Welcome to join our EBV oncology team!
Viral Oncology Laboratory
The Principle Investigator:
Name: Chih-Wen Peng (Ponpon)
Degree: Ph. D. in Plant Virology, Oregon State University
Postdoctral Trainee: Dept. of Medicine and Microbiology and
Molecular Genetics, Harvard Medical
School
Position: Professor, Department of Life Science, National Dong
Hwa University
E. mail: pengcw@gms.ndhu.edu.tw
The Principle Investigator:
Name: Chih-Wen Peng (Ponpon)
Degree: Ph. D. in Plant Virology, Oregon State University
Postdoctral Trainee: Dept. of Medicine and Microbiology and
Molecular Genetics, Harvard Medical
School
Position: Professor, Department of Life Science, National Dong
Hwa University
E. mail: pengcw@gms.ndhu.edu.tw
Biography
Chih-Wen Peng, PhD, is a professor in the Institute of Medical Sciences, Tzu Chi University. He received his B.S. degree from National Chung-Hsing University and his PhD from Oregon State University. After his PhD, he was a post-doctoral fellow in Dr. Eliott Kieff’s lab in Harvard Medical School focusing on virus and host interactions to elucidate how EBV nuclear antigens trigger the latency dependent transcription program. He joined the faculty at department of Life Sciences in 2004 and at the Institute of Medical Sciences of Tzu Chi University in 2015. Dr. Peng has conducted proteomic and epigenetic research to dissect how Epstein-Barr Virus (EBV) exploits or subverts the cellular factors to establish and to maintain the persistency in host cells.
Research
Epstein Barr Virus (EBV) was discovered in cultures of Burkitt Lymphoma (BL) cells, an endemic African pediatric B-cell lymphoma. EBV is now also implicated in causation of B- and NKT-cell proliferative
Diseases, Hodgkin's Disease, Nasopharyngeal Carcinoma, and Antral Gastric Carcinomas. Consistent with these oncogenic effects, EBV infection of primary human B-lymphocytes causes continuous lymphoblastoid cell proliferation (LCLs), in vitro, and in patients with deficient T-cell immune responses. EBV-transformed B cell growth requires five EBV nuclear antigen proteins (EBNAs), two integral membrane proteins (LMPs), and may also be affected by EBV non-protein-coding small RNAs. Our research interest is to uncover the mechanistic insight of EBV-mediated transformation of human B lymphocytes through targeting to the working model of key viral latent proteins. We have identified some cellular factors are involved in the establishment and maintence of EBV latency program. In addition, we also advance to anti-EBV compounds discovery. Epstein-Barr Virus (EBV) was the first human tumor virus shown to associate with a broad spectrum of cancers originating from lymphocytes and epithelial cells. EBV related studies have been of huge importance to our understanding of how viruses can cause cancer. The establishment of lifelong latent infection in host cells is a prerequisite process of EBV-induced tumoriegenesis.
Our research interests focus on: (I) Understanding of how EBV latent genes interact and modulate cellular factors to build up the permanent infection in host cells. (II) Identification of new biomarkers and therapeutic targets for EBV associated cancers. (III) Development of new anti-virus protocol for being applied to translation medicine research of EBV-associated malignancies.
Epstein Barr Virus (EBV) was discovered in cultures of Burkitt Lymphoma (BL) cells, an endemic African pediatric B-cell lymphoma. EBV is now also implicated in causation of B- and NKT-cell proliferative
Diseases, Hodgkin's Disease, Nasopharyngeal Carcinoma, and Antral Gastric Carcinomas. Consistent with these oncogenic effects, EBV infection of primary human B-lymphocytes causes continuous lymphoblastoid cell proliferation (LCLs), in vitro, and in patients with deficient T-cell immune responses. EBV-transformed B cell growth requires five EBV nuclear antigen proteins (EBNAs), two integral membrane proteins (LMPs), and may also be affected by EBV non-protein-coding small RNAs. Our research interest is to uncover the mechanistic insight of EBV-mediated transformation of human B lymphocytes through targeting to the working model of key viral latent proteins. We have identified some cellular factors are involved in the establishment and maintence of EBV latency program. In addition, we also advance to anti-EBV compounds discovery. Epstein-Barr Virus (EBV) was the first human tumor virus shown to associate with a broad spectrum of cancers originating from lymphocytes and epithelial cells. EBV related studies have been of huge importance to our understanding of how viruses can cause cancer. The establishment of lifelong latent infection in host cells is a prerequisite process of EBV-induced tumoriegenesis.
