The Gα12/13 family of heterotrimeric G proteins and the small GTPase RhoA link the Kaposi sarcoma-associated herpes virus G protein-coupled receptor to heme oxygenase-1 expression and tumorigenesis

Heme oxygenase-1 (HO-1), an inducible enzyme that metabolizes the heme group, is highly expressed in human Kaposi sarcoma lesions. Its expression is up-regulated by the G protein-coupled receptor from the Kaposi sarcoma-associated herpes virus (vGPCR). Although recent evidence shows that HO-1 contri...

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Detalles Bibliográficos
Autores: Martín, M.J., Tanos, T., García, A.B., Martin, D., Gutkind, J.S., Coso, O.A., Marinissen, M.J.
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2007
País:Argentina
Institución:Universidad Nacional de Buenos Aires. Facultad de Ciencias Exactas y Naturales
Repositorio:Biblioteca Digital (UBA-FCEN)
Idioma:inglés
OAI Identifier:paperaa:paper_00219258_v282_n47_p34510_Martin
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_00219258_v282_n47_p34510_Martin
Access Level:acceso abierto
Palabra clave:Kaposi sarcoma lesions
Oncogenic activity
Tumor growth
Tumorigenesis
Cells
Enzyme activity
Gene expression
RNA
Tumors
Proteins
G protein coupled receptor
guanine nucleotide binding protein
guanine nucleotide binding protein alpha12
guanine nucleotide binding protein alpha13
guanosine triphosphatase
heme oxygenase 1
heme oxygenase inhibitor
heterotrimeric guanine nucleotide binding protein
protoporphyrin
RhoA guanine nucleotide binding protein
short hairpin RNA
unclassified drug
vasculotropin A
chemokine receptor
G protein coupled receptor, Human herpesvirus 8
G protein-coupled receptor, Human herpesvirus 8
guanine nucleotide binding protein alpha subunit
photosensitizing agent
RHOA protein, human
VEGFA protein, human
allograft
animal cell
animal experiment
animal model
article
carcinogenesis
cell proliferation
cell strain 3T3
cell survival
controlled study
enzyme activity
human
human cell
Human herpesvirus 8
Kaposi sarcoma
mouse
nonhuman
nude mouse
priority journal
protein expression
protein function
tumor growth
animal
drug antagonism
drug effect
drug screening
gene expression regulation
genetics
metabolism
promoter region
secretion
virus cell transformation
Herpesviridae
Murinae
Mus
Mus musculus
Animals
Cell Transformation, Viral
Gene Expression Regulation, Neoplastic
GTP-Binding Protein alpha Subunits, Gq-G11
Heme Oxygenase-1
Herpesvirus 8, Human
Humans
Mice
Mice, Nude
NIH 3T3 Cells
Photosensitizing Agents
Promoter Regions (Genetics)
Protoporphyrins
Receptors, Chemokine
rhoA GTP-Binding Protein
Vascular Endothelial Growth Factor A
Xenograft Model Antitumor Assays
Descripción
Sumario:Heme oxygenase-1 (HO-1), an inducible enzyme that metabolizes the heme group, is highly expressed in human Kaposi sarcoma lesions. Its expression is up-regulated by the G protein-coupled receptor from the Kaposi sarcoma-associated herpes virus (vGPCR). Although recent evidence shows that HO-1 contributes to vGPCR-induced tumorigenesis and vascular endothelial growth factor (VEGF) expression, the molecular steps that link vGPCR to HO-1 remain unknown. Here we show that vGPCR induces HO-1 expression and transformation through the Gα12/13 family of heterotrimeric G proteins and the small GTPase RhoA. Targeted small hairpin RNA knockdown expression of Gα12, Gα13, or RhoA and inhibition of RhoA activity impair vGPCR-induced transformation and ho-1 promoter activity. Knockdown expression of RhoA also reduces vGPCR-induced VEFG-A secretion and blocks tumor growth in a murine allograft tumor model. NIH-3T3 cells expressing constitutively activated Gα13 or RhoA implanted in nude mice develop tumors displaying spindle-shaped cells that express HO-1 and VEGF-A, similarly to vGPCR-derived tumors. RhoAQL-induced tumor growth is reduced 80% by small hairpin RNA-mediated knockdown expression of HO-1 in the implanted cells. Likewise, inhibition of HO-1 activity by chronic administration of the HO-1 inhibitor tin protoporphyrin IX to mice reduces RhoAQL-induced tumor growth by 70%. Our study shows that vGPCR induces HO-1 expression through the Gα12/13/RhoA axes and shows for the first time a potential role for HO-1 as a therapeutic target in tumors where RhoA has oncogenic activity.