CRAM-A indicates IFN-gamma-associated inflammatory response in breast cancer


SARMADI P., Tunali G. , Esendagli-Yilmaz G., YILMAZ K. B. , ESENDAĞLI G.

MOLECULAR IMMUNOLOGY, cilt.68, sa.2, ss.692-698, 2015 (SCI İndekslerine Giren Dergi) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 68 Konu: 2
  • Basım Tarihi: 2015
  • Doi Numarası: 10.1016/j.molimm.2015.10.019
  • Dergi Adı: MOLECULAR IMMUNOLOGY
  • Sayfa Sayıları: ss.692-698

Özet

Atypical chemokine receptors (ACKRs) function as endpoint regulators of chemokine gradients. These non-signaling receptors that are transiently expressed under inflammatory conditions have critical roles in the control or maintenance of immune responses. Alternatively, here, CCRL2 (ACKR5) expression was determined to be constitutive in breast cancer cells. Increased amount of CCRL2 was also found in breast tumor tissues with high immune infiltration. Its expression was upregulated in the presence of pro-inflammatory cytokines, IL-1 beta, TNF-alpha, IL-6, and especially IFN-gamma. Moreover, an alternative