Our research interests focus on: (I) Understanding of how EBV latent genes interact and modulate cellular factors to build up the permanent infection in host cells. (II) Identification of new biomarkers and therapeutic targets for EBV associated cancers. (III) Development of new anti-virus protocol for being applied to translation medicine research of EBV-associated malignancies.
The achievement of PI’s current research work:
During the past five years, the PI’s research work focused on exploring the working model by which EBNA1 or EBNA2 recruit cellular factors to support the establishment and maintenance of EBV latent infection in host B cells. His research group employed protein affinity pull-down and LC-MS/MS analyses to identify the cellular proteins bound to EBNA2 and EBNA1, respectively. The innovative studies about the interactions between the above viral gene products and cellular factors led to gain advanced knowledge with respect to the establishment and maintenance of EBV persistent infection in host cells, which is expected to be a critical requirement for such oncogenic virus to induce tumorigenesis in hosts.
Firstly, nucleophosmin (NPM1) and the protein ariginine methyl transferase were found to be EBNA2 associated. Peng’s group found dramatic NPM1expression was induced in EBV positively infected B cells after three days of viral infection, and EBNA2 were shown to have a role in the transactivation of the NPM1 promoter. Depletion of NPM1 with the lentivirus-expressed short-hairpin RNAs (shRNAs) effectively abrogated EBNA2-dependent transcription and transformation outgrowth of lymphoblastoid cells. Notably, Peng’s team found the ATP-bound state of NPM1 was required to induce assembly of a protein complex containing EBNA2, RBP-Jk, and NPM1 by stabilizing the interaction of EBNA2 with RBP-Jk. In a NPM1-knockdown cell line, an EBNA2-mediated transcription defect was shown to be fully restored by the ectopic expression of NPM1. Their findings highlight the essential role of NPM1 in chaperoning EBNA2 onto the promoter of EBV oncogene latency-associated membrane protein 1 (LMP1), which is coordinated with the subsequent activation of transcriptional cascades through RBP-Jk during EBV infection (See reference 1). Furthermore, Peng’s group also demonstrated that protein ariginine methyltransferase 5 (PRMT5) substantially recognizes EBNA2 330-365 ariginine-glycinerich domain and mediates methylation of ariginine residues and subsequently leads to promote EBNA2 binding to the cognate elements (See reference 2).
Secondly, recent collaboration between Dr. Peng’s group and Dr. Song’s group (Jikui Song , Department of Biochemistry University of California, Riverside) has led to unravel the crystal structure of the coiled-coil and MYND tandem domains of BS69/ZMYND11, a candidate tumor suppressor, in complex with an EBNA2 peptide containing a PXLXP motif. They found that the coiled-coil and MYND domains of BS69 cooperate in binding to EBNA2. They showed that EBNA2 interacts with BS69 and down-regulates its expression at both mRNA and protein levels in EBV-associated B cells. Ectopic BS69 coiled-coil-MYND dual domain is recruited to viral target promoters through interaction with EBNA2, inhibits EBNA2-mediated transcription activation, and impairs proliferation of lymphoblastoid cell lines (LCLs). This study identifies the BS69 C-terminal domains as an inhibitor of EBNA2 and likely mediates a host defense response to EBV infection, which may have important implications in development of novel therapeutic strategies against EBV infection (See reference 4).
