NDLI: Andrographolide Inhibits Epstein–Barr Virus Lytic Reactivation in EBV-Positive Cancer Cell Lines through the Modulation of Epigenetic-Related Proteins

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Andrographolide Inhibits Epstein–Barr Virus Lytic Reactivation in EBV-Positive Cancer Cell Lines through the Modulation of Epigenetic-Related Proteins

Content Provider	MDPI
Author	Malat, Praphatson Ekalaksananan, Tipaya Heawchaiyaphum, Chukkris Suebsasana, Supawadee Roytrakul, Sittiruk Yingchutrakul, Yodying Pientong, Chamsai
Copyright Year	2022
Description	Reactivation of Epstein–Barr virus (EBV) is associated with EBV-associated malignancies and is considered to be a benefit target for treatment. Andrographolide is claimed to have antiviral and anti-tumor activities. Therefore, this study aimed to investigate the effect of andrographolide on the inhibition of EBV lytic reactivation in EBV-positive cancer cells. The cytotoxicity of andrographolide was firstly evaluated in EBV-positive cancer cells; P3HR1, AGS-EBV and HONE1-EBV cells, using an MTT assay. Herein, the spontaneous expression of EBV lytic genes; BALF5, BRLF1 and BZLF1, was significantly inhibited in andrographolide-treated cells. Accordingly, andrographolide inhibited the expression of Zta and viral production in sodium butyrate (NaB)-induced EBV lytic reactivation. Additionally, proteomics and bioinformatics analysis revealed the differentially expressed proteins that inhibit EBV lytic reactivation in all treated cell lines were functionally related with the histone modifications and chromatin organization, such as histone H3-K9 modification and histone H3-K27 methylation. Taken together, andrographolide inhibits EBV reactivation in EBV-positive cancer cells by inhibiting EBV lytic genes, probably, through the histone modifications.
Starting Page	4666
e-ISSN	14203049
DOI	10.3390/molecules27144666
Journal	Molecules
Issue Number	14
Volume Number	27
Language	English
Publisher	MDPI
Publisher Date	2022-07-21
Access Restriction	Open
Subject Keyword	Molecules Biochemical Research Andrographolide Epstein–barr Virus Lytic Reactivation Bzlf1 Histone Modifications
Content Type	Text
Resource Type	Article

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