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Inflammation and Cancer pp 25–52Cite as

The Role of Inflammation in Colon Cancer

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Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 816))

Abstract

Colorectal cancer (CRC) is the one of the leading causes of cancer-related deaths in the world. CRC is responsible for more than 600,000 deaths annually and incidence rates are increasing in most of the developing countries. Epidemiological and laboratory investigations suggest that environmental factors such as western style dietary habits, tobacco-smoking, and lack of physical activities are considered as risks for CRC. Molecular pathobiology of CRC implicates pro-inflammatory conditions to promote the tumor malignant progression, invasion, and metastasis. It is well known that patients with inflammatory bowel disease are at higher risk of CRC. Many evidences exist reiterating the link between Inflammation and CRC. Inflammation involves interaction between various immune cells, inflammatory cells, chemokines, cytokines, and pro-inflammatory mediators, such as cyclooxygenase (COX) and lipoxygenase (LOX) pathways, which may lead to signaling towards, tumor cell proliferation, growth, and invasion. Thus, this review will focus on mechanisms by which pro-inflammatory mediators and reactive oxygen/nitrogen species play a role in promoting CRC. Based on these mechanisms, various preventive strategies, involving anti-inflammatory agents, such as COX inhibitors, COX-LOX inhibitors, iNOS inhibitors, natural supplements/agents, and synthetic agents, that blocks the inflammatory pathways and suppress CRC are discussed in this review.

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Abbreviations

CRC:

Colorectal cancer

CAC:

Colitis-associated cancer

IBD:

Inflammatory bowel disease

NSAIDs:

Non-steroidal anti-inflammatory drugs

NK:

Natural killer cells

DC:

Dendritic cells

ACF:

Aberrant crypt foci

T reg:

T regulatory cells

5-ASA:

5-aminosalicylic acid

MCP-1:

Monocytes chemo attractant protein 1

PGE2 :

Prostaglandin E2

IL-8:

Interleukin-8

IL-6:

Interleukin-6

IL-10:

Interleukin 10

TNF-α:

Tumor necrosis factor- α

COX-2:

Cyclooxygenase-2

PGI2 :

Prostaglandin I2

PGD2 :

Prostaglandin D2

LT:

Leukotriene

HPETE:

Hydroperoxyeicosatetraenoic acid

EETs:

Epoxy-eicosatrienoic acids

EPA:

Eicosapentaenoic acid

DHA:

Decosahexaenoic acid

PUFAs:

Polyunsaturated fatty acids (PUFAs)

LX:

Lipoxins

RVs:

Resolvins

AOM:

Azoxymethane

NO:

Nitric oxide

NF-κB:

Nuclear factor–κB

MMP:

Matrix metalloproteinase

PI3K:

Phosphatidylinositol 3-kinase

mPGES:

Microsomal prostaglandin E synthase

VEGF:

Vascular endothelial growth factor

FLAP:

Five lox activating protein

DP1:

PGD2 receptor

ROS:

Reactive oxygen species

RNS:

Reactive nitrogen species

NO:

Nitric oxide

iNOS:

Inducible nitric oxide synthase

nNOS:

Neuronal nitric oxide synthase

eNOS:

Endothelial nitric oxide synthase

APC:

Adenomatous polyposis coli

LPS:

Lipopolysaccharide

IL-1β:

Interleukin-1β

AA:

Arachidonic acid

NO-NSAID:

NO-releasing NSAID

IL-4:

Interleukin 4

COXibs:

COX-2-specific inhibitors

FAP:

Familial adenomatous polyposis

L-NAME:

L-nitro arginine methyl ester

Se-PBIT:

Selenium [S,S’-1,4-phenylenebis(1,2-ethanediyl) bis-isothiourea]

GI:

Gastrointestinal

MIP:

Macrophage inflammatory protein

MCP:

Monocytes chemo attractant protein

ABC:

ATP-binding cassette

DMH:

Dimethyl hydrazine

MDFs:

Mucin depleted foci

DSS:

Dextran sulfate sodium

EPA-FFA:

Eicosapentaenoic acid-free fatty acid

ONA:

Oleanolic acid

OT:

18α-olean-12-ene-3β-23,28-triol

18R-RvE1:

5,12,18R-trihydroxy-EPA

LXA4 :

lipoxins A4

ABC:

ATP-binding cassette

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Acknowledgements

We want to acknowledge the Grant support NCI-R01-94962; NCI-CN-53300 for the work quoted in this chapter and Dr. Julie Sando for her scientific and language editing of this chapter.

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  1. Center for Cancer Prevention and Drug Development, Department of Medicine, Hematology Oncology Section, PCS Cancer Center, University of Oklahoma Health Sciences Center, Oklahoma City, OK, 73104, USA

    Naveena B. Janakiram & Chinthalapally V. Rao

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  1. Naveena B. Janakiram
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Correspondence to Naveena B. Janakiram or Chinthalapally V. Rao .

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  1. Dept of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA

    Bharat B. Aggarwal

  2. Dept of Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA

    Bokyung Sung

  3. Dep Experimental Therapeutics, The University of Texas M.D. Anderson Cancer Center, Houston, Texas, USA

    Subash Chandra Gupta

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Janakiram, N.B., Rao, C.V. (2014). The Role of Inflammation in Colon Cancer. In: Aggarwal, B., Sung, B., Gupta, S. (eds) Inflammation and Cancer. Advances in Experimental Medicine and Biology, vol 816. Springer, Basel. https://doi.org/10.1007/978-3-0348-0837-8_2

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