Thirdly, both nucleolin (NCL) and ribosomal protein L4 (RPL4) were identified as EBNA1-associated proteins by Peng’s group. EBNA1’s N-terminal 100 aa and NCL’s RNA-binding domains were shown to be critical for EBNA1/NCL interaction. Despite low-level stable association, NCL shRNA knockdowns revealed wild-type NCL, but not an NCL ATP binding site point mutant to be critical for EBNA1 binding to EBV episomes, transcription, and genome maintenance. The research work identify NCL and NCL K429 as potential targets for inhibition of EBNA1’s role in EBV mediated tumorigenesis (Reference 3).The followed up study finds that EBNA1 complexes with Ribosome Protein L4 (RPL4) and Nucleolin to stabilize EBNA1 binding to oriP. Cooperation of RPL4’s N terminus with Nucleolin K429 is necessary for EBNA1 oriP binding and episome maintenance, whereas RPL4’s C-terminal K380 and K393 induce H3K4me2, which promotes EBNA1 transactivation of oriP. These discoveries strikingly enhance the understanding of the complexity of EBNA1’s interactions with host proteins and EBV episomes and reveal new targets for inhibition of EBV genome persistence (Reference 5).
Significance of PI’s research work
Treating of EBV associated malignancies poses a great challenge to both physicians and patients because of its less common nature and more disease heterogeneity, as compared to most other cancers. In addition, EBV-induced lymphoproliferative disease (EBV-LPD) after transplantation remains a serious and life-threatening complication. Although patients with early stage disease can often achieve long-lasting remissions with a combination of chemotherapy and radiation, current treatments for most EBV-infected T/NK or some B neoplasms are unsatisfactory. Despite that no effective anti-EBV compounds have been identified, the presence of EBV in tumour cells offers an opportunity for the development of new therapeutic strategies based on targeting the unique virus dependent surviving pathways. Therapies involving novel mechanisms that target important EBV oncogenes or viral-dependent signaling pathways are critically required. Good anti-EBV protocols will be expected to exhibit promising anti-tumour effects by showing their strong capability to deplete the cell viability of EBV-infected cancer cells.
Selected publications:
1. Cheng-Der Liu, Ya-Lyn Chen, Yi-Li Min, Bo Zhao, Chi-Ping Cheng, Myung-Soo Kang, Shu-Jun Chiu, Elliott Kieff, and Chih-Wen *Peng. 2012, The Nuclear Chaperone Nucleophosmin Escorts an Epstein-Barr Virus Nuclear Antigen to Establish Transcriptional Cascades for Latent Infection in Human B Cells. PLoS Pathog, 8: e1003084 (1-16). (IF=7.562; R/C= 10/119 )
2. Liu, CD, Cheng, CP, Fang, JS, Chen, LC, CW *Peng. 2013, Modulation of Epstein-Barr Virus Nuclear Antigen 2-Dependent Transcription by Protein Arginine Methyltransferase 5. Biochemical and Biophysical Research Communications, 430:1097-1102. (IF:297:RC=180/290)
3. Ya-Lyn Chen, Cheng-Der Liu, Chi-Ping-Cheng, Bo Zhao, Hao-Jen Hsu, Chih-Long Shen, Shu-Jiun Chiu, Elliott Kieff, and Chih-Wen *Peng. 2014 Nucleolin is important for Epstein-Barr Virus Nuclear Antigen mediated episome binding,maintenance, and transcription. Proc Natl Acad Sci USA. 111(1):243-248. (IF=9.674; R/C= 4/57)
4. Matthew R. Harter, Cheng-Der Liu, Chih-Lung Shen, Elsie Gonzalez-Hurtado, Zhi-Min Zhang, Muyu Xu, Ernest Martinez, Chih-Wen *Peng, and Jikui *Song. 2016 BS69/ZMYND11 is a potential EBNA2-targeting suppressor for EBV infection. PLoS Pathog 12(2): e1005414. (IF=7.562; R/C= 10/119 )
5. Chih-Lung Shen, Cheng-Der Liu, Ren-In You, Yung-Hao Ching, Jun Liang, Liangru Ke,Ya-Lin Chen, Hong-Chi Chen , Hao-Jen Hsu, Je-Wen Liou, Kieff Elliott, and Chih-Wen *Peng. 2016 Ribosomal Protein L4 is essential for Epstein-Barr virus Nuclear Antigen 1 functions. Proc. Natl. Acad. Sci USA. Feb 23;113(8):2229-34. (IF=9.674; R/C= 4/57)
Research Grants:
