EBV encoded miR-BHRF1-1 potentiates viral lytic replication by downregulating host p53 in nasopharyngeal carcinoma

Zijian Li; Xue Chen; Lili Li; Sufang Liu; Lifang Yang; Xiaoqian Ma; Min Tang; Ann M. Bode; Zigang Dong; Lunquan Sun; Ya Cao

doi:10.1016/j.biocel.2011.11.007

EBV encoded miR-BHRF1-1 potentiates viral lytic replication by downregulating host p53 in nasopharyngeal carcinoma

Zijian Li
, Xue Chen
, Lili Li
, Sufang Liu
, Lifang Yang
, Xiaoqian Ma
, Min Tang
, Ann M. Bode
, Zigang Dong
, Lunquan Sun
, Ya Cao

The Hormel Institute

Research output: Contribution to journal › Article › peer-review

42 Scopus citations

Abstract

miRNAs (microRNAs) are a class of non-coding small RNAs. The Epstein-Barr-virus (EBV) encoded miR-BHRF1-1 is barely expressed in most nasopharyngeal carcinoma (NPC) cells with EBV latent infection. Here, we used a strategy of overexpression and inhibition of miR-BHRF1-1 and showed that miR-BHRF1-1 is involved in TPA-induced accumulation of EBV lytic proteins and viral copies in late lytic cycle. The data further suggested that the miR-BHRF1-1-potentiated induction of EBV lytic replication was accompanied by inhibiting p53 expression. Our results demonstrated that the EBV original pathogen miR-BHRF1-1 is involved in the control of EBV late lytic replication by directly targeting the host p53 gene.

Original language	English (US)
Pages (from-to)	275-279
Number of pages	5
Journal	International Journal of Biochemistry and Cell Biology
Volume	44
Issue number	2
DOIs	https://doi.org/10.1016/j.biocel.2011.11.007
State	Published - Feb 2012

Bibliographical note

Funding Information:
This research was supported by the International (Regional) Cooperation and Exchange Projects of National Natural Science Foundation of China (NO: 30640420462), National Natural Science Foundation of China (NO: 30873010), Joint Research Fund for Overseas Chinese Scholars and Scholars in Hong Kong and Macao of National Natural Science Foundation of China (NO: 81028012), Innovative Project of Graduate of Central South University (NO: 2340-77328). National Program on Key Basic Research Project (973 Program) (NO: 2011CB504305). NSFC-NIH Joint Biomedical Program (NO: 81161120410).

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

SDG 3 Good Health and Well-being

Keywords

Epstein-Barr-virus
Host-pathogen interaction
Late lytic replication
miR-BHRF1-1
p53

Publisher link

10.1016/j.biocel.2011.11.007

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title = "EBV encoded miR-BHRF1-1 potentiates viral lytic replication by downregulating host p53 in nasopharyngeal carcinoma",

abstract = "miRNAs (microRNAs) are a class of non-coding small RNAs. The Epstein-Barr-virus (EBV) encoded miR-BHRF1-1 is barely expressed in most nasopharyngeal carcinoma (NPC) cells with EBV latent infection. Here, we used a strategy of overexpression and inhibition of miR-BHRF1-1 and showed that miR-BHRF1-1 is involved in TPA-induced accumulation of EBV lytic proteins and viral copies in late lytic cycle. The data further suggested that the miR-BHRF1-1-potentiated induction of EBV lytic replication was accompanied by inhibiting p53 expression. Our results demonstrated that the EBV original pathogen miR-BHRF1-1 is involved in the control of EBV late lytic replication by directly targeting the host p53 gene.",

keywords = "Epstein-Barr-virus, Host-pathogen interaction, Late lytic replication, miR-BHRF1-1, p53",

author = "Zijian Li and Xue Chen and Lili Li and Sufang Liu and Lifang Yang and Xiaoqian Ma and Min Tang and Bode, \{Ann M.\} and Zigang Dong and Lunquan Sun and Ya Cao",

note = "Funding Information: This research was supported by the International (Regional) Cooperation and Exchange Projects of National Natural Science Foundation of China (NO: 30640420462), National Natural Science Foundation of China (NO: 30873010), Joint Research Fund for Overseas Chinese Scholars and Scholars in Hong Kong and Macao of National Natural Science Foundation of China (NO: 81028012), Innovative Project of Graduate of Central South University (NO: 2340-77328). National Program on Key Basic Research Project (973 Program) (NO: 2011CB504305). NSFC-NIH Joint Biomedical Program (NO: 81161120410).",

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journal = "International Journal of Biochemistry and Cell Biology",

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AU - Li, Zijian

AU - Chen, Xue

AU - Li, Lili

AU - Liu, Sufang

AU - Yang, Lifang

AU - Ma, Xiaoqian

AU - Tang, Min

AU - Bode, Ann M.

AU - Dong, Zigang

AU - Sun, Lunquan

AU - Cao, Ya

N1 - Funding Information: This research was supported by the International (Regional) Cooperation and Exchange Projects of National Natural Science Foundation of China (NO: 30640420462), National Natural Science Foundation of China (NO: 30873010), Joint Research Fund for Overseas Chinese Scholars and Scholars in Hong Kong and Macao of National Natural Science Foundation of China (NO: 81028012), Innovative Project of Graduate of Central South University (NO: 2340-77328). National Program on Key Basic Research Project (973 Program) (NO: 2011CB504305). NSFC-NIH Joint Biomedical Program (NO: 81161120410).

PY - 2012/2

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N2 - miRNAs (microRNAs) are a class of non-coding small RNAs. The Epstein-Barr-virus (EBV) encoded miR-BHRF1-1 is barely expressed in most nasopharyngeal carcinoma (NPC) cells with EBV latent infection. Here, we used a strategy of overexpression and inhibition of miR-BHRF1-1 and showed that miR-BHRF1-1 is involved in TPA-induced accumulation of EBV lytic proteins and viral copies in late lytic cycle. The data further suggested that the miR-BHRF1-1-potentiated induction of EBV lytic replication was accompanied by inhibiting p53 expression. Our results demonstrated that the EBV original pathogen miR-BHRF1-1 is involved in the control of EBV late lytic replication by directly targeting the host p53 gene.

AB - miRNAs (microRNAs) are a class of non-coding small RNAs. The Epstein-Barr-virus (EBV) encoded miR-BHRF1-1 is barely expressed in most nasopharyngeal carcinoma (NPC) cells with EBV latent infection. Here, we used a strategy of overexpression and inhibition of miR-BHRF1-1 and showed that miR-BHRF1-1 is involved in TPA-induced accumulation of EBV lytic proteins and viral copies in late lytic cycle. The data further suggested that the miR-BHRF1-1-potentiated induction of EBV lytic replication was accompanied by inhibiting p53 expression. Our results demonstrated that the EBV original pathogen miR-BHRF1-1 is involved in the control of EBV late lytic replication by directly targeting the host p53 gene.

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KW - Host-pathogen interaction

KW - Late lytic replication

KW - miR-BHRF1-1

KW - p53

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EBV encoded miR-BHRF1-1 potentiates viral lytic replication by downregulating host p53 in nasopharyngeal carcinoma

Abstract

Bibliographical note

UN SDGs

Keywords

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