numbers 15K08496, 18H02664 and herpesvirus, can enhance L1 retrotransposition [140], which may highlight the importance of L1 in 18K19449, the Program on the Innovative Development and the Application of New Drugs for Hepatitis B from Japan Agency for Medical Research and Development (AMED), and grants from the Takeda Science Foundation, Recently, we have also reported that capsaicin, a compound with anti-tumor activity, can suppress LG1rarnettrfootrr2a0n1s5paonsdit iAokna[e1d4a1M]. eTdhicisalr eRseuseltasrcuhgFgoeustnsdtahteiopno(sTs.Hib.i)l.ity that some anti-tumor agents might exert their anti-tumor effect through the inhibition of L1 retrotransposition. Given that L1 plays important Conflicts of Interest: The authors declare no conflicts of interest. roles in HBV-related HCC tumorigenesis, L1 may be a novel prime therapeutic target for HBV-related HCC. Research in this regard will provide insights into HCC and other types of tumors. Publisher Copyright: {\textcopyright} 2019 by the authors. Licensee MDPI, Basel, Switzerland.",
year = "2019",
month = feb,
day = "1",
doi = "10.3390/ijms20030645",
language = "English",
volume = "20",
journal = "International Journal of Molecular Sciences",
issn = "1661-6596",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "3",
}
