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Functional Impacts of Signal Integration: Regulation of Inflammation-Related Transcription Factors by Heterotrimeric G Proteins

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From Molecular to Modular Tumor Therapy

Part of the book series: The Tumor Microenvironment ((TTME,volume 3))

Abstract

Oncogenic mutations of G proteins and G protein-coupled receptors (GPCRs) have been identified in various endocrine tumors for almost 20 years. Chronic inflammation contributes to tumorigenesis by the induction of cytokine and chemokine production and leukocyte infiltration. Many inflammatory mediators and chemoattractants elicit their effects by stimulating specific GPCRs. The subsequent activation of various G proteins often results in the modulation of transcription factors via complex signaling networks. Human herpesviruses can even resort to hijacking such control by making their own constitutive GPCRs that eventually lead to the development of Kaposi’s sarcoma. Increasing evidence indicates that inflammation-related transcription factors such as STAT3 and NFκB are common effectors of converging streams of G protein signals, which further signifies the importance of G protein-mediated regulations of inflammatory actions and tumorigenesis. This chapter aims to review the regulations of transcription factors mediated by G proteins and the biological relevance of cross-communications between different signaling cascades.

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Abbreviations

A1R, A2AR, A2BR, A3R:

Types 1, 2A, 2B and 3 adenosine receptors

Akt:

Protein kinase B

AP-1:

Activator protein-1

AT1R:

Type 1 angiotension II receptor

ATF-2:

Activating transcription factor-2

ASMC:

Airway smooth muscle cells

Bax:

Bcl-2-associated X protein

Bcl-2:

B-cell CLL/lymphoma 2

bFGF:

Basic fibroblast growth factor

BK1R, BK2R:

Types 1 and 2 bradykinin receptors

BLT1, BLT2 :

Types 1 and 2 leukotriene B4 receptors

C5a:

Complement 5a

cAMP:

Cyclic AMP

CaM:

Calmodulin

CaMKII:

Calmodulin kinase II

CBP:

CREB-binding protein

CCR:

CC chemokine receptor

C/EBPδ:

CCAAT/enhancer binding protein δ

CHO:

Chinese hamster ovary cells

COX-2:

Cyclooxygenase-2

CREB:

Cyclic AMP-responsive element binding protein

c-Src:

Cellular-sarcoma

CXCR:

CXC chemokine receptor

DAG:

Diacylglycerol

Egr-3:

Early growth response-3

EGF:

Epidermal growth factor

EP4:

Prostaglandin E4 receptor

Epac:

Exchange proteins directly activated by cAMP

EPRAP:

EP4 receptor-associated protein

ERK:

Extracellular signal-regulated kinase

fMLP:

N-formyl-methionyl-leucyl-phenylalaine

G-CSF:

Granulocyte colony-stimulating factor

GM-CSF:

Granulocyte/macrophage colony-stimulating factor

G protein:

Heterotrimeric guanine nucleotide binding regulatory protein

GPCR:

G protein-coupled receptor

GRPR:

Gastrin-releasing peptide-preferring receptor

H1R, H2R:

Types 1 and 2 histamine receptors

HCMV:

Human cytomegalovirus

hBD-3:

Human β-defensin-3

HEK293:

Human embryonic kidney 293 cells

HEL:

Human erythroleukemia cells

hIP:

Human prostacyclin receptor

HUVEC:

Human umbilical vein endothelial cells

ICAM-1:

Intercellular cell adhesion molecule-1

IFN-γ:

Interferon-γ

IκB:

Inhibitor of κB

IKK:

Inhibitor of κB kinase

IL:

Interleukin

iNOS:

Inducible nitric oxide synthase

IP3 :

Inositol trisphosphate

Jak:

Janus kinase

JNK:

c-Jun N-terminal kinase

KSHV-GPCR:

Kaposi sarcoma herpesvirus-encoded G protein-coupled receptor

LHSCC:

Laryngeal and hypopharyngeal squamous cell carcinomas

LPA:

Lysophosphatidic acid

LPS:

Lipopolysaccharide

mAKAP:

Muscle A kinase-anchoring protein

MAPK:

Mitogen-activated protein kinase

MCP-1:

Monocyte chemotactic protein-1

M-CSF:

Macrophage-colony stimulating factor

Mcl-1:

Myeloid cell leukemia sequence 1

MEK1/2:

Mitogen-activated protein kinase kinase 1/2

MIP-1α:

Macrophage inflammatory protein-1α

MIP-1β:

Macrophage inflammatory protein-1β

MMP:

Matrix metallopeptidase

NFAT:

Nuclear factor of activated T-cells

NFκB:

Nuclear factor κB

NPC:

Nasopharyngeal carcinoma

p38:

p38 mitogen-activated protein kinase

PAF:

Platelet-activating factor

PAI-1:

Plasminogen activator inhibitor-1

PAR:

Protease-activated receptor

PDK-1:

3′-phosphoinositide-dependent protein kinase-1

PGE2:

Prostanglandin E2

PI3K:

Phosphatidylinositol 3-kinase

PKA:

Protein kinase A

PKC:

Protein kinase C

PIP2:

Phosphatidylinositol bisphosphate

PLC:

Phospholipase C

PPAR:

Peroxisome proliferator-activated receptor

ROS:

Reactive oxygen species

RyR2:

Ryanodine receptor 2

SST2R, SST4R:

Types 2 and 4 somatostatin receptors

STAT:

Signal transducer and activator of transcription

Tac1:

Tachykinin 1

TIMP-1:

Tissue inhibitor of metalloprotease-1

TNF-α:

Tumor necrosis factor-α

TRAIL:

TNF-related apoptosis-inducing ligand

TXA2 :

Thromboxane A2 receptor

Tyk2:

Tyrosine kinase 2

US28:

Viral chemokine receptor US28

VCAM-1:

Vascular cell adhesion molecule-1

VEGF:

Vascular endothelial growth factor

VSMC:

Vascular smooth muscle cells.

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Acknowledgements

Studies by the authors are supported in part by the Hong Kong Jockey Club, Research Grant Council (HKUST 644306, 643306 and 663108) and University Grant Council of Hong Kong (AoE/B-15/01) to YHW.

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  1. Biotechnology Research Institute and Department of Biochemistry, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong, SAR, China

    Wendy Wing Shan Yeung, Maurice Kwok Chung Ho & Yung Hou Wong

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    Albrecht Reichle

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Yeung, W.W.S., Ho, M.K.C., Wong, Y.H. (2010). Functional Impacts of Signal Integration: Regulation of Inflammation-Related Transcription Factors by Heterotrimeric G Proteins. In: Reichle, A. (eds) From Molecular to Modular Tumor Therapy. The Tumor Microenvironment, vol 3. Springer, Dordrecht. https://doi.org/10.1007/978-90-481-9531-2_9

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