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Article: A case report on a large, peduncular intra-abdominal hepatocellular carcinoma extending into the retroperitoneum.

Omer, Dana M / Dozier, Jordan / Cao, Zongxian / Zhu, Hongfa / McCain, Donald A

2021 Volume 9, Issue 3, Page(s) 1288–1291

Abstract: Here, we discuss a relatively uncommon presentation of a hepatocellular carcinoma and discuss its preoperative planning and surgical intervention required to reach complete resection. ...

Abstract	Here, we discuss a relatively uncommon presentation of a hepatocellular carcinoma and discuss its preoperative planning and surgical intervention required to reach complete resection.
Language	English
Publishing date	2021-01-08
Publishing country	England
Document type	Case Reports
ZDB-ID	2740234-4
ISSN	2050-0904
ISSN	2050-0904
DOI	10.1002/ccr3.3751
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Article ; Online: Pepcan-12 (RVD-hemopressin) is a CB2 receptor positive allosteric modulator constitutively secreted by adrenals and in liver upon tissue damage.

Petrucci, Vanessa / Chicca, Andrea / Glasmacher, Sandra / Paloczi, Janos / Cao, Zongxian / Pacher, Pal / Gertsch, Jürg

Scientific reports

2017 Volume 7, Issue 1, Page(s) 9560

Abstract: Pepcan-12 (RVD-hemopressin; RVDPVNFKLLSH) is the major peptide of a family of endogenous peptide endocannabinoids (pepcans) shown to act as negative allosteric modulators (NAM) of cannabinoid CB1 receptors. Noradrenergic neurons have been identified to ... ...

Abstract	Pepcan-12 (RVD-hemopressin; RVDPVNFKLLSH) is the major peptide of a family of endogenous peptide endocannabinoids (pepcans) shown to act as negative allosteric modulators (NAM) of cannabinoid CB1 receptors. Noradrenergic neurons have been identified to be a specific site of pepcan production. However, it remains unknown whether pepcans occur in the periphery and interact with peripheral CB2 cannabinoid receptors. Here, it is shown that pepcan-12 acts as a potent (K
MeSH term(s)	Adrenal Glands/injuries ; Adrenal Glands/metabolism ; Allosteric Regulation ; Chromatography, Liquid ; Hemoglobins/chemistry ; Hemoglobins/metabolism ; Liver/injuries ; Liver/metabolism ; Metabolome ; Metabolomics/methods ; Peptide Fragments/chemistry ; Peptide Fragments/metabolism ; Protein Binding ; Receptor, Cannabinoid, CB2/chemistry ; Receptor, Cannabinoid, CB2/metabolism ; Reperfusion Injury/etiology ; Reperfusion Injury/metabolism ; Reperfusion Injury/pathology ; Structure-Activity Relationship ; Tandem Mass Spectrometry
Chemical Substances	Hemoglobins ; Peptide Fragments ; RVD-hemopressin, human ; Receptor, Cannabinoid, CB2
Language	English
Publishing date	2017-08-25
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-09808-8
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Article ; Online: Cannabidiol attenuates alcohol-induced liver steatosis, metabolic dysregulation, inflammation and neutrophil-mediated injury.

Wang, Yuping / Mukhopadhyay, Partha / Cao, Zongxian / Wang, Hua / Feng, Dechun / Haskó, György / Mechoulam, Raphael / Gao, Bin / Pacher, Pal

Scientific reports

2017 Volume 7, Issue 1, Page(s) 12064

Abstract: Cannabidiol (CBD) is a non-psychoactive component of marijuana, which has anti-inflammatory effects. It has also been approved by FDA for various orphan diseases for exploratory trials. Herein, we investigated the effects of CBD on liver injury induced ... ...

