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

37 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).

Keywords

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

UN SDGs

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

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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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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).

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

Abstract

Bibliographical note

Keywords

UN SDGs

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