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The Intricacy of ROS in Cancer Therapy Resistance

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  • First Online:
Handbook of Oxidative Stress in Cancer: Mechanistic Aspects

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Abstract

Cancer is one of the notable causes of death universally due to the emergence of therapy resistance despite the evolution of encouraging therapeutic blueprints. Increased levels of reactive oxygen species (ROS) and antioxidant defense systems leading to alteration of the redox balancing are the typical sources for cancer initiation, progression, and therapy resistance. The elevated ROS levels in cancer and therapy-resistant cells are due to the dysfunction of mitochondria and alteration of metabolism in the cancer cells. The oxidative stress induced by ROS has a dichotomous role in the regulation of cancer and therapy resistance; it may augment cancer progression leading to the therapy resistance or may facilitate cancer cell death depending upon the intensity and the extent of exposure of ROS. So, strategies have been employed either to inhibit or to increase ROS along with the manipulation of the antioxidant defense systems for sensitizing and killing the cancer cells. In this chapter, we have discussed the current understanding of the role of ROS in cancer and therapy resistance, and precisely, the sources, activation, and regulation of ROS, the dichotomous role of ROS in cancer progression and inhibition, and the molecular mechanisms involved in the ROS-mediated cancer therapy resistance.

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Abbreviations

3-MA:

3-Methyladenine

8-OG:

8-Oxoguanine

8OHG:

8-Hydroxyguanine

ABC:

ATP-binding cassette

AKR:

Aldo-ketoreductases

Akt:

Protein kinase B

AMPK:

AMP-activated protein kinase

ARE:

Antioxidant responsive element

ARF:

Alternative reading frame

ATM:

Ataxia-telangiectasia mutated

ATP:

Adenosine triphosphate

ATR:

ATM and Rad3-related

BRCA1:

Breast Cancer gene 1

Cdk:

Cyclin-dependent kinase

Chk:

Checkpoint kinase

COX2:

Cyclo-oxygenase 2

CXCL14:

C-X-C motif chemokine 14

Cyt-c:

Cytochrome- c

DDH:

Dihydrodiol dehydrogenase

DDR:

DNA damage response

DNA:

Deoxyribonucleicacid

DNMT1:

DNA methyltransferase 1

dNTP:

Deoxyribonucleotide triphosphate

DSB:

Double-strand break

EMT:

Epithelial to mesenchymal transition

ERK:

Extracellular signal-regulated kinase

ETC:

Electron transport chain

FADH2:

Flavin adenine Dinucleotide

FAK:

Focal adhesion kinase

FAO:

Fatty acid oxidation

FOXO:

Forkhead box transcription factor

G6PD:

Glucose-6-phosphate dehydrogenase

GPX:

Glutathione peroxidase

GR:

Glutathione reductase

GSH:

Reduced Glutathione

GSSG:

Oxidized Glutathione

HIF1α:

Hypoxia-inducible factor 1α

HMGB1:

High-mobility group box 1

I-CAM:

Intercellular adhesion molecule 1

IL:

Interleukin

LC3:

Microtubule-associated protein 1A/1B-light chain 3

LDHA:

Lactate dehydrogenase A

LKB1:

Liver kinase B 1

MAPK:

Mitogen-activated protein kinase

MDR1:

Multidrug resistance 1

MEF:

Mouse embryonic fibroblasts

MIF:

Migration inhibitory factor

MMP:

Matrix metalloproteinases

MNC:

Multinucleated cells

MSH1:

MutS protein homolog 1

NADP:

Nicotinamide adenine dinucleotide phosphate

NADPH:

Nicotinamide adenine dinucleotide phosphate reduced

NF-kB:

Nuclear factor- kB

NRF2:

Nuclear factor erythroid 2-related factor 2

OGG1:

8-Oxoguanine DNA glycosylase 1

PAH:

Polycyclic aromatic hydrocarbon

PDGF:

Platelet-derived growth factor

P-gp:

P-glycoprotein

PI3K:

Phosphoinositide 3-kinase

PINK1:

PTEN-induced kinase 1

PPP:

Pentose phosphate pathway

PRX:

Peroxiredoxins

Rac1:

Ras-related C3 botulinum toxin substrate 1

ROS:

Reactive oxygen species

RUNX3:

Runt-related transcription factor 3

SOD:

Superoxide dismutase

Src:

Proto-oncogene c-Src

TNF:

Tumor necrosis factor

Trx:

Thioredoxins

VDAC:

Voltage-dependent anion-selective channel

VEGF:

Vascular-endothelial growth factor

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Acknowledgment

We would like to acknowledge Department of Science and Technology (DST-INSPIRE-IF130677), University Grants Commission (UGC), Council of Scientific and Industrial Research (CSIR), Indian Council of Medical Research (ICMR), Science and Engineering Research Board (SERB-J C Bose National Fellowship), Ministry of Human Resource and Development (MHRD), Government of India; Indian Institute of Technology Kharagpur, India; and German Academic Exchange Service (DAAD), Germany, for providing financial support.

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Authors and Affiliations

  1. School of Medical Science and Technology, Indian Institute of Technology Kharagpur, Kharagpur, West Bengal, India

    Chandan Kanta Das, Ranabir Majumder, Pritam Roy & Mahitosh Mandal

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  1. Chandan Kanta Das
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  2. Ranabir Majumder
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  3. Pritam Roy
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  4. Mahitosh Mandal
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Corresponding author

Correspondence to Mahitosh Mandal .

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Editors and Affiliations

  1. Department of Biochemistry and Biophysic, University of Kalyani Department of Biochemistry and Biophysic, Kalyani, West Bengal, India

    Sajal Chakraborti

  2. Dept of Veterinary Pathobiology, University of Missouri, College Vet, Columbia, MO, USA

    Bimal K Ray

  3. Saroj Gupta Cancer Centre & Research Ins, Kolkata, India

    Sushanta Roychowdhury

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Das, C.K., Majumder, R., Roy, P., Mandal, M. (2021). The Intricacy of ROS in Cancer Therapy Resistance. 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_125-1

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