1. Study on the mechanism of EBV latent infection in B cells.
NSC 101-2320-B-320 -005 -MY3 (08. 2012~ 07. 2015)
2. EBV nuclear antigen 1 mediated transcription and development of high throughput assay systems.
NHRI 9910 BC (01. 2009~12.2013)
3. The Mechanistic Insight of miRNAs and Cytokines in EBV Pathogenesis
NHRI (01. 01.2014~12.31.2015)
4. MOST 105 2016.08.01-2019.07.31
5. MOST 106 2017.08.01-2020.07.31
1. Study on the mechanism of EBV latent infection in B cells.
NSC 101-2320-B-320 -005 -MY3 (08. 2012~ 07. 2015)
2. EBV nuclear antigen 1 mediated transcription and development of high throughput assay systems.
NHRI 9910 BC (01. 2009~12.2013)
3. The Mechanistic Insight of miRNAs and Cytokines in EBV Pathogenesis
NHRI (01. 01.2014~12.31.2015)
4. MOST 105 2016.08.01-2019.07.31
5. MOST 106 2017.08.01-2020.07.31
Lab Members:
4 Graduate Students
1 Research Assistant
2 Undergraduate Students
4 Graduate Students
1 Research Assistant
2 Undergraduate Students
Publications:
1. Tsai, C.-H., Cheng, C.-P., Peng, C-.W., Lin, B.-Y., Lin, N.-S., and Y.-H. Hsu. 1999. Sufficient length of a poly(A)
tail for the formation of a potential pseudoknot is required for efficient replication of bamboo mosaic potexvirus RNA.
J. Virol. 73, 2703-2709.
2. Peng, C. W., and V. V. *Dolja. 2000. Leader Proteinase of the Beet Yellows closterovirus: Mutational analysis of the
function in genome amplification. J. Virol. 74, 9766-9770.
3. Peng C. W., V. V. Peremyslov, A. R. Mushegian, W. O. Dawson, and V. V. *Dolja. 2001. Functional specialization
and evolution of the leader proteinases in the family closteroviridae. J. Virol 75, 12153-12160.
4. Peng, C. W., V. V. Peremyslov, E. J. Snijder, and V. V. *Dolja. 2002. A competent- chimera of plant and animal viruses.
Virology 294, 75-84 .
5. Cheng, J. H., C.W. Peng, Y. H. Hsu, C. H. Tsai. 2002. The Synthesis of Minus-Strand RNA of Bamboo Mosaic Potexvirus
Initiates from Multiple Sites within the Poly(A) Tail. J. Virol. 76, 6114-6120.
6. Peng, C.W., A.J. Napuli, and V. V. Dolja. 2003. Leader Proteinase of Beet Yellows Virus Functions in Long-Distance
transport. J. Virol 77,2843-2849.
7. Peng , C.W., Y. Xio, B. Zhao, *E. Kieff and S. Harada. 2004. The direct interactions between Epstein-Barr Virus Leader
Nuclear Protein LP and the EBNA2 acidic domain underlie coordinate transcriptional regulation. Proc. Natl. Acad.
Sci. USA 101, 1033-1038.
8. Peng, C.W., Bo Zhao and E. Kieff. 2004. Four EBNA2 domains are important for EBNA LP coactivation with EBNA2.
J Virol. 78(20):11439-42.
