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Molecular Cross-Talk Between Nuclear Receptors and Nuclear Factor-κB

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From Molecular to Modular Tumor Therapy

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

Abstract

Nuclear receptors can function as ligand-activated transcription factors but can even so cross-talk with other transcription factors. In this respect, NF-κB, a central regulator of both inflammation and tumorigenesis, can cross-react with and is negatively affected by these nuclear receptors. In current medicine, the nuclear receptor ligands for the glucocorticoid receptor form still the mainstay for treatment of inflammation-based afflictions. However, also other nuclear receptor ligands can affect inflammatory processes. In this respect, the cross-talk of various nuclear receptors with each other has been given renewed attention in recent literature. We will discuss the cross-talk of nuclear receptors with NF-κB and each other in the context of the attenuating control of inflammatory and tumor-promoting mechanisms, using the well described glucocorticoid receptor as a focal point.

Abbreviated title: NR:NF-κB cross-talk

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Abbreviations

AF:

Activation function

AMPK:

AMP-activated protein kinase

AP-1:

Activator protein-1

APOC3:

Apolipoprotein C-III

ARE:

Adenylate-uridylate (AU)-rich element

ATF:

Activating transcription factor

Bcl:

B-cell lymphoma

Brg:

Brahma-related gene

Brm:

Brahma

C:

Carboxy

cAMP:

Cyclic adenosine monophosphate

CAR:

Constitutive androstane receptor (NR1I3)

C/EBP:

CCAAT enhancer-binding protein

CBP:

CREB-binding protein

CC10:

Clara cell secretory 10 kDa protein

cdc37:

Cell division cycle 37 protein

Cdk:

Cyclin-dependent kinase

c-FLIP:

Cellular-FLICE inhibitory protein

ChIP:

Chromatin immunoprecipitation

CK2:

Casein kinase 2

COUP-TFII:

Chicken ovalbumin upstream promoter-transcription factor II (NR2F2)

COX-2:

Cyclo-oxygenase-2

CREB:

cAMP-responsive element-binding protein

CRM1:

Chromosome region maintenance, synonym: exportin1

Cyp3a4:

Cytochrome P450, subfamily IIIA, polypeptide 4

DBD:

DNA-binding domain

Dexras1:

DEX-induced Ras1

Dok-1:

Downstream of tyrosine kinase 1

DRIP205:

Vitamin D receptor-interacting protein complex component (MED1)

DUSP:

Dual specificity phosphatase

eNOS:

Endothelial nitric oxide synthetase

EMSA:

Electrophoretic mobility shift assay

ER:

Estrogen receptor (NR3A1, NR3A2)

ERE:

Estrogen response elemnt

ERK:

Extracellular signal-regulated kinase

ERR:

Estrogen-related receptor (NR3B1, NR3B2, NR3B3)

ELKS:

Protein rich in amino acids E, L, K and S

FKBP:

FK506-binding protein

FXR:

Farnesoid X receptor (NR1H4)

GC:

Glucocorticoid

GILZ:

GC-induced leucine zipper

GR:

Glucocorticoid receptor (NR3C1)

GRE:

Glucocorticoid response element

H3:

Histone H3

H4:

Histone H4

HAT:

Histone acetyl transferase

HDAC:

Histone deacetylase

HNF-4:

Hepatocyte nuclear factor-4 (NR2A1, NR2A2)

Hsp:

Heat shock protein

ICAM:

Intercellular adhesion molecule

Ifit1:

Interferon-induced with tetratricopeptide repeats 1

IFN:

Interferon

IκB:

Inhibitor of NF-κB

IKK:

IκB kinase

IL:

Interleukin

iNOS:

Inducible nitric oxide synthetase

IP-10:

Interferon-inducible protein of 10 kDa

IRF:

Interferon regulatory factor

JNK:

c-Jun N-terminal kinase

KO:

Knock-out

LBD:

Ligand-binding domain

LPS:

Lipopolysaccharide

LXR:

Liver X receptor (NR1H2, NR1H3)

MAPK:

Mitogen-activated protein kinase

MEKK:

