Effect of aldosterone on the amplification of oncolytic vaccinia virus in human cancer lines
JX-594 is an oncolytic virus derived from the Wyeth vaccinia strain that causes replication-dependent cytolysis and antitumor immunity. Starting with a cross-examination of clinical-trial samples from advanced hepatocellular carcinoma patients having high levels of aldosterone and virus amplificatio...
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| Published in | Clinical and molecular hepatology Vol. 17; no. 3; pp. 213 - 219 |
|---|---|
| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Korea (South)
Korean Association for the Study of the Liver
01.09.2011
The Korean Association for the Study of the Liver 대한간학회 |
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| Online Access | Get full text |
| ISSN | 1738-222X 2287-2728 2093-8047 2093-8047 2287-285X |
| DOI | 10.3350/kjhep.2011.17.3.213 |
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| Abstract | JX-594 is an oncolytic virus derived from the Wyeth vaccinia strain that causes replication-dependent cytolysis and antitumor immunity. Starting with a cross-examination of clinical-trial samples from advanced hepatocellular carcinoma patients having high levels of aldosterone and virus amplification in JX-594 treatment, we investigated the association between virus amplification and aldosterone in human cancer cell lines.
Cell proliferation was determined by a cell-counting-kit-based colorimetric assay, and vaccinia virus quantitation was performed by quantitative polymerase chain reaction (qPCR) and a viral plaque assay. Also, the intracellular pH was measured using a pH-sensitive dye.
Simultaneous treatment with JX-594 and aldosterone significantly increased viral replication in A2780, PC-3, and HepG2 cell lines, but not in U2OS cell lines. Furthermore, the aldosterone treatment time altered the JX-594 replication according to the cell line. The JX-594 replication peaked after 48 and 24 hours of treatment in PC-3 and HepG2 cells, respectively. qPCR showed that JX-594 entry across the plasma membrane was increased, however, the changes are not significant by the treatment. This was inhibited by treatment with spironolactone (an aldosterone-receptor inhibitor). JX-594 entry was significantly decreased by treatment with EIPA [5-(N-ethyl-N-isopropyl)amiloride; a Na(+)/H(+)-exchange inhibitor], but aldosterone significantly restored JX-594 entry even in the presence of EIPA. Intracellular alkalization was observed after aldosterone treatment but was acidified by EIPA treatment.
Aldosterone stimulates JX-594 amplification via increased virus entry by affecting the H(+) gradient. |
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| AbstractList | JX-594 is an oncolytic virus derived from the Wyeth vaccinia strain that causes replication-dependent cytolysis and antitumor immunity. Starting with a cross-examination of clinical-trial samples from advanced hepatocellular carcinoma patients having high levels of aldosterone and virus amplification in JX-594 treatment, we investigated the association between virus amplification and aldosterone in human cancer cell lines.
Cell proliferation was determined by a cell-counting-kit-based colorimetric assay, and vaccinia virus quantitation was performed by quantitative polymerase chain reaction (qPCR) and a viral plaque assay. Also, the intracellular pH was measured using a pH-sensitive dye.
Simultaneous treatment with JX-594 and aldosterone significantly increased viral replication in A2780, PC-3, and HepG2 cell lines, but not in U2OS cell lines. Furthermore, the aldosterone treatment time altered the JX-594 replication according to the cell line. The JX-594 replication peaked after 48 and 24 hours of treatment in PC-3 and HepG2 cells, respectively. qPCR showed that JX-594 entry across the plasma membrane was increased, however, the changes are not significant by the treatment. This was inhibited by treatment with spironolactone (an aldosterone-receptor inhibitor). JX-594 entry was significantly decreased by treatment with EIPA [5-(N-ethyl-N-isopropyl)amiloride; a Na(+)/H(+)-exchange inhibitor], but aldosterone significantly restored JX-594 entry even in the presence of EIPA. Intracellular alkalization was observed after aldosterone treatment but was acidified by EIPA treatment.