9. Peng*, CW., B Zhao HC Chen, ML Chou, , CY Lai, SZ Lin, SY Shu, and E. Kieff*. 2007, Hsp72 up regulates Epstein-Barr
Virus EBNALP co-activation with EBNA2. Blood. 109(12) 5447-5454. (First and corresponding author)
10. Chang YJ, Liu JW, Lin PC, Sun LY, Peng CW, Luo GH, Chen TM, Lee RP, Lin SZ, Harn HJ, and Chiou TW. 2009,
Mesenchymal stem cells facilitate recovery from chemically induced liver damage and decrease liver fibrosis.
Life Sci. 23; 85(13-14):517-25.
11. T-L *Chiu, Su CC, Wang MR, and CW Peng. 2009, AAV2-mediated interleukin-12 in the treatment of malignant brain
tumors through activation of NK cells. International Journal of oncology. Dec;35(6):1361-7.
12. Lin, RH, Peng, CW, Lin, YC, Peng, HL, HC *Huang. 2011, The XopE2 effector protein of Xanthomonas campestris pv.
vesicatoria is involved in virulence and in the suppression of the hypersensitive response. Botanical Studies,
52:55-72.
13. Yu, SH, Yang, PM, Peng, CW, Yu, YC, SJ *Chiu. 2011, Securin depletion sensitizes human colon cancer cells to
fisetin-duced apoptosis. Cancer Letters, 300:96- 104.
14. Bo Zhao, James Zoub, Hongfang Wang, Eric Johannsen, Chih-Wen Peng, John Quackenbush, Jessica C.
Mar, Cynthia Casson Mortond, Matthew L. Freedman, Stephen C. Blacklowd, Jon C. Asterd, Bradley E. Bernsteinc, and
Elliott Kieff. 2011, Epstein-Barr virus exploits intrinsic B-lymphocyte transcription programs to achieve immortal cell
growth. Proc Natl Acad Sci U S A.,108:14902-14907
15. Chiu, TL*, Peng, CW, MJ Wang. 2011, Enhanced anti-glioblastoma activity of microglia by AAV2-mediated IL-12
through TRAIL and phagocytosis in vitro. Oncol Rep., 25:1373-1380.
16. Chen, YL, Tsai, HL, CW *Peng. 2012, EGCG debilitates the persistence of EBV latency by reducing the DNA
binding potency of nuclear antigen 1. Biochemical and Biophysical Research Communications, 417:1093-
1099.
17. Yang, PM, Tseng, HH, Peng, CW, Chen, WS, SJ *Chiu. 2012, Dietary flavonoid fisetin targets caspase-3-deficient
human breast cancer MCF-7 cells by induction of caspase-7- associated apoptosis and inhibition of autophagy.
INTERNATIONAL JOURNAL OF ONCOLOGY, 40:469-478
18. Liu, CD, Chen, YL, Min, YL, Zhao, B, Cheng, CP, Kang, M, Chiu, SJ, Kieff, E, CW *Peng. 2012, The Nuclear Chaperone
Nucleophosmin Escorts an Epstein-Barr Virus Nuclear Antigen to Establish Transcriptional Cascades for Latent
Infection in Human B Cells. PLOS Pathog. 8: e1003084 (1-16).
19. Liu, CD, Cheng, CP, Fang, JS, Chen, LC, CW *Peng. 2013, Modulation of Epstein-Barr Virus Nuclear Antigen
2-Dependent Transcription by Protein Arginine Methyltransferase 5. Biochemical and Biophysical Research
Communications, 430:1097-1102.
20. Yi-Chu Yu, Pei-Ming Yang, Qiu-Yu Chuah, Yao-Huei Huang, Chih-Wen Peng, Yi-Jang Lee, and Shu-Jun Chiu1.
2013. Radiation-induced senescence in securin-deficient cancer cells promotes cell invasion involving
the IL-6/STAT3 and PDGF-BB/PDGFR pathways. Scientific Reports, 3:1675-1685.
