Mucins and Toll-like receptors

Kith and kin in infection and cancer

Research output: Contribution to journalShort survey

19 Citations (Scopus)

Abstract

Inflammation is underlying biological phenomenon common in infection and cancer. Mucins are glycoproteins which establish a physical barrier for undesirable entry of foreign materials through epithelial surfaces. A deregulated expression and an anomalous glycosylation pattern of mucins are known in large number of cancers. TLRs are class of receptors which recognize the molecular patterns of invading pathogens and activate complex inflammatory pathways to clear them. Aberrant expression of TLRs is observed in many cancers. A highly orchestrated action of mucins and TLRs is well evolved host defence mechanism; however, a link between the two in other non-infectious conditions has received less attention. Here we present an overview as to how mucins and TLRs give protection to the host and are deregulated during carcinogenesis. Further, we propose the possible mechanisms of cross-regulation between them in pathogenesis of cancer. As both mucins and TLRs are therapeutically important class of molecules, an understanding of the underlying molecular mechanisms connecting the two will open new avenues for the therapeutic targeting of cancer.

Original languageEnglish (US)
Pages (from-to)110-119
Number of pages10
JournalCancer Letters
Volume321
Issue number2
DOIs
StatePublished - Aug 28 2012

Fingerprint

Toll-Like Receptors
Mucins
Infection
Neoplasms
Biological Phenomena
Architectural Accessibility
Glycosylation
Glycoproteins
Carcinogenesis
Inflammation

Keywords

  • Cancer
  • Infection
  • Inflammation
  • Mucins
  • Toll-like receptors

ASJC Scopus subject areas

  • Oncology
  • Cancer Research

Cite this

Mucins and Toll-like receptors : Kith and kin in infection and cancer. / Tarang, Shikha; Kumar, Sushil; Batra, Surinder Kumar.

In: Cancer Letters, Vol. 321, No. 2, 28.08.2012, p. 110-119.

Research output: Contribution to journalShort survey

@article{aa4ecd78d30b47afa00699a886b7d337,
title = "Mucins and Toll-like receptors: Kith and kin in infection and cancer",
abstract = "Inflammation is underlying biological phenomenon common in infection and cancer. Mucins are glycoproteins which establish a physical barrier for undesirable entry of foreign materials through epithelial surfaces. A deregulated expression and an anomalous glycosylation pattern of mucins are known in large number of cancers. TLRs are class of receptors which recognize the molecular patterns of invading pathogens and activate complex inflammatory pathways to clear them. Aberrant expression of TLRs is observed in many cancers. A highly orchestrated action of mucins and TLRs is well evolved host defence mechanism; however, a link between the two in other non-infectious conditions has received less attention. Here we present an overview as to how mucins and TLRs give protection to the host and are deregulated during carcinogenesis. Further, we propose the possible mechanisms of cross-regulation between them in pathogenesis of cancer. As both mucins and TLRs are therapeutically important class of molecules, an understanding of the underlying molecular mechanisms connecting the two will open new avenues for the therapeutic targeting of cancer.",
keywords = "Cancer, Infection, Inflammation, Mucins, Toll-like receptors",
author = "Shikha Tarang and Sushil Kumar and Batra, {Surinder Kumar}",
year = "2012",
month = "8",
day = "28",
doi = "10.1016/j.canlet.2012.01.040",
language = "English (US)",
volume = "321",
pages = "110--119",
journal = "Cancer Letters",
issn = "0304-3835",
publisher = "Elsevier Ireland Ltd",
number = "2",

}

TY - JOUR

T1 - Mucins and Toll-like receptors

T2 - Kith and kin in infection and cancer

AU - Tarang, Shikha

AU - Kumar, Sushil

AU - Batra, Surinder Kumar

PY - 2012/8/28

Y1 - 2012/8/28

N2 - Inflammation is underlying biological phenomenon common in infection and cancer. Mucins are glycoproteins which establish a physical barrier for undesirable entry of foreign materials through epithelial surfaces. A deregulated expression and an anomalous glycosylation pattern of mucins are known in large number of cancers. TLRs are class of receptors which recognize the molecular patterns of invading pathogens and activate complex inflammatory pathways to clear them. Aberrant expression of TLRs is observed in many cancers. A highly orchestrated action of mucins and TLRs is well evolved host defence mechanism; however, a link between the two in other non-infectious conditions has received less attention. Here we present an overview as to how mucins and TLRs give protection to the host and are deregulated during carcinogenesis. Further, we propose the possible mechanisms of cross-regulation between them in pathogenesis of cancer. As both mucins and TLRs are therapeutically important class of molecules, an understanding of the underlying molecular mechanisms connecting the two will open new avenues for the therapeutic targeting of cancer.

AB - Inflammation is underlying biological phenomenon common in infection and cancer. Mucins are glycoproteins which establish a physical barrier for undesirable entry of foreign materials through epithelial surfaces. A deregulated expression and an anomalous glycosylation pattern of mucins are known in large number of cancers. TLRs are class of receptors which recognize the molecular patterns of invading pathogens and activate complex inflammatory pathways to clear them. Aberrant expression of TLRs is observed in many cancers. A highly orchestrated action of mucins and TLRs is well evolved host defence mechanism; however, a link between the two in other non-infectious conditions has received less attention. Here we present an overview as to how mucins and TLRs give protection to the host and are deregulated during carcinogenesis. Further, we propose the possible mechanisms of cross-regulation between them in pathogenesis of cancer. As both mucins and TLRs are therapeutically important class of molecules, an understanding of the underlying molecular mechanisms connecting the two will open new avenues for the therapeutic targeting of cancer.

KW - Cancer

KW - Infection

KW - Inflammation

KW - Mucins

KW - Toll-like receptors

UR - http://www.scopus.com/inward/record.url?scp=84860919269&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84860919269&partnerID=8YFLogxK

U2 - 10.1016/j.canlet.2012.01.040

DO - 10.1016/j.canlet.2012.01.040

M3 - Short survey

VL - 321

SP - 110

EP - 119

JO - Cancer Letters

JF - Cancer Letters

SN - 0304-3835

IS - 2

ER -