Abstract	Cannabidiol (CBD) is a non-psychoactive component of marijuana, which has anti-inflammatory effects. It has also been approved by FDA for various orphan diseases for exploratory trials. Herein, we investigated the effects of CBD on liver injury induced by chronic plus binge alcohol feeding in mice. CBD or vehicle was administered daily throughout the alcohol feeding study. At the conclusion of the feeding protocol, serums samples, livers or isolated neutrophils were utilized for molecular biology, biochemistry and pathology analysis. CBD significantly attenuated the alcohol feeding-induced serum transaminase elevations, hepatic inflammation (mRNA expressions of TNFα, MCP1, IL1β, MIP2 and E-Selectin, and neutrophil accumulation), oxidative/nitrative stress (lipid peroxidation, 3-nitrotyrosine formation, and expression of reactive oxygen species generating enzyme NOX2). CBD treatment also attenuated the respiratory burst of neutrophils isolated from chronic plus binge alcohol fed mice or from human blood, and decreased the alcohol-induced increased liver triglyceride and fat droplet accumulation. Furthermore, CBD improved alcohol-induced hepatic metabolic dysregulation and steatosis by restoring changes in hepatic mRNA or protein expression of ACC-1, FASN, PPARα, MCAD, ADIPOR-1, and mCPT-1. Thus, CBD may have therapeutic potential in the treatment of alcoholic liver diseases associated with inflammation, oxidative stress and steatosis, which deserves exploration in human trials.
MeSH term(s)	Animals ; Cannabidiol/pharmacology ; Cells, Cultured ; Central Nervous System Depressants/pharmacology ; Energy Metabolism/drug effects ; Energy Metabolism/genetics ; Ethanol/pharmacology ; Fatty Liver, Alcoholic/genetics ; Fatty Liver, Alcoholic/metabolism ; Fatty Liver, Alcoholic/prevention & control ; Gene Expression Regulation/drug effects ; Humans ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/prevention & control ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Mice, Inbred C57BL ; Neutrophil Infiltration/drug effects ; Neutrophils/drug effects ; Neutrophils/metabolism ; Oxidative Stress/drug effects
Chemical Substances	Central Nervous System Depressants ; Cannabidiol (19GBJ60SN5) ; Ethanol (3K9958V90M)
Language	English
Publishing date	2017-09-21
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-017-10924-8
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Article ; Online: Electodiagnostic and Advanced Neuro-imaging Characterization for Successful Treatment of a Spinal Extradural Arachnoid Cyst.

Tanaka, Tomoko / Boddepalli, Raja S / Miller, Douglas C / Cao, Zongxian / Sindhwani, Vivek / Coates, Joan R / Govindarajan, Raghav / Litofsky, N Scott

World neurosurgery

2017

Abstract: Background: Spinal extradural arachnoid cysts (SEAC) are relatively uncommon. However, several large cysts have presented with spinal cord compression requiring surgical intervention.: Case description: We report a patient with progressively ... ...

Abstract	Background: Spinal extradural arachnoid cysts (SEAC) are relatively uncommon. However, several large cysts have presented with spinal cord compression requiring surgical intervention. Case description: We report a patient with progressively enlarging SEAC causing worsening right S1 radiculopathy and gastrocnemius muscle atrophy. Electromyography (EMG) and nerve conduction studies (NCS) revealed an S1 motor radiculopathy. Serial magnetic resonance imaging (MRI) findings confirmed enlargement of the small cyst originating from the sacral thecal sac on the right while two smaller cyst on the left remained stable. Dynamic computed tomography (CT) myelogram revealed connection to the thecal sac behind the right S1 nerve root. We performed a right hemilaminectomy from L5 to S2 to expose the cyst pedicle, which was ligated and marsupialized the cyst. After surgery, the patient showed clinical and electrodiagnostic improvement. Conclusion: This case illustrates the principles of timely surgical intervention after advanced diagnostic imaging and electrodiagnostic testing to improve neurological function and minimize complications.
Language	English
Publishing date	2017-10-11
Publishing country	United States
Document type	Journal Article
ZDB-ID	2534351-8
ISSN	1878-8769 ; 1878-8750
ISSN (online)	1878-8769
ISSN	1878-8750
DOI	10.1016/j.wneu.2017.10.003
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Article ; Online: A critical role for IFN regulatory factor 1 in NKT cell-mediated liver injury induced by alpha-galactosylceramide.

Cao, Zongxian / Dhupar, Rajeev / Cai, Changchun / Li, Peiyuan / Billiar, Timothy R / Geller, David A

Journal of immunology (Baltimore, Md. : 1950)

2010 Volume 185, Issue 4, Page(s) 2536–2543

Abstract: NKT cells are remarkably abundant in mouse liver. Compelling experimental evidence has suggested that NKT cells are involved in the pathogenesis of many liver diseases. Activation of NKT cells with alpha-galactosylceramide (alpha-GalCer) causes liver ... ...

