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TRP Channels, Oxidative Stress, and Cancer

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Handbook of Oxidative Stress in Cancer: Mechanistic Aspects

Abstract

Transient receptor potential (TRP) channels have evolved as trigger for many physiological and pathophysiological conditions including cancer. These are non-selective cation-specific ion channels and are activated by many endogenous and exogenous stimuli including certain chemicals, changes in osmotic condition, and temperature. Until now, studies on TRP channels regarding its role in cancer progression are only handful. Most of the studies in this specific area have been done using either in vitro or in vivo models. Recent development in bioinformatics and big data analysis provided an advanced platform to study tumor biology, target identification, genetic analysis, and anti-cancer drug development. Exploiting this combination of strategies new research is being carried out to link TRP channels, oxidative stress, and cancer pathology. Certain TRP channel family members have been identified to be up- or downregulated and play either tumor enhancer or suppressor functions. TRPM2 and TRPA1 are the two main redox-sensor ion channels that have been relatively well-investigated in relation to cancer and the present chapter highlights the major roles played by these channels in cancer pathophysiology. The chapter briefly discusses certain tumor-specific expression pattern of TRP channels, their biological role under oxidative stress, and possible use of some proof of concepts for developing therapeutic strategies for cancer management.

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Abbreviations

AKT::

Protein kinase B (PKB)

also known as AKT

ATP::

Adenosine triphosphate

bFGF::

Basic fibroblast growth factor

Ca2+::

Calcium

[Ca2+]i::

Intracellular calcium

CADPR::

Cyclic ADP ribose

CaM::

Calmodulin

DAG::

Diacylglycerol

ECM::

Extracellular matrix

ERK::

Extracellular signal-regulated kinase

FOXO3a::

Fork head box transcription factor 3a

GSH::

Glutathione

GSH-Px::

Glutathione peroxidase

H2O2::

Hydrogen peroxide

HIF::

Hypoxia-inducible factor

IC50::

Half maximal inhibitory concentration

ICGC::

International cancer genome consortium

InsP3::

Inositol 1,4,5-triphosphate

IR-injury::

Ischemia-reperfusion injury

JNK::

c-Jun N-terminal kinase

KO::

Knock out

MCL-1::

Myeloid leukemia cell-1

mTOR::

The mammalian target of rapamycin

NAC::

N-acetyl-L-cysteine

NRF2::

Nuclear factor erythroid 2-related factor 2

OCR::

Oxygen consumption rate

PARG::

Poly (ADP-ribose) glycohydrolase

PARP::

Poly (ADP-ribose) polymerase

PDGF::

Platelet-derived growth factor

PI3K::

Phosphoinositide 3-kinase

PLC::

Phospholipase C

PYK2::

Proline-rich tyrosine kinase-2

RAS::

Rat sarcoma; a family of oncogene

SCLC::

Small cell lung carcinoma

SOD::

Superoxide dismutase

TGF::

Transforming growth factor

TRP channels::

Transient receptor potential channels

VEGF::

Vascular endothelial growth factor

VEGFR::

Vascular endothelial growth factor receptor

WT::

Wild type

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Correspondence to Amritlal Mandal .

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© 2021 Springer Nature Singapore Pte Ltd.

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Mandal, A., Varghese, M.V., James, J., Chakraborti, S. (2021). TRP Channels, Oxidative Stress, and Cancer. In: Chakraborti, S., Ray, B.K., Roychowdhury, S. (eds) Handbook of Oxidative Stress in Cancer: Mechanistic Aspects. Springer, Singapore. https://doi.org/10.1007/978-981-15-4501-6_80-1

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  • DOI: https://doi.org/10.1007/978-981-15-4501-6_80-1

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  • Publisher Name: Springer, Singapore

  • Print ISBN: 978-981-15-4501-6

  • Online ISBN: 978-981-15-4501-6

  • eBook Packages: Springer Reference Biomedicine and Life SciencesReference Module Biomedical and Life Sciences

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