21. Ya-Lyn Chen, Cheng-Der Liu, Chi-Ping Cheng, Bo Zhao, Hao-Jen Hsu, Chih-Long Shen, Shu-Jiun Chiu, Elliot Kieff, and
Chih-Wen *Peng. Nucleolin is important for Epstain-Barr Viorus Nuclear Antigen 1 dependent episome binding,
maintenance, transcription. Proc Natl Acad Sci USA. 111(1):243-248
22. Yao-Huei Huang, Pei-Ming Yang, Qiu-Yu Chuah, Yi-Jang Lee, Chih-Wen Peng, and Shu-Jun *Chiu. 2014 Autophage
promotes radiation-induced senescence but inhibits bystander effects in human breast cancer cells. Autophage 10:7,
1-17.
23. Matthew R Harter, Cheng-Der Liu, Chih-Lung Shen, Elsie Gonzalez-Hurtado, Zhi-Min Zhang, Muyu Xu, Ernest Martinez
Chih-Wen *Peng, and Jikui *Song. BS69/ZMYND11 C-Terminal Domains Bind and Inhibit EBNA2. Feb. 06 2016
PLOS Pathog. 12(2):E1005414 ·
24. Chih-Lung Shen, Cheng-Der Liu, Ren-In You,Yung-Hao Ching, Jun Liang, Liangru Ke, Ya-Lin Chen, Hong-Chi Chen,
Hao-Jen Hsu, Je-Wen Liou, Elliott Kieff, and Chih-Wen *Peng. Ribosome Protein L4 is essential for Epstein-Barr Virus
Nuclear Antigen 1 function. 2016 Proc Natl Acad Sci USA. 113(8):2229-2234
25. Tsai MH, Chang CH, Tsai RK, Hong YR, Chuang TH, Fan KT, Peng CW, Wu CY, Hsu WL, Wang LS, Chen LK, Yu HS.
2016 Cross-regulation of Pro-inflammatory Cytokines by Interleukin-10 and MiR-155 in Orientia tsutsugamushi-infected
Human Macrophages Prevents Cytokine Storm. J Invest Dermatol. 2016 Jul;136(7):1398-407Feb 24. (IF=7.216; R/C=
1/63)
26. Wang C, Zhou H, Xue Y, Liang J, Narita Y, Gerdt C, Zheng AY, Jiang R, Trudeau S, Peng CW, Gewurz BE, Zhao B.
Epstein-Barr Virus Nuclear Antigen Leader Protein Coactivates EP300. J Virol. 2018 Apr 13;92(9).
27. Jhang JF, Hsu YH, Peng CW, Jiang YH, Ho HC, Kuo HC. Epstein-Barr Virus Presence As A Potential Etiology of
Persistent Bladder Inflammation in Human Interstitial Cystitis/Bladder Pain Syndrome. J Urol. 2018 Apr 10
28. Shen CL, Huang WH, Hsu HJ, Yang JH, Peng CW. GAP31 from an ancient medicinal plant exhibits anti-viral activity
through targeting to Epstein-Barr virus nuclear antigen 1. Antiviral Res. 2019 Apr;164:123-130.
1. Tsai, C.-H., Cheng, C.-P., Peng, C-.W., Lin, B.-Y., Lin, N.-S., and Y.-H. Hsu. 1999. Sufficient length of a poly(A)
tail for the formation of a potential pseudoknot is required for efficient replication of bamboo mosaic potexvirus RNA.
J. Virol. 73, 2703-2709.
2. Peng, C. W., and V. V. *Dolja. 2000. Leader Proteinase of the Beet Yellows closterovirus: Mutational analysis of the
function in genome amplification. J. Virol. 74, 9766-9770.
3. Peng C. W., V. V. Peremyslov, A. R. Mushegian, W. O. Dawson, and V. V. *Dolja. 2001. Functional specialization
and evolution of the leader proteinases in the family closteroviridae. J. Virol 75, 12153-12160.
4. Peng, C. W., V. V. Peremyslov, E. J. Snijder, and V. V. *Dolja. 2002. A competent- chimera of plant and animal viruses.
Virology 294, 75-84 .
5. Cheng, J. H., C.W. Peng, Y. H. Hsu, C. H. Tsai. 2002. The Synthesis of Minus-Strand RNA of Bamboo Mosaic Potexvirus
Initiates from Multiple Sites within the Poly(A) Tail. J. Virol. 76, 6114-6120.