Abstract	NKT cells are remarkably abundant in mouse liver. Compelling experimental evidence has suggested that NKT cells are involved in the pathogenesis of many liver diseases. Activation of NKT cells with alpha-galactosylceramide (alpha-GalCer) causes liver injury through mechanisms that are not well understood. We undertook studies to characterize the key pathways involved in alpha-GalCer-induced liver injury. We found that expression of the transcription factor IFN regulatory factor 1 (IRF-1) in mouse liver was dramatically upregulated by alpha-GalCer treatment. Neutralization of either TNF-alpha or IFN-gamma inhibited alpha-GalCer-mediated IRF-1 upregulation. alpha-GalCer-induced liver injury was significantly suppressed in IRF-1 knockout mice or in wild-type C56BL/6 mice that received a microRNA specifically targeting IRF-1. In contrast, overexpression of IRF-1 greatly potentiated alpha-GalCer-induced liver injury. alpha-GalCer injection also induced a marked increase in hepatic inducible NO synthase expression in C56BL/6 mice, but not in IRF-1 knockout mice. Inducible NO synthase knockout mice exhibited significantly reduced liver injury following alpha-GalCer treatment. Finally, we demonstrated that both NKT cells and hepatocytes expressed IRF-1 in response to alpha-GalCer. However, it appeared that the hepatocyte-derived IRF-1 was mainly responsible for alpha-GalCer-induced liver injury, based on the observation that inhibition of IRF-1 by RNA interference did not affect alpha-GalCer-induced NKT cell activation. Our findings revealed a novel mechanism of NKT cell-mediated liver injury in mice, which has implications in the development of human liver diseases.
MeSH term(s)	Animals ; Blotting, Western ; Flow Cytometry ; Galactosylceramides/administration & dosage ; Galactosylceramides/immunology ; Gene Expression/drug effects ; Gene Knockout Techniques ; Hepatocytes/immunology ; Hepatocytes/metabolism ; Interferon Regulatory Factor-1/genetics ; Interferon Regulatory Factor-1/immunology ; Interferon Regulatory Factor-1/physiology ; Interferon-gamma/immunology ; Interferon-gamma/metabolism ; Liver/drug effects ; Liver/immunology ; Liver/metabolism ; Liver Diseases/etiology ; Liver Diseases/immunology ; Liver Diseases/metabolism ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Natural Killer T-Cells/immunology ; Natural Killer T-Cells/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Tumor Necrosis Factor-alpha/immunology ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances	Galactosylceramides ; Interferon Regulatory Factor-1 ; Tumor Necrosis Factor-alpha ; alpha-galactosylceramide ; Interferon-gamma (82115-62-6) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2010-08-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1000092
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Article: Interferon-gamma induces autophagy with growth inhibition and cell death in human hepatocellular carcinoma (HCC) cells through interferon-regulatory factor-1 (IRF-1)

Li, Peiyuan / Du, Qiang / Cao, Zongxian / Guo, Zhong / Evankovich, John / Yan, Wei / Chang, Ying / Shao, Lifang / Stolz, Donna Beer / Tsung, Allan / Geller, David A

Cancer letters. 2012 Jan. 28, v. 314, no. 2

2012

Abstract: Interferon-gamma (IFN-γ) is a pleiotropic cytokine with immunomodulatory, anti-viral, and anti-proliferative effects. In this study, we examined the effects of IFN-γ on autophagy and cell growth in human hepatocellular carcinoma (HCC) cells. IFN-γ ... ...

Abstract	Interferon-gamma (IFN-γ) is a pleiotropic cytokine with immunomodulatory, anti-viral, and anti-proliferative effects. In this study, we examined the effects of IFN-γ on autophagy and cell growth in human hepatocellular carcinoma (HCC) cells. IFN-γ inhibited cell growth of Huh7 cells with non-apoptotic cell death. IFN-γ induced autophagosome formation and conversion/turnover of microtubule associated protein 1 light chain 3 (LC3) protein. Furthermore, overexpression of IRF-1 also induced autophagy in Huh7 cells. Silencing IRF-1 expression with target small hairpin RNA blocked autophagy induced by IFN-γ. Silencing of the autophagy signals Beclin-1 or Atg5 attenuated the inhibitory effect of IFN-γ on Huh7 cells with decreased cell death. Additionally, IFN-γ activated autophagy in freshly cultured human HCC cells. Together, these findings show that IFN-γ induces autophagy through IRF-1 signaling pathway and the induction of autophagy contributes to the growth-inhibitory effect of IFN-γ with cell death in human liver cancer cells.
Keywords	RNA ; autophagy ; cell growth ; cytokines ; growth retardation ; hepatoma ; human growth ; humans ; interferon-gamma ; signal transduction
Language	English
Dates of publication	2012-0128
Size	p. 213-222.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2011.09.031
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Cannabidiol Protects against Doxorubicin-Induced Cardiomyopathy by Modulating Mitochondrial Function and Biogenesis.