Aldosterone stimulates JX-594 amplification via increased virus entry by affecting the H(+) gradient. Background/AimsJX-594 is an oncolytic virus derived from the Wyeth vaccinia strain that causes replication-dependent cytolysis and antitumor immunity. Starting with a cross-examination of clinical-trial samples from advanced hepatocellular carcinoma patients having high levels of aldosterone and virus amplification in JX-594 treatment, we investigated the association between virus amplification and aldosterone in human cancer cell lines.MethodsCell proliferation was determined by a cell-counting-kit-based colorimetric assay, and vaccinia virus quantitation was performed by quantitative polymerase chain reaction (qPCR) and a viral plaque assay. Also, the intracellular pH was measured using a pH-sensitive dye.ResultsSimultaneous treatment with JX-594 and aldosterone significantly increased viral replication in A2780, PC-3, and HepG2 cell lines, but not in U2OS cell lines. Furthermore, the aldosterone treatment time altered the JX-594 replication according to the cell line. The JX-594 replication peaked after 48 and 24 hours of treatment in PC-3 and HepG2 cells, respectively. qPCR showed that JX-594 entry across the plasma membrane was increased, however, the changes are not significant by the treatment. This was inhibited by treatment with spironolactone (an aldosterone-receptor inhibitor). JX-594 entry was significantly decreased by treatment with EIPA [5-(N-ethyl-N-isopropyl)amiloride; a Na+/H+-exchange inhibitor], but aldosterone significantly restored JX-594 entry even in the presence of EIPA. Intracellular alkalization was observed after aldosterone treatment but was acidified by EIPA treatment.ConclusionsAldosterone stimulates JX-594 amplification via increased virus entry by affecting the H+ gradient. Background/Aims: JX-594 is an oncolytic virus derived from the Wyeth vaccinia strain that causes replication-dependent cytolysis and antitumor immunity. Starting with a cross-examination of clinical-trial samples from advanced hepatocellular carcinoma patients having high levels of aldosterone and virus amplification in JX-594 treatment, we investigated the association between virus amplification and aldosterone in human cancer cell lines. Methods: Cell proliferation was determined by a cell-counting-kit-based colorimetric assay, and vaccinia virus quantitation was performed by quantitative polymerase chain reaction (qPCR) and a viral plaque assay. Also, the intracellular pH was measured using a pH-sensitive dye. Results: Simultaneous treatment with JX-594 and aldosterone significantly increased viral replication in A2780, PC-3, and HepG2 cell lines, but not in U2OS cell lines. Furthermore, the aldosterone treatment time altered the JX-594 replication according to the cell line. The JX-594replication peaked after 48 and 24 hours of treatment in PC-3 and HepG2 cells, respectively. qPCR showed that JX-594 entry across the plasma membrane was increased, however, the changes are not significant by the treatment. This was inhibited by treatment with spironolactone (an aldosterone-receptor inhibitor). JX-594 entry was significantly decreased by treatment with EIPA [5-(N-ethyl-N-isopropyl)amiloride; a Na^+/H^+-exchange inhibitor], but aldosterone significantly restored JX-594 entry even in the presence of EIPA. Intracellular alkalization was observed after aldosterone treatment but was acidified by EIPA treatment. Conclusions: Aldosterone stimulates JX-594 amplification via increased virus entry by affecting the H^ gradient. KCI Citation Count: 0 JX-594 is an oncolytic virus derived from the Wyeth vaccinia strain that causes replication-dependent cytolysis and antitumor immunity. Starting with a cross-examination of clinical-trial samples from advanced hepatocellular carcinoma patients having high levels of aldosterone and virus amplification in JX-594 treatment, we investigated the association between virus amplification and aldosterone in human cancer cell lines.BACKGROUND/AIMSJX-594 is an oncolytic virus derived from the Wyeth vaccinia strain that causes replication-dependent cytolysis and antitumor immunity. Starting with a cross-examination of clinical-trial samples from advanced hepatocellular carcinoma patients having high levels of aldosterone and virus amplification in JX-594 treatment, we investigated the association between virus amplification and aldosterone in human cancer cell lines.Cell proliferation was determined by a cell-counting-kit-based colorimetric assay, and vaccinia virus quantitation was performed by quantitative polymerase chain reaction (qPCR) and a viral plaque assay. Also, the intracellular pH was measured using a pH-sensitive dye.METHODSCell proliferation was determined by a cell-counting-kit-based colorimetric assay, and vaccinia virus quantitation was performed by quantitative polymerase chain reaction (qPCR) and a viral plaque assay. Also, the intracellular pH was measured using a pH-sensitive dye.Simultaneous treatment with JX-594 and aldosterone significantly increased viral replication in A2780, PC-3, and HepG2 cell lines, but not in U2OS cell lines. Furthermore, the aldosterone treatment time altered the JX-594 replication according to the cell line. The JX-594 replication peaked after 48 and 24 hours of treatment in PC-3 and HepG2 cells, respectively. qPCR showed that JX-594 entry across the plasma membrane was increased, however, the changes are not significant by the treatment. This was inhibited by treatment with spironolactone (an aldosterone-receptor inhibitor). JX-594 entry was significantly decreased by treatment with EIPA [5-(N-ethyl-N-isopropyl)amiloride; a Na(+)/H(+)-exchange inhibitor], but aldosterone significantly restored JX-594 entry even in the presence