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Mol. Cells 2011; 32(2): 173-179

Published online May 27, 2011

https://doi.org/10.1007/s10059-011-0066-y

© The Korean Society for Molecular and Cellular Biology

Association between Epstein-Barr Virus Infection and Chemoresistance to Docetaxel in Gastric Carcinoma

Hee Jong Shin, Do Nyun Kim, and Suk Kyeong Lee*

Research Institute of Immunobiology, Department of Medical Lifescience, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea

Correspondence to : *Correspondence: sukklee@catholic.ac.kr

Received: April 8, 2011; Revised: May 20, 2011; Accepted: May 23, 2011

Abstract

Epstein-Barr virus (EBV) is associated with human can-cers such as nasopharyngeal carcinoma, Burkitt’s lym-phoma, Hodgkin’s disease, and gastric carcinoma (GC). EBV is associated with about 10% of all GC cases globally. EBV-associated GC has distinct features from EBV-ne-gative GC. However, it is still unclear if EBV infection has any effect on GC chemoresistance. Cell proliferation assay, cell cycle analysis, and active caspase Western blot revealed that the EBV-positive GC cell line (AGS-EBV) showed chemoresistance to docetaxel compared to the EBV-negative GC cell line (AGS). Docetaxel treatment increased expression of Bax similarly in AGS and AGS-EBV cell lines. However, Bcl-2 induction was markedly higher in AGS-EBV cells, after docetaxel treatment. Although docetaxel increased the expression of p53 to a similar extent in both cell lines, induction of p21 in AGS-EBV cells was lower than in AGS cells. Furthermore, expression of survivin was higher in AGS-EBV cells than in AGS cells following docetaxel treatment as well as at basal state. EBV-lytic gene expression was induced by docetaxel treatment in AGS-EBV cells. The results suggest that EBV infection and lytic induction confers chemoresistance to GC, possibly by regulating cellular and EBV latent and lytic gene expression.

Keywords apoptosis, cell cycle related genes, chemoresistance, docetaxel, EBV-positive gastric carcinoma

Article

Research Article

Mol. Cells 2011; 32(2): 173-179

Published online August 31, 2011 https://doi.org/10.1007/s10059-011-0066-y

Copyright © The Korean Society for Molecular and Cellular Biology.

Association between Epstein-Barr Virus Infection and Chemoresistance to Docetaxel in Gastric Carcinoma

Hee Jong Shin, Do Nyun Kim, and Suk Kyeong Lee*

Research Institute of Immunobiology, Department of Medical Lifescience, College of Medicine, The Catholic University of Korea, Seoul 137-701, Korea

Correspondence to:*Correspondence: sukklee@catholic.ac.kr

Received: April 8, 2011; Revised: May 20, 2011; Accepted: May 23, 2011

Abstract

Epstein-Barr virus (EBV) is associated with human can-cers such as nasopharyngeal carcinoma, Burkitt’s lym-phoma, Hodgkin’s disease, and gastric carcinoma (GC). EBV is associated with about 10% of all GC cases globally. EBV-associated GC has distinct features from EBV-ne-gative GC. However, it is still unclear if EBV infection has any effect on GC chemoresistance. Cell proliferation assay, cell cycle analysis, and active caspase Western blot revealed that the EBV-positive GC cell line (AGS-EBV) showed chemoresistance to docetaxel compared to the EBV-negative GC cell line (AGS). Docetaxel treatment increased expression of Bax similarly in AGS and AGS-EBV cell lines. However, Bcl-2 induction was markedly higher in AGS-EBV cells, after docetaxel treatment. Although docetaxel increased the expression of p53 to a similar extent in both cell lines, induction of p21 in AGS-EBV cells was lower than in AGS cells. Furthermore, expression of survivin was higher in AGS-EBV cells than in AGS cells following docetaxel treatment as well as at basal state. EBV-lytic gene expression was induced by docetaxel treatment in AGS-EBV cells. The results suggest that EBV infection and lytic induction confers chemoresistance to GC, possibly by regulating cellular and EBV latent and lytic gene expression.

Keywords: apoptosis, cell cycle related genes, chemoresistance, docetaxel, EBV-positive gastric carcinoma

Mol. Cells
Sep 30, 2023 Vol.46 No.9, pp. 527~572
COVER PICTURE
Chronic obstructive pulmonary disease (COPD) is marked by airspace enlargement (emphysema) and small airway fibrosis, leading to airflow obstruction and eventual respiratory failure. Shown is a microphotograph of hematoxylin and eosin (H&E)-stained histological sections of the enlarged alveoli as an indicator of emphysema. Piao et al. (pp. 558-572) demonstrate that recombinant human hyaluronan and proteoglycan link protein 1 (rhHAPLN1) significantly reduces the extended airspaces of the emphysematous alveoli by increasing the levels of TGF-β receptor I and SIRT1/6, as a previously unrecognized mechanism in human alveolar epithelial cells, and consequently mitigates COPD.

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