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JCR 2016
جستجوی مقالات
سه شنبه 25 آذر 1404
Iranian Biomedical Journal
، جلد ۲۷، شماره ۱، صفحات ۳۴-۴۵
عنوان فارسی
چکیده فارسی مقاله
کلیدواژههای فارسی مقاله
عنوان انگلیسی
A New Insight Into p53-Inhibiting Genes in Epstein–Barr Virus-Associated Gastric Adenocarcinoma
چکیده انگلیسی مقاله
Background:
The
p53
mutation is uncommon in
Epstein–Barr virus
-linked gastric carcinoma, but its suppression occurs through mechanisms such as
ubiquitin specific peptidase 7 (
USP7) inhibitions via
Epstein–Barr virus nuclear antigen-1 (
EBNA1) activity. This study aimed to evaluate the effect of EBNA1 on
p53
-inhibiting gene expression and the impact of USP7 inhibition on
p53
suppression.
Methods:
MKN-45 cells were transfected with the
EBNA1
plasmid. A stable EBNA1 expression cell line was developed through selection based on hygromycin B resistance.
Murine double minute (
MDM)4
,
MDM2
,
sirtuin
(
SIRT)3
,
histone deacetylase (
HDAC)1
,
proteasome 26S subunit, Non-ATPase (
PSMD)10
,
USP7
, and
p53
expression were checked using real-time PCR. Also, cells containing EBNA1 or control plasmid were treated with GNE-6776, and the expression of the interested genes and cell survival were assessed.
Results:
MDM4
,
MDM2
, and
PSMD10
were significantly upregulated in the MKN-45 cell line following
EBNA1
transfection. Morphological changes were observed in the cells harboring
EBNA1
after 20 days. In the control cells, USP7 inhibition significantly upregulated the
HDAC1
,
PSMD10
,
MDM4
, and
MDM2
genes after 24 h, but downregulated these genes after four days. In the
EBNA1
-harboring cells,
MDM2
,
MDM4
, and
PSMD10
genes were significantly upregulated after 24 h, and this effect was sustained for all genes except for
MDM4
, even after four days. Furthermore, USP7 inhibition induced apoptosis in both cell groups.
Conclusion:
EBNA1 enhances the expression of p53-inhibiting genes. Two events—p53 protein overexpression and apoptosis activation—followed the suppression of the USP7 protein and provided evidence for its possible function. The significance of the EBNA1-USP7 interaction in p53 suppression warrants additional investigation and possibly reconsideration.
کلیدواژههای انگلیسی مقاله
Herpesvirus 4, Tumor suppressor protein p53, USP7 protein
نویسندگان مقاله
| Seyed Mohammad Ali Hashemi
Department of Microbiology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran
| Abdolvahab Moradi
Department of Microbiology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran
| Seyed Younes Hosseini
Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
| Hadi Razavi Nikoo
Department of Microbiology, School of Medicine, Golestan University of Medical Sciences, Gorgan, Iran
| Taravat Bamdad
Department of Virology, School of Medical Sciences, Tarbiat Modarres University, Tehran, Iran
| Zahra Faghih
Shiraz Institute for Cancer Research, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
| Jamal Sarvari*
Department of Bacteriology and Virology, School of Medicine, Shiraz University of Medical Sciences, Shiraz, Iran
| Alijan Tabarraei
Infectious Diseases Research Center, Golestan University of Medical Sciences, Gorgan, Iran
نشانی اینترنتی
http://ibj.pasteur.ac.ir/browse.php?a_code=A-10-5038-1&slc_lang=en&sid=1
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کد مقاله (doi)
زبان مقاله منتشر شده
en
موضوعات مقاله منتشر شده
Cancer Biology
نوع مقاله منتشر شده
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