Hao, Enkui / Mukhopadhyay, Partha / Cao, Zongxian / Erdélyi, Katalin / Holovac, Eileen / Liaudet, Lucas / Lee, Wen-Shin / Haskó, György / Mechoulam, Raphael / Pacher, Pál

Molecular medicine (Cambridge, Mass.)

2015 Volume 21, Page(s) 38–45

Abstract: Doxorubicin (DOX) is a widely used, potent chemotherapeutic agent; however, its clinical application is limited because of its dose-dependent cardiotoxicity. DOX's cardiotoxicity involves increased oxidative/nitrative stress, impaired mitochondrial ... ...

Abstract	Doxorubicin (DOX) is a widely used, potent chemotherapeutic agent; however, its clinical application is limited because of its dose-dependent cardiotoxicity. DOX's cardiotoxicity involves increased oxidative/nitrative stress, impaired mitochondrial function in cardiomyocytes/endothelial cells and cell death. Cannabidiol (CBD) is a nonpsychotropic constituent of marijuana, which is well tolerated in humans, with antioxidant, antiinflammatory and recently discovered antitumor properties. We aimed to explore the effects of CBD in a well-established mouse model of DOX-induced cardiomyopathy. DOX-induced cardiomyopathy was characterized by increased myocardial injury (elevated serum creatine kinase and lactate dehydrogenase levels), myocardial oxidative and nitrative stress (decreased total glutathione content and glutathione peroxidase 1 activity, increased lipid peroxidation, 3-nitrotyrosine formation and expression of inducible nitric oxide synthase mRNA), myocardial cell death (apoptotic and poly[ADP]-ribose polymerase 1 [PARP]-dependent) and cardiac dysfunction (decline in ejection fraction and left ventricular fractional shortening). DOX also impaired myocardial mitochondrial biogenesis (decreased mitochondrial copy number, mRNA expression of peroxisome proliferator-activated receptor γ coactivator 1-alpha, peroxisome proliferator-activated receptor alpha, estrogen-related receptor alpha), reduced mitochondrial function (attenuated complex I and II activities) and decreased myocardial expression of uncoupling protein 2 and 3 and medium-chain acyl-CoA dehydrogenase mRNA. Treatment with CBD markedly improved DOX-induced cardiac dysfunction, oxidative/nitrative stress and cell death. CBD also enhanced the DOX-induced impaired cardiac mitochondrial function and biogenesis. These data suggest that CBD may represent a novel cardioprotective strategy against DOX-induced cardiotoxicity, and the above-described effects on mitochondrial function and biogenesis may contribute to its beneficial properties described in numerous other models of tissue injury.
MeSH term(s)	Animals ; Antibiotics, Antineoplastic/adverse effects ; Cannabidiol/administration & dosage ; Cannabidiol/pharmacology ; Cardiomyopathies/drug therapy ; Cardiomyopathies/etiology ; Cardiomyopathies/metabolism ; Cardiomyopathies/pathology ; Cardiomyopathies/physiopathology ; Cardiotonic Agents/administration & dosage ; Cardiotonic Agents/pharmacology ; Cardiotoxicity ; Cell Death ; Disease Models, Animal ; Doxorubicin/adverse effects ; Enzyme Activation/drug effects ; Hemodynamics ; Male ; Matrix Metalloproteinase 2/metabolism ; Matrix Metalloproteinase 9/metabolism ; Mice ; Mitochondria, Heart/drug effects ; Mitochondria, Heart/metabolism ; Oxidative Stress/drug effects
Chemical Substances	Antibiotics, Antineoplastic ; Cardiotonic Agents ; Cannabidiol (19GBJ60SN5) ; Doxorubicin (80168379AG) ; Matrix Metalloproteinase 2 (EC 3.4.24.24) ; Matrix Metalloproteinase 9 (EC 3.4.24.35)
Language	English
Publishing date	2015-01-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.2119/molmed.2014.00261
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Article ; Online: Mast cells play a critical role in the systemic inflammatory response and end-organ injury resulting from trauma.

Cai, Changchun / Cao, Zongxian / Loughran, Patricia A / Kim, Sodam / Darwiche, Sophie / Korff, Sebastian / Billiar, Timothy R

Journal of the American College of Surgeons

2011 Volume 213, Issue 5, Page(s) 604–615

Abstract: Background: Much of the morbidity after trauma results from excessive activation of the innate immune system. This is manifested as a systemic inflammatory response and associated end-organ damage. Although mast cells are known to be important in many ... ...

