Chemokines and chemokine receptors as promoters of prostate cancer growth and progression

Nicole Salazar, Miguel Castellan, Samir S. Shirodkar, Bal L. Lokeshwar

Research output: Contribution to journalArticle

44 Scopus citations

Abstract

Prostate cancer (CaP) is estimated to be first in incidence among cancers, with more than 240,000 new cases in 2012 in the United States. Chemokines and their receptors provide survival, proliferation, and invasion characteristics to CaP cells in both primary sites of cancer and metastatic locations. The emerging data demonstrate that many chemokines and their receptors are involved in the multistep process of CaP, leading to metastasis, and, further, that these factors act cooperatively to enhance other mechanisms of tumor cell survival, growth, and metastasis. Changes of chemokine receptor cohorts may be necessary to activate tumor-promoting signals. Chemokine receptors can activate downstream effectors, such as mitogen-activated protein kinases, by complex mechanisms of ligand-de-pendent activation of cryptic growth factors; guanosine triphosphate-binding, protein-coupled activation of survival kinases; or transactivation of other receptors such as ErbB family members. We describe vanguard research in which more than the classic view of chemokine receptor biology was clarified. Control of chemokines and inhibition of their receptor activation may add critical tools to reduce tumor growth, especially in chemo-hormonal refractory CaP that is both currently incurable and the most aggressive form of the disease, accounting for most of the more than 28,000 annual deaths.

Original languageEnglish (US)
Pages (from-to)77-91
Number of pages15
JournalCritical Reviews in Eukaryotic Gene Expression
Volume23
Issue number1
DOIs
StatePublished - 2013
Externally publishedYes

Keywords

  • Apoptosis
  • Chemokine receptors
  • Chemokines
  • Gene regulation
  • Growth factor receptors
  • Invasion
  • Metastasis
  • Motility
  • Prostate cancer
  • Survival signaling

ASJC Scopus subject areas

  • Molecular Biology
  • Genetics

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