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Impact and Application of Nutraceuticals on Inflammation-Induced Colorectal Cancer Development

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Molecular Oncology: Underlying Mechanisms and Translational Advancements

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Abstract

Chronic inflammation has been shown to contribute to several diseases including colorectal cancer, which is the third leading death cancer in the world. During the past several decades, scientific research on biology of inflammation-induced colorectal cancer has been raised to become a mainstream of biomedical investigation and pharmaceutical development. Due to the important role played by inflammation in common diseases, attempting to prevent or treat them by suppressing the cellular and chemical mediators is an active area of medical research. Most of the prevailing approaches include steroids, non-steroidal anti-inflammatory drugs and immune selective anti-inflammatory derivatives are fraught with side effects. There is an urgent need for an alternative, effective, and well-tolerated treatment with negative side effects, such as the natural compound therapy. Healthy diet includes low intake of carbohydrates and fats (high percentage of unsaturated fat), high intake of fruits and vegetables, and more physical excises. Moreover, bioactive compounds in food or diet, nutrients, are essential for the prevention of inflammation-induced colorectal cancer from in vitro cells and in vivo animal models, and loss of nutrients can lead to more serious illness. The mediators and signaling pathways of inflammation-induced colorectal cancer have been alleviated by the interaction with bioactive food components, which play a crucial role in the development, treatment or prevention of inflammation-induced colorectal cancer.

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Abbreviations

AOM/DSS:

Azoxymethane/dextran sulfate sodium

AP-1:

Activator protein-1

ARF:

Alternate reading frame

BBR:

Berberine

BFCs:

Bioactive food compounds

CD:

Crohn’s disease

COX-2:

Cyclooxygenase-2

CRC:

Colorectal cancer

CVD:

Cardiovascular diseases

EGCG:

Epigallocatechin gallate

ERK5:

Extracellular signal-regulated kinase-5

ERKs:

Extracellular signal-regulated kinases

GCSF:

Granulocyte stimulating factor

GI:

Gastrointestinal

GLA:

Gamma linolenic acid

IBD:

Inflammatory bowel disease

IFN:

Interferon

IL-:

Interleukin-

JAK/STAT:

Janus kinase/signal transducers and activators of transcription

JNKs:

c-Jun NH2-terminal kinases

LPS:

lipopolysaccharides

MAPK:

Mitogen-activated protein kinases

MCSF:

Macrophage stimulating factors

NFκB:

Nuclear factor kappa B

Nrf-2:

Nuclear erythroid 2-related factor 2

PEITC:

Phenethyl isothiocyanate

PPARs:

Peroxisome proliferator-activated receptors

PYCARD:

PYD and CARD domain containing

ROS:

Reactive oxygen species

SEER:

Surveillance, epidemiology, and end results

SFN:

Sulforaphane

TGF:

Transforming growth factor

TNF:

Tumor necrosis factor

UC:

Ulcerative colitis

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Authors and Affiliations

  1. Department of Health & Nutritional Sciences, South Dakota State University, Brookings, SD, 57007, USA

    Yi Liu

  2. Department of Cancer Biology, Mayo Clinic, Jacksonville, FL, 32224, USA

    Yi Liu

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  1. Yi Liu
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Correspondence to Yi Liu .

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  1. Institute of Biomedical and Genetic Engineering (IBGE), Islamabad, Pakistan

    Ammad Ahmad Farooqi

  2. Institute of Biomedical and Genetic Engineering (IBGE), Islamabad, Pakistan

    Muhammad Ismail

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Liu, Y. (2017). Impact and Application of Nutraceuticals on Inflammation-Induced Colorectal Cancer Development. In: Farooqi, A., Ismail, M. (eds) Molecular Oncology: Underlying Mechanisms and Translational Advancements. Springer, Cham. https://doi.org/10.1007/978-3-319-53082-6_14

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