Abstract	Background: Much of the morbidity after trauma results from excessive activation of the innate immune system. This is manifested as a systemic inflammatory response and associated end-organ damage. Although mast cells are known to be important in many immune responses, their role in the systemic response to severe trauma is unknown. Study design: C57BL/6J-KitW-sh/BsmJ (mast cell deficient) and wild type mice were subjected to 1.5 hours of hemorrhagic shock plus bilateral femur fracture and soft tissue injury (HS/T), followed by resuscitation at 4.5 hours. Blood withdrawal volumes, mean arterial pressures, circulating cytokine, chemokine, high mobility group box-1 (HMGB-1), double strain DNA (dsDNA), transaminase levels, and histology in liver and lung were compared between groups. Results: Mast cell deficient mice exhibited greater hemodynamic stability than wild type mice. At baseline, the mast cell deficient mice exhibited no difference in any of the organ injury or inflammatory markers measured. As expected, wild type mice subjected to HS/T exhibited end-organ damage manifested by marked increases in circulating alanine transaminase, aspartate aminotransferase, and dsDNA levels, as well as histologic evidence of tissue necrosis. In clear contrast, mast cell deficient mice exhibited almost no tissue damage. Similarly, the magnitude of increased circulating cytokine and chemokine induced by HS/T was much less in the mast cell deficient mice than in the wild type group. Conclusions: Mast cell deficiency resulted in a damped systemic inflammatory response, greatly attenuated multiple organ injury, and more stable hemodynamics in HS/T. So mast cells appear to be a critical component of the initial host response to severe injury.
MeSH term(s)	Alanine Transaminase/blood ; Animals ; Aspartate Aminotransferases/blood ; Biomarkers/blood ; Blood Pressure ; DNA/blood ; Disease Models, Animal ; Femoral Fractures/immunology ; Femoral Fractures/pathology ; Fluorescent Antibody Technique ; HMGB1 Protein/blood ; Interleukin-10/blood ; Interleukin-1beta/blood ; Interleukin-6/blood ; Liver/pathology ; Lung/pathology ; Macrophage Activation ; Mast Cells/immunology ; Mice ; Mice, Inbred C57BL ; Microscopy, Confocal ; Necrosis/immunology ; Shock, Hemorrhagic/immunology ; Shock, Hemorrhagic/pathology ; Soft Tissue Injuries/immunology ; Soft Tissue Injuries/pathology ; Systemic Inflammatory Response Syndrome/immunology ; Tumor Necrosis Factor-alpha/blood
Chemical Substances	Biomarkers ; HMGB1 Protein ; Interleukin-1beta ; Interleukin-6 ; Tumor Necrosis Factor-alpha ; Interleukin-10 (130068-27-8) ; DNA (9007-49-2) ; Aspartate Aminotransferases (EC 2.6.1.1) ; Alanine Transaminase (EC 2.6.1.2)
Language	English
Publishing date	2011-09-14
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	1181115-8
ISSN	1879-1190 ; 1072-7515
ISSN (online)	1879-1190
ISSN	1072-7515
DOI	10.1016/j.jamcollsurg.2011.08.009
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Article: Apigenin inhibits VEGF and HIF-1 expression via PI3K/AKT/p70S6K1 and HDM2/p53 pathways

Fang, Jing / Xia, Chang / Cao, Zongxian / Zheng, Jenny Z / Reed, Eddie / Jiang, Bing-Hua

FASEB journal : 2005 Mar., v. 19, no. 3

2005

Abstract: Apigenin is a nontoxic dietary flavonoid that has been shown to possess anti-tumor properties and therefore poses special interest for the development of a novel chemopreventive and/or chemotherapeutic agent for cancer. Ovarian cancer is one of the most ... ...