of EIPA. Intracellular alkalization was observed after aldosterone treatment but was acidified by EIPA treatment.RESULTSSimultaneous treatment with JX-594 and aldosterone significantly increased viral replication in A2780, PC-3, and HepG2 cell lines, but not in U2OS cell lines. Furthermore, the aldosterone treatment time altered the JX-594 replication according to the cell line. The JX-594 replication peaked after 48 and 24 hours of treatment in PC-3 and HepG2 cells, respectively. qPCR showed that JX-594 entry across the plasma membrane was increased, however, the changes are not significant by the treatment. This was inhibited by treatment with spironolactone (an aldosterone-receptor inhibitor). JX-594 entry was significantly decreased by treatment with EIPA [5-(N-ethyl-N-isopropyl)amiloride; a Na(+)/H(+)-exchange inhibitor], but aldosterone significantly restored JX-594 entry even in the presence of EIPA. Intracellular alkalization was observed after aldosterone treatment but was acidified by EIPA treatment.Aldosterone stimulates JX-594 amplification via increased virus entry by affecting the H(+) gradient.CONCLUSIONSAldosterone stimulates JX-594 amplification via increased virus entry by affecting the H(+) gradient. |
| Author | Lee, Yu Kyoung Cho, Euna Kim, Jeong Eun Kim, Mi Kyung Lee, Hyun Ju Cho, Mong Gui, Shao Ran Rho, Jasung Lee, Yeon Sook Hwang, Tae-Ho |
| AuthorAffiliation | 3 Department of Gastroenterology, Pusan National University College of Medicine, Busan, Korea 2 Department of Pharmacology, Pusan National University School of Medicine, Busan, Korea 1 Department of Pharmacology, Pusan National University School of Korean Medicine, Busan, Korea 4 Research Center for Hepatic and Biliary Cancer Center, Pusan National University Yangsan Hospital, Pusan National University College of Medicine, Yangsan, Korea |
| AuthorAffiliation_xml | – name: 1 Department of Pharmacology, Pusan National University School of Korean Medicine, Busan, Korea – name: 4 Research Center for Hepatic and Biliary Cancer Center, Pusan National University Yangsan Hospital, Pusan National University College of Medicine, Yangsan, Korea – name: 3 Department of Gastroenterology, Pusan National University College of Medicine, Busan, Korea – name: 2 Department of Pharmacology, Pusan National University School of Medicine, Busan, Korea |
| Author_xml | – sequence: 1 givenname: Hyun Ju surname: Lee fullname: Lee, Hyun Ju organization: Department of Pharmacology, Pusan National University School of Korean Medicine, Busan, Korea – sequence: 2 givenname: Jasung surname: Rho fullname: Rho, Jasung organization: Department of Pharmacology, Pusan National University School of Korean Medicine, Busan, Korea – sequence: 3 givenname: Shao Ran surname: Gui fullname: Gui, Shao Ran organization: Department of Pharmacology, Pusan National University School of Medicine, Busan, Korea – sequence: 4 givenname: Mi Kyung surname: Kim fullname: Kim, Mi Kyung organization: Department of Pharmacology, Pusan National University School of Medicine, Busan, Korea – sequence: 5 givenname: Yu Kyoung surname: Lee fullname: Lee, Yu Kyoung organization: Department of Pharmacology, Pusan National University School of Medicine, Busan, Korea – sequence: 6 givenname: Yeon Sook surname: Lee fullname: Lee, Yeon Sook organization: Department of Pharmacology, Pusan National University School of Medicine, Busan, Korea – sequence: 7 givenname: Jeong Eun surname: Kim fullname: Kim, Jeong Eun organization: Department of Pharmacology, Pusan National University School of Korean Medicine, Busan, Korea – sequence: 8 givenname: Euna surname: Cho fullname: Cho, Euna organization: Department of Pharmacology, Pusan National University School of Medicine, Busan, Korea – sequence: 9 givenname: Mong surname: Cho fullname: Cho, Mong organization: Department of Gastroenterology, Pusan National University College of Medicine, Busan, Korea – sequence: 10 givenname: Tae-Ho surname: Hwang fullname: Hwang, Tae-Ho organization: Department of Pharmacology, Pusan National University School of Korean Medicine, Busan, Korea., Research Center for Hepatic and Biliary Cancer Center, Pusan National University Yangsan Hospital, Pusan National University College of Medicine, Yangsan, Korea |
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| Snippet | JX-594 is an oncolytic virus derived from the Wyeth vaccinia strain that causes replication-dependent cytolysis and antitumor immunity. Starting with a... Background/AimsJX-594 is an oncolytic virus derived from the Wyeth vaccinia strain that causes replication-dependent cytolysis and antitumor immunity. Starting... Background/Aims: JX-594 is an oncolytic virus derived from the Wyeth vaccinia strain that causes replication-dependent cytolysis and antitumor immunity.... |
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| SubjectTerms | Adrenal glands Aldosterone - pharmacology Amiloride - analogs & derivatives Amiloride - pharmacology Animals Ascites Cancer Carcinoma, Hepatocellular - blood Carcinoma, Hepatocellular - virology Cell Line, Tumor Edema Gene expression Hormones Humans Hydrocortisone - blood Hydrogen-Ion Concentration Infections Liver Neoplasms - blood Liver Neoplasms - virology Mineralocorticoid Receptor Antagonists - pharmacology Neuroprotective Agents - pharmacology Oncolytic Virotherapy Original Patients Rabbits Signal transduction Spironolactone - pharmacology Vaccinia virus - drug effects Vaccinia virus - genetics Vaccinia virus - metabolism Vaccinia virus - physiology Virus Replication - drug effects Viruses 내과학 |
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| Title | Effect of aldosterone on the amplification of oncolytic vaccinia virus in human cancer lines |
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