6. Peng, C.W., A.J. Napuli, and V. V. Dolja. 2003. Leader Proteinase of Beet Yellows Virus Functions in Long-Distance
transport. J. Virol 77,2843-2849.
7. Peng , C.W., Y. Xio, B. Zhao, *E. Kieff and S. Harada. 2004. The direct interactions between Epstein-Barr Virus Leader
Nuclear Protein LP and the EBNA2 acidic domain underlie coordinate transcriptional regulation. Proc. Natl. Acad.
Sci. USA 101, 1033-1038.
8. Peng, C.W., Bo Zhao and E. Kieff. 2004. Four EBNA2 domains are important for EBNA LP coactivation with EBNA2.
J Virol. 78(20):11439-42.
9. Peng*, CW., B Zhao HC Chen, ML Chou, , CY Lai, SZ Lin, SY Shu, and E. Kieff*. 2007, Hsp72 up regulates Epstein-Barr
Virus EBNALP co-activation with EBNA2. Blood. 109(12) 5447-5454. (First and corresponding author)
10. Chang YJ, Liu JW, Lin PC, Sun LY, Peng CW, Luo GH, Chen TM, Lee RP, Lin SZ, Harn HJ, and Chiou TW. 2009,
Mesenchymal stem cells facilitate recovery from chemically induced liver damage and decrease liver fibrosis.
Life Sci. 23; 85(13-14):517-25.
11. T-L *Chiu, Su CC, Wang MR, and CW Peng. 2009, AAV2-mediated interleukin-12 in the treatment of malignant brain
tumors through activation of NK cells. International Journal of oncology. Dec;35(6):1361-7.
12. Lin, RH, Peng, CW, Lin, YC, Peng, HL, HC *Huang. 2011, The XopE2 effector protein of Xanthomonas campestris pv.
vesicatoria is involved in virulence and in the suppression of the hypersensitive response. Botanical Studies,
52:55-72.
13. Yu, SH, Yang, PM, Peng, CW, Yu, YC, SJ *Chiu. 2011, Securin depletion sensitizes human colon cancer cells to
fisetin-duced apoptosis. Cancer Letters, 300:96- 104.
14. Bo Zhao, James Zoub, Hongfang Wang, Eric Johannsen, Chih-Wen Peng, John Quackenbush, Jessica C.
Mar, Cynthia Casson Mortond, Matthew L. Freedman, Stephen C. Blacklowd, Jon C. Asterd, Bradley E. Bernsteinc, and
Elliott Kieff. 2011, Epstein-Barr virus exploits intrinsic B-lymphocyte transcription programs to achieve immortal cell
growth. Proc Natl Acad Sci U S A.,108:14902-14907
15. Chiu, TL*, Peng, CW, MJ Wang. 2011, Enhanced anti-glioblastoma activity of microglia by AAV2-mediated IL-12
through TRAIL and phagocytosis in vitro. Oncol Rep., 25:1373-1380.
16. Chen, YL, Tsai, HL, CW *Peng. 2012, EGCG debilitates the persistence of EBV latency by reducing the DNA
binding potency of nuclear antigen 1. Biochemical and Biophysical Research Communications, 417:1093-
1099.
17. Yang, PM, Tseng, HH, Peng, CW, Chen, WS, SJ *Chiu. 2012, Dietary flavonoid fisetin targets caspase-3-deficient
human breast cancer MCF-7 cells by induction of caspase-7- associated apoptosis and inhibition of autophagy.
INTERNATIONAL JOURNAL OF ONCOLOGY, 40:469-478
18. Liu, CD, Chen, YL, Min, YL, Zhao, B, Cheng, CP, Kang, M, Chiu, SJ, Kieff, E, CW *Peng. 2012, The Nuclear Chaperone
Nucleophosmin Escorts an Epstein-Barr Virus Nuclear Antigen to Establish Transcriptional Cascades for Latent
Infection in Human B Cells. PLOS Pathog. 8: e1003084 (1-16).
