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Editor | Epstein-Barr Virus (EBV) is the first human tumor virus discovered (1964).
More than 90% of adults worldwide have been infected with EBV.
B cells are EBV host cells, EBV.
It will be latent in the body's memory B cells for life, and usually does not produce any symptoms
.
However, EBV infection can cause 2% of malignant tumors, including a variety of lymphomas (Hodgkin’s lymphoma, Burkitt’s lymphoma, etc.
) and epithelial cell carcinomas (nasopharyngeal carcinoma and 10% of gastric cancer)
.
Worldwide, approximately 200,000 cancers are caused by EBV infection each year, and 140,000 patients die as a result
.
In different cancer types, EBV expresses different gene products, such as patients with nasopharyngeal carcinoma: EBV expresses EBV-encoded small RNAs (EBERs), EBV-encoded BART microRNAs (BART microRNAs), Epstein-Barr nuclear antigen 1 (EBNA1) ), Latent membrane protein 1 (LMP1), and Latent membrane protein 2 (LMP2).
LMP1 is a key gene for the growth and transformation of viruses.
It is a more researched oncogene and plays an important role in the formation of nasopharyngeal carcinoma
.
However, in Burkitt lymphoma patients: only EBERs, BART microRNAs, and EBNA1 are expressed.
BART microRNAs do not affect the growth and transformation ability of the virus.
The growth and transformation ability of EBNA1 is controversial, and the function of EBERs has not been clearly studied
.
Therefore, what role EBV plays in the formation of Burkitt’s lymphoma remains unclear
.
EBERs are small RNAs encoded by EBV, including EBER1 and EBER2, about 170 bp long, and they can bind to host proteins to form nucleoprotein complexes
.
The growth and transformation ability of EBERs in different EBV virus strains is controversial.
EBERs does not affect the growth and transformation of B95-8 (virus strain isolated from patients with infectious mononucleosis in the United States) and P3HR1 (virus strain isolated from patients with lymphoma) Ability, but affects the growth and transformation ability of Akata (a virus strain isolated from Japanese lymphoma patients)
.
Therefore, it is unclear what role EBERs play in virus growth and transformation ability
.
On October 22, 2021, the Henri-Jacques Delecluse team of the German Cancer Research Center (the first author is Dr.
Li Zhe) published an article The Epstein–Barr virus noncoding RNA EBER2 transactivates the UCHL1 deubiquitinase to accelerate cell growth in the PNAS magazine, revealing EBER2 in EB virus can promote the growth and transformation ability of UCHL1 by activating UCHL1, and reveals the difference of EBER2 requirements of different EBV strains
.
M81 is a virus strain isolated from patients with nasopharyngeal carcinoma in Hong Kong.
The M81 EBER2 knockout strain was obtained through the EBV-BAC recombination system.
EBV can efficiently transform B cells into lymphoid cell lines (LCLs) with immortal proliferation ability in vitro.
It provides a good model for studying the growth and transformation ability of EBV
.
The study found that the growth and transformation ability of the M81 EBER2 knockout strain was significantly reduced, and it was verified in vivo (mouse model)
.
Further mass spectrometry analysis revealed that EBER2 mainly regulates the expression of ubiquitin carboxy-terminal hydrolase-1 (UCHL1) to promote the growth and transformation of the virus
.
Specifically, UCHL1 regulates the expression of Cyclin B1 through deubiquitination, which in turn affects the cell growth cycle
.
More importantly, EBER2 can regulate the expression of UCHL1 in EBV-negative Burkitt lymphoma cell lines, indicating that EBER2 may play an important role in the formation of Burkitt lymphoma
.
How does EBER2 regulate the expression of UCHL1? Previous literature reports: EBER2 can bind to the host protein NONO, NONO can bind to the PU.
1 protein, and the transcription factor PU.
1 can bind to the UCHL1 promoter to initiate UCHL1 transcription and translation
.
Therefore, the author speculates whether EBER2 can bind to PU.
1 and affect the ability of PU.
1 to bind to the UCHL1 promoter? This hypothesis was verified by RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) experiments: EBER2 can indirectly bind PU.
1 protein and promote PU.
1 to bind to the UCHL1 promoter, thereby regulating UCHL1 transcription and translation
.
Bioinformatics analysis also found that a piece of UCHL1 mRNA can perfectly hybridize with EBER2 sequence
.