Abstract	Apigenin is a nontoxic dietary flavonoid that has been shown to possess anti-tumor properties and therefore poses special interest for the development of a novel chemopreventive and/or chemotherapeutic agent for cancer. Ovarian cancer is one of the most common causes of cancer death among women. Here we demonstrate that apigenin inhibits expression of vascular endothelial growth factor (VEGF) in human ovarian cancer cells. VEGF plays an important role in tumor angiogenesis and growth. We found that apigenin inhibited VEGF expression at the transcriptional level through expression of hypoxia-inducible factor 1[alpha] (HIF-1[alpha]). Apigenin inhibited expression of HIF-1[alpha] and VEGF via the PI3K/AKT/p70S6K1 and HDM2/p53 pathways. Apigenin inhibited tube formation in vitro by endothelial cells. These findings reveal a novel role of apigenin in inhibiting HIF-1 and VEGF expression that is important for tumor angiogenesis and growth, identifying new signaling molecules that mediate this regulation.--Fang, J., Xia, C., Cao, Z., Zheng, J. Z., Reed, E., Jiang, B.-H. Apigenin inhibits VEGF and HIF-1 expression via PI3K/AKT/p70S6K1 and HDM2/p53 pathways.
Language	English
Dates of publication	2005-03
Size	p. 342-353.
Document type	Article
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
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Article: Insulin-like growth factor-I induces cyclooxygenase-2 expression via PI3K, MAPK and PKC signaling pathways in human ovarian cancer cells.

Cao, Zongxian / Liu, Ling-Zhi / Dixon, Dan A / Zheng, Jenny Z / Chandran, Bala / Jiang, Bing-Hua

Cellular signalling

2007 Volume 19, Issue 7, Page(s) 1542–1553

Abstract: Elevated levels of insulin-like growth factor-I (IGF-I) are associated with ovarian carcinogenesis and progression. However, the molecular mechanisms by which IGF-I contributes to ovarian cancer development remain to be elucidated. Cyclooxygenase-2 (COX- ... ...

Abstract	Elevated levels of insulin-like growth factor-I (IGF-I) are associated with ovarian carcinogenesis and progression. However, the molecular mechanisms by which IGF-I contributes to ovarian cancer development remain to be elucidated. Cyclooxygenase-2 (COX-2) is a crucial player in the pathogenesis of human malignancies. Herein we showed that IGF-I efficiently induced COX-2 expression and PGE(2) biosynthesis at physiologically relevant concentrations in human ovarian cancer cells. IGF-I treatment significantly increased COX-2 transcriptional activation. IGF-I also stabilized COX-2 mRNA through the COX-2 3'-untranslated region (3'-UTR), which appeared independent of the conserved AU-rich elements. We next investigated the signaling pathways involved in IGF-I-induced COX-2 expression. We found that PI3K inhibitor wortmannin or LY294002 blocked COX-2 expression induced by IGF-I. Wortmannin treatment or a dominant negative PI3K mutant significantly inhibited IGF-I-induced COX-2 mRNA stabilization, but only slightly decreased COX-2 transcriptional activation. We showed that ERK1/2 and p38 MAPKs were required for IGF-I-induced COX-2 expression and that activation of both pathways by IGF-I increased COX-2 transcriptional activation and its mRNA stability. IGF-I stimulated PKC activation in the cells and pretreatment with PKC inhibitor bisindolylmaleimide prevented IGF-I-induced COX-2 transcriptional activation and mRNA stabilization, and inhibited COX-2 mRNA and protein expression. Taken together, our data demonstrate that IGF-I induces COX-2 expression in human ovarian cancer cells, which is mediated by three parallel signaling cascades--PI3K, MAPK, and PKC pathways that differentially regulate COX-2 expression at transcriptional and post-transcriptional levels.
MeSH term(s)	Cyclooxygenase 2/biosynthesis ; Cyclooxygenase 2/genetics ; Dinoprostone/biosynthesis ; Enzyme Activation/drug effects ; Enzyme Induction/drug effects ; Female ; Gene Expression Regulation, Enzymologic/drug effects ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Insulin-Like Growth Factor I/pharmacology ; MAP Kinase Signaling System/drug effects ; Mitogen-Activated Protein Kinase 1/metabolism ; Mitogen-Activated Protein Kinase 3/metabolism ; Models, Biological ; Ovarian Neoplasms/enzymology ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Phosphatidylinositol 3-Kinases/metabolism ; Protein Kinase C/metabolism ; RNA Stability/drug effects ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Signal Transduction/drug effects ; Transcriptional Activation/drug effects ; Up-Regulation/drug effects ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	RNA, Messenger ; Insulin-Like Growth Factor I (67763-96-6) ; Cyclooxygenase 2 (EC 1.14.99.1) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Protein Kinase C (EC 2.7.11.13) ; Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; Mitogen-Activated Protein Kinase 3 (EC 2.7.11.24) ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2007-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1002702-6
ISSN	0898-6568
ISSN	0898-6568
DOI	10.1016/j.cellsig.2007.01.028
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