19. Liu, CD, Cheng, CP, Fang, JS, Chen, LC, CW *Peng. 2013, Modulation of Epstein-Barr Virus Nuclear Antigen
2-Dependent Transcription by Protein Arginine Methyltransferase 5. Biochemical and Biophysical Research
Communications, 430:1097-1102.
20. Yi-Chu Yu, Pei-Ming Yang, Qiu-Yu Chuah, Yao-Huei Huang, Chih-Wen Peng, Yi-Jang Lee, and Shu-Jun Chiu1.
2013. Radiation-induced senescence in securin-deficient cancer cells promotes cell invasion involving
the IL-6/STAT3 and PDGF-BB/PDGFR pathways. Scientific Reports, 3:1675-1685.
21. Ya-Lyn Chen, Cheng-Der Liu, Chi-Ping Cheng, Bo Zhao, Hao-Jen Hsu, Chih-Long Shen, Shu-Jiun Chiu, Elliot Kieff, and
Chih-Wen *Peng. Nucleolin is important for Epstain-Barr Viorus Nuclear Antigen 1 dependent episome binding,
maintenance, transcription. Proc Natl Acad Sci USA. 111(1):243-248
22. Yao-Huei Huang, Pei-Ming Yang, Qiu-Yu Chuah, Yi-Jang Lee, Chih-Wen Peng, and Shu-Jun *Chiu. 2014 Autophage
promotes radiation-induced senescence but inhibits bystander effects in human breast cancer cells. Autophage 10:7,
1-17.
23. Matthew R Harter, Cheng-Der Liu, Chih-Lung Shen, Elsie Gonzalez-Hurtado, Zhi-Min Zhang, Muyu Xu, Ernest Martinez
Chih-Wen *Peng, and Jikui *Song. BS69/ZMYND11 C-Terminal Domains Bind and Inhibit EBNA2. Feb. 06 2016
PLOS Pathog. 12(2):E1005414 ·
24. Chih-Lung Shen, Cheng-Der Liu, Ren-In You,Yung-Hao Ching, Jun Liang, Liangru Ke, Ya-Lin Chen, Hong-Chi Chen,
Hao-Jen Hsu, Je-Wen Liou, Elliott Kieff, and Chih-Wen *Peng. Ribosome Protein L4 is essential for Epstein-Barr Virus
Nuclear Antigen 1 function. 2016 Proc Natl Acad Sci USA. 113(8):2229-2234
25. Tsai MH, Chang CH, Tsai RK, Hong YR, Chuang TH, Fan KT, Peng CW, Wu CY, Hsu WL, Wang LS, Chen LK, Yu HS.
2016 Cross-regulation of Pro-inflammatory Cytokines by Interleukin-10 and MiR-155 in Orientia tsutsugamushi-infected
Human Macrophages Prevents Cytokine Storm. J Invest Dermatol. 2016 Jul;136(7):1398-407Feb 24. (IF=7.216; R/C=
1/63)
26. Wang C, Zhou H, Xue Y, Liang J, Narita Y, Gerdt C, Zheng AY, Jiang R, Trudeau S, Peng CW, Gewurz BE, Zhao B.
Epstein-Barr Virus Nuclear Antigen Leader Protein Coactivates EP300. J Virol. 2018 Apr 13;92(9).
27. Jhang JF, Hsu YH, Peng CW, Jiang YH, Ho HC, Kuo HC. Epstein-Barr Virus Presence As A Potential Etiology of
Persistent Bladder Inflammation in Human Interstitial Cystitis/Bladder Pain Syndrome. J Urol. 2018 Apr 10
28. Shen CL, Huang WH, Hsu HJ, Yang JH, Peng CW. GAP31 from an ancient medicinal plant exhibits anti-viral activity
through targeting to Epstein-Barr virus nuclear antigen 1. Antiviral Res. 2019 Apr;164:123-130.
