Correction:Drp1-dependent remodeling of mitochondrial morphology triggered by EBV-LMP1 increases cisplatin resistance

Correction to:Signal Transduction and Targeted Therapy(2020)5:56,https://doi.org/10.1038/s41392-020-0151-9,published online 20 May 2020 In this article1 an error was noticed in Fig.3d left(p-Drp1 Ser637).The images were misassigned.And one writing error was found in Fig.S1c.The correct figures are given.The authors confirm that these corrections do not change the result interpretation or conclusions of the article.

Drp1-dependent remodeling of mitochondrial morphology triggered by EBV-LMP1 increases cisplatin resistance

Latent membrane protein 1(LMP1)is a major Epstein–Barr virus(EBV)-encoded oncoprotein involved in latency infection that regulates mitochondrial functions to facilitate cell survival.Recently,mitochondrial fission has been demonstrated as a crucial mechanism in oncovirus-mediated carcinogenesis.Mitochondrial dynamin-related protein 1(Drp1)-mediated mitochondrial fission has an impact on the chemoresistance of cancers.However,the mechanism by which oncogenic stress promotes mitochondrial fission,potentially contributing to tumorigenesis,is not entirely understood.The role of Drp1 in the oncogenesis and prognosis of EBV-LMP1-positive nasopharyngeal carcinoma(NPC)was determined in our study.We show that EBV-LMP1 exhibits a new function in remodeling mitochondrial morphology by activating Drp1.A high level of p-Drp1(Ser616)or a low level of p-Drp1(Ser637)correlates with poor overall survival and disease-free survival.Furthermore,the protein level of p-Drp1(Ser616)is related to the clinical stage(TNM stage)of NPC.Targeting Drp1 impairs mitochondrial function and induces cell death in LMP1-positive NPC cells.In addition,EBV-LMP1 regulates Drp1 through two oncogenic signaling axes,AMPK and cyclin B1/Cdk1,which promote cell survival and cisplatin resistance in NPC.Our findings provide novel insight into the role of EBV-LMP1-driven mitochondrial fission in regulating Drp1 phosphorylation at serine 616 and serine 637.Disruption of Drp1 could be a promising therapeutic strategy for LMP1-positive NPC.

Targeting the signaling in Epstein-Barr virus-associated diseases: mechanism, regulation, and clinical study

Epstein-Barr virus-associated diseases are important global health concerns.As a group I carcinogen,EBV accounts for 1.5%of human malignances,including both epithelial-and lymphatic-originated tumors.Moreover,EBV plays an etiological and pathogenic role in a number of non-neoplastic diseases,and is even involved in multiple autoimmune diseases(SADs).In this review,we summarize and discuss some recent exciting discoveries in EBV research area,which including DNA methylation alterations,metabolic reprogramming,the changes of mitochondria and ubiquitin-proteasome system(UPS),oxidative stress and EBV lytic reactivation,variations in non-coding RNA(ncRNA),radiochemotherapy and immunotherapy.Understanding and learning from this advancement will further confrm the far-reaching and future value of therapeutic strategies in EBV-associated diseases.