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Microbe-Induced Oxidative Stress in Cancer Development and Efficacy of Probiotics as Therapeutics in Preventing Its Onset and Progression

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Handbook of Oxidative Stress in Cancer: Therapeutic Aspects

Abstract

Within the metaorganisms, cross-communication between commensal organisms and the host is crucial for the maintenance of physiological homeostasis. At times, microbiota becomes accountable for breaching homeostasis by creating a microenvironment favoring uncontrolled cell growth. Chronic infection and inflammation act as inciting factors for reactive oxygen species generation promoting damage to DNA, proteins, and lipids. Oxidative stress activates a variety of transcription factors that in turn control the expression of several inflammatory cytokines and chemokines. Consecutive changes including altered cell growth, genetic instability, and inhibition of apoptosis create a proper carcinogenic milieu. Apart from the complicated side effects associated with prevailing anticancer therapies, their safety, stability, and affordability are in question. At present, significant immunomodulating properties of probiotic bacteria are being considered as a promising tool in cancer treatment. In addition, to boost the innate defense mechanisms of hosts, probiotics can act as antigenotoxic, anticarcinogenic, and antioxidative agents. In this chapter, the role of pathogenic microbes in oxidative stress-induced cancer and the effectiveness of probiotics as a future therapeutic strategy in preventing cancer onset and progression through manipulating intestinal microflora are highlighted.

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Abbreviations

4-HNE:

4-Hydroxynonenal

8-OHdG:

8-Hydroxydeoxyguanosine

8-oxo-dG:

8-Oxo-2′-deoxyguanosine

ADH:

Alcohol dehydrogenase

AID:

Activation-induced cytidine deaminase

AMPK:

Adenosine monophosphate-activated protein kinase

AMPs:

Antimicrobial peptides

APC:

Anaphase promoting complex

APRIL:

A proliferation-inducing ligand

AQP3:

Aquaporin 3

ATP:

Adenosine triphosphate

AvrA:

Avirulence protein A

BAD:

BCL-2-associated death promoter

BAFF:

B cell-activating factor

BAX:

BCL-2 associated X

BCL-2:

B-cell lymphoma 2

BER:

Base excision repair

BFT:

B. fragilis toxin

BLIMP:

B lymphocyte-induced maturation protein 1

cagA:

Cytotoxin-associated gene A

CD:

Crohn’s disease

CDKs:

Cyclin-dependent kinases

CDT:

Cytolethal distending toxin

CIDR:

Succeeding cysteine-rich interdomain region

CLRs:

C-type lectin receptors

CNF1:

Cytotoxic necrotizing factor 1

COX:

Cyclooxygenase

CRC:

Colorectal cancer

CTCL:

Cutaneous T-cell lymphoma

CTL:

Cytotoxic T lymphocytes

CXCL:

C-X-C motif chemokine ligand

CYP:

Cytochrome P450

DC:

Dendritic cell

DDR:

DNA damage responses

DNA:

Deoxyribonucleic acid

DNase I:

Deoxyribonuclease I

DPPH:

2,2-Diphenyl-1-picrylhydrazyl

DSBs:

Double-strand breaks

EBV:

Epstein-Barr virus

ERK:

Extracellular regulated kinase

ETBF:

Enterotoxigenic B. fragilis

Etk/BMX:

Epithelial and endothelial tyrosine kinase/bone marrow X

FOXO3a:

Forkhead box O3a

GEC:

Gingival epithelial cell

GI:

Gastrointestinal

GPRs:

G-protein-coupled receptors

GPX1:

Glutathione peroxidase 1

HCC:

Hepatocellular carcinoma

HDAC:

Histone deacetylase

HIF-1α:

Hypoxia-inducible factor 1α

HNE:

4-Hydroxy-2-nonenal

HRE:

Hypoxia response element

HSP:

Heat shock protein

IARC:

International Agency for Research on Cancer

IBD:

Inflammatory bowel disease

IFN-γ:

Interferon-γ

IgA:

Immunoglobulin A

IL:

Interleukin

JAK1/STAT3:

Janus kinase 1/signal transducer and activator of transcription 3

JNK:

c-Jun N-terminal kinases

LPS:

Lipopolysaccharide

MALT:

Mucosa-associated lymphoid tissue

MDA:

Malondialdehyde

MDSC:

Myeloid-derived suppressor cells

miRNA:

MicroRNA

NDK:

Nucleoside diphosphate kinase

NF-κβ:

Nuclear factor κ light-chain enhancer of activated B cells

NK:

Natural killer

NLRX1:

NOD-like receptor family member X1

NO:

Nitric oxide

NOX:

NADPH oxidase

Nrf2:

Nuclear factor erythroid 2-related factor 2

OSCC:

Oral squamous cell carcinoma

PBMC:

Peripheral blood mononuclear cells

PfEMP1:

P. falciparum erythrocyte membrane protein 1

PGN:

Peptidoglycan

PI3K/Akt:

Phosphatidylinositol 3-kinase/protein kinase B

PKC:

Protein kinase C

pro-MMP-9:

Pro-matrix metalloproteinase-9

PTEN:

Phosphatase and tensin homolog deleted on chromosome 10

RNI:

Reactive nitrogen intermediates

RNS:

Reactive nitrogen species

ROI:

Reactive oxygen intermediate

ROS:

Reactive oxygen species

SabA:

Sialic acid–binding adhesin

SCFA:

Short-chain fatty acid

SE:

Staphylococcal enterotoxin

Sir2:

Silent information regulator 2

SMO:

Spermine oxidase

SNP:

Single-nucleotide polymorphism

SOD2:

Superoxide dismutase 2

T4SS:

Type IV secretion systems

TER:

Transepithelial resistance

TGF-β:

Tumor growth factor β

TLR:

Toll-like receptor

TNF-α:

Tumor necrosis factor α

UC:

Ulcerative colitis

VacA:

Vacuolating cytotoxin A

WHO:

World Health Organization

Wnt:

Wingless-related integration site

ZO:

Zonula occludens

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Acknowledgments

The financial assistance from DAE-BRNS, Government of India (Project No. 37 (1)/20/15/2014-BRNS), and CSIR, Government of India (Project No. 27(0322)/17/EMR-II) is thankfully acknowledged.

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Correspondence to Somasri Dam .

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Biswas, P., Pal, S., Das, M., Dam, S. (2022). Microbe-Induced Oxidative Stress in Cancer Development and Efficacy of Probiotics as Therapeutics in Preventing Its Onset and Progression. In: Chakraborti, S. (eds) Handbook of Oxidative Stress in Cancer: Therapeutic Aspects. Springer, Singapore. https://doi.org/10.1007/978-981-16-1247-3_159-1

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  • DOI: https://doi.org/10.1007/978-981-16-1247-3_159-1

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  • Publisher Name: Springer, Singapore

  • Print ISBN: 978-981-16-1247-3

  • Online ISBN: 978-981-16-1247-3

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

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