MKK kinase, synonyms: MKKK, MAPKKK, MAP3K

MHC:

Major histocompatibility complex

MK:

MAPK-activated protein kinase

MKK:

MAPK kinase, synonyms: MEK, MAPKK, MAP2K

MMP:

Matrix metalloproteinase

MMTV:

Mouse mammary tumor virus

MR:

Mineralocorticoid receptor (NR3C2)

MSK:

Mitogen-and stress-activated protein kinase

NCoR:

Nuclear corepressor

NEMO:

NF-κB essential modulator, synonym: IKKγ

NGFIB:

Nerve Growth factor IB (NR4A1)

NF-κB:

Nuclear Factor-κB

NIK:

NF-κB-inducing kinase

nGRE:

negative GRE

NLS:

Nuclear localization signal

NOR1:

Neuron-derived orphan receptor 1 (NR4A3)

NR:

Nuclear receptor

Nurr1:

Nuclear receptor related 1 (NR4A2)

PAI-1:

Plasminogen activator inhibitor type 1

PGC-1:

PPARγ coactivator-1

Pin1:

Protein NIMA(never in mitosis gene a)-interacting

PKA:

Protein kinase A

PKC:

Protein kinase C

PPAR:

Peroxisome proliferator-activated receptor-α (NR1C1, NR1C2, NR1C3)

PR:

Progesterone receptor (NR3C3)

P-TEFb:

Positive transcription elongation factor b

PXR:

Pregnane X receptor (NR1I2)

RA:

Retinoic acid

RANKL:

Receptor activator of NF-κB ligand

RANTES:

Regulated upon activation, normal T-cell expressed and secreted

RIP:

Receptor-interacting protein

Rel-HD:

Rel homology domain

RNA Pol II:

RNA polymerase II

SGK:

Serum and glucocorticoid-inducible kinase

SHP:

Small heterodimer partner (NR0B2)

SLAP:

Src-like adaptor protein

SLPI:

Secretory leukocyte protease inhibitor 1

SMRT:

Silencing mediator for retinoid and thyroid-hormone receptors

SOCS:

Suppressor of cytokine signalling

SP-A:

Surfactant protein A

SRC:

Steroid receptor coactivator

SUMO:

Small ubiquitin-related modifier

SWI/SNF-:

Switching of yeast mating type/sucrose non-fermenting

TA:

Transactivation domain

TAK1:

TGF-activated kinase 1

TAB2/3:

TAK-binding protein

TANK:

TRAF family member-associated NF-κB activator

TBK1:

TANK-binding kinase 1

TLR:

Toll-like receptor

TNF:

Tumor necrosis factor-α

TNF-R:

TNF-receptor

TR:

Thyroid hormone receptor (NR1A1, NR1A2)

TRADD:

TNF-R-associated death domain

TRAF:

TNF-R-associated factor

Trip6:

Thyroid receptor-interacting protein 6

TTP:

Tristetraprolin

VCAM:

Vascular cell adhesion molecule

VDR:

Vitamin D receptor (NR1I1)

ZDF rat:

Zucker diabetic fatty rat

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Acknowledgements

This work was financially supported by grants from Interuniversity Attraction Poles (IAP) 6/18 (to GH), a GOA from Ghent University (to GH). I.M.E. Beck and K. De Bosscher are postdoctoral fellows of the Research Foundation - Flanders (FWO–Vlaanderen).

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  1. Laboratory of Eukaryotic Gene Expression and Signal Transduction (LEGEST), Department of Physiology, Ghent University, K.L. Ledeganckstraat 35, B-9000, Gent, Belgium

    Ilse M. E. Beck, Guy Haegeman & Karolien De Bosscher

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  1. , Department of Hematology and Oncology, University Hospital Regensburg, Franz-Josef-Strauss-Allee 11, Regensburg, 93042, Germany

    Albrecht Reichle

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Beck, I.M.E., Haegeman, G., De Bosscher, K. (2010). Molecular Cross-Talk Between Nuclear Receptors and Nuclear Factor-κB. 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_10

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