Through the analysis of EBER2 and UCHL1 mRNA mutations, it was found that the expression of UCHL1 was significantly reduced, indicating that RNA-RNA interaction would affect the expression of UCHL1
.
EBER2 Northern blot experiment also confirmed that EBER2 can hybridize with UCHL1 mRNA
.
The study found that B95-8 and P3HR1 do not need EBER, but M81 and Akata need EBER to promote growth and transformation, suggesting that there may be other viral genes that affect the expression of UCHL1
.
In order to find the gene of the virus, the authors constructed a series of exchange mutants.
The gene from B95-8 was exchanged into the M81 genome, and the gene from M81 was exchanged into the B95-8 genome
.
Theoretically, if the gene is important for the phenotype of B95-8 or M81, the phenotype of the exchange strain will disappear or weaken
.
The author found that LMP1 is another key gene that affects the expression of UCHL1.
Due to the polymorphism of the LMP1 gene, the ability of B95-8 LMP1 to induce the expression of UCHL1 is significantly stronger than that of M81 LMP1
.
Interestingly, the B95-8 LMP1 and P3HR1 LMP1 gene sequences are exactly the same, and the M81 LMP1 and Akata LMP1 sequences are exactly the same, which explains why B95-8 and P3HR1 do not require EBER, but M81 and Akata require EBER to promote cells.
Growth transformation
.
The Henri-Jacques Delecluse team (the first author is Dr.
Li Zhe) reported in Nature Microbiology in September 2019 that non-coding RNA in the Epstein-Barr virus can induce the production of the virus by inducing an inflammatory response
.
This is another important work of the team in non-coding RNA: EBER2 can promote the growth and transformation of the virus by activating UCHL1, and reveals why some virus strains need EBER2, and some virus strains do not need EBER2, and clarify different EBV Virus strains can use different strategies to transform B cells, and it has been proved at the molecular level that EBER2 may promote the formation of Burkitt’s lymphoma.
This series of work has enriched everyone’s understanding of EBV non-coding RNA
.
Original link: https:// Plate maker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author has all legal rights, and offenders must be investigated
.
More than 90% of adults worldwide have been infected with EBV.
B cells are EBV host cells, EBV.
It will be latent in the body's memory B cells for life, and usually does not produce any symptoms
.
However, EBV infection can cause 2% of malignant tumors, including a variety of lymphomas (Hodgkin’s lymphoma, Burkitt’s lymphoma, etc.
) and epithelial cell carcinomas (nasopharyngeal carcinoma and 10% of gastric cancer)
.
Worldwide, approximately 200,000 cancers are caused by EBV infection each year, and 140,000 patients die as a result
.
In different cancer types, EBV expresses different gene products, such as patients with nasopharyngeal carcinoma: EBV expresses EBV-encoded small RNAs (EBERs), EBV-encoded BART microRNAs (BART microRNAs), Epstein-Barr nuclear antigen 1 (EBNA1) ), Latent membrane protein 1 (LMP1), and Latent membrane protein 2 (LMP2).
LMP1 is a key gene for the growth and transformation of viruses.
It is a more researched oncogene and plays an important role in the formation of nasopharyngeal carcinoma
.
However, in Burkitt lymphoma patients: only EBERs, BART microRNAs, and EBNA1 are expressed.
BART microRNAs do not affect the growth and transformation ability of the virus.
The growth and transformation ability of EBNA1 is controversial, and the function of EBERs has not been clearly studied
.
Therefore, what role EBV plays in the formation of Burkitt’s lymphoma remains unclear
.
EBERs are small RNAs encoded by EBV, including EBER1 and EBER2, about 170 bp long, and they can bind to host proteins to form nucleoprotein complexes
.
The growth and transformation ability of EBERs in different EBV virus strains is controversial.
EBERs does not affect the growth and transformation of B95-8 (virus strain isolated from patients with infectious mononucleosis in the United States) and P3HR1 (virus strain isolated from patients with lymphoma) Ability, but affects the growth and transformation ability of Akata (a virus strain isolated from Japanese lymphoma patients)
.
Therefore, it is unclear what role EBERs play in virus growth and transformation ability
.
On October 22, 2021, the Henri-Jacques Delecluse team of the German Cancer Research Center (the first author is Dr.
Li Zhe) published an article The Epstein–Barr virus noncoding RNA EBER2 transactivates the UCHL1 deubiquitinase to accelerate cell growth in the PNAS magazine, revealing EBER2 in EB virus can promote the growth and transformation ability of UCHL1 by activating UCHL1, and reveals the difference of EBER2 requirements of different EBV strains
.
M81 is a virus strain isolated from patients with nasopharyngeal carcinoma in Hong Kong.
The M81 EBER2 knockout strain was obtained through the EBV-BAC recombination system.
EBV can efficiently transform B cells into lymphoid cell lines (LCLs) with immortal proliferation ability in vitro.
It provides a good model for studying the growth and transformation ability of EBV
.
The study found that the growth and transformation ability of the M81 EBER2 knockout strain was significantly reduced, and it was verified in vivo (mouse model)
.
Further mass spectrometry analysis revealed that EBER2 mainly regulates the expression of ubiquitin carboxy-terminal hydrolase-1 (UCHL1) to promote the growth and transformation of the virus
.
Specifically, UCHL1 regulates the expression of Cyclin B1 through deubiquitination, which in turn affects the cell growth cycle
.
More importantly, EBER2 can regulate the expression of UCHL1 in EBV-negative Burkitt lymphoma cell lines, indicating that EBER2 may play an important role in the formation of Burkitt lymphoma
.
How does EBER2 regulate the expression of UCHL1? Previous literature reports: EBER2 can bind to the host protein NONO, NONO can bind to the PU.
1 protein, and the transcription factor PU.
1 can bind to the UCHL1 promoter to initiate UCHL1 transcription and translation
.
Therefore, the author speculates whether EBER2 can bind to PU.
1 and affect the ability of PU.
1 to bind to the UCHL1 promoter? This hypothesis was verified by RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) experiments: EBER2 can indirectly bind PU.
1 protein and promote PU.
1 to bind to the UCHL1 promoter, thereby regulating UCHL1 transcription and translation
.
Bioinformatics analysis also found that a piece of UCHL1 mRNA can perfectly hybridize with EBER2 sequence
.
Through the analysis of EBER2 and UCHL1 mRNA mutations, it was found that the expression of UCHL1 was significantly reduced, indicating that RNA-RNA interaction would affect the expression of UCHL1
.
EBER2 Northern blot experiment also confirmed that EBER2 can hybridize with UCHL1 mRNA
.
The study found that B95-8 and P3HR1 do not need EBER, but M81 and Akata need EBER to promote growth and transformation, suggesting that there may be other viral genes that affect the expression of UCHL1
.
In order to find the gene of the virus, the authors constructed a series of exchange mutants.
The gene from B95-8 was exchanged into the M81 genome, and the gene from M81 was exchanged into the B95-8 genome
.
Theoretically, if the gene is important for the phenotype of B95-8 or M81, the phenotype of the exchange strain will disappear or weaken
.
The author found that LMP1 is another key gene that affects the expression of UCHL1.
Due to the polymorphism of the LMP1 gene, the ability of B95-8 LMP1 to induce the expression of UCHL1 is significantly stronger than that of M81 LMP1
.
Interestingly, the B95-8 LMP1 and P3HR1 LMP1 gene sequences are exactly the same, and the M81 LMP1 and Akata LMP1 sequences are exactly the same, which explains why B95-8 and P3HR1 do not require EBER, but M81 and Akata require EBER to promote cells.
Growth transformation
.
The Henri-Jacques Delecluse team (the first author is Dr.
Li Zhe) reported in Nature Microbiology in September 2019 that non-coding RNA in the Epstein-Barr virus can induce the production of the virus by inducing an inflammatory response
.
This is another important work of the team in non-coding RNA: EBER2 can promote the growth and transformation of the virus by activating UCHL1, and reveals why some virus strains need EBER2, and some virus strains do not need EBER2, and clarify different EBV Virus strains can use different strategies to transform B cells, and it has been proved at the molecular level that EBER2 may promote the formation of Burkitt’s lymphoma.
This series of work has enriched everyone’s understanding of EBV non-coding RNA
.
Original link: https:// Plate maker: Notes for reprinting on the 11th [Non-original article] The copyright of this article belongs to the author of the article.
Personal forwarding and sharing are welcome.
Reprinting is prohibited without permission.
The author has all legal rights, and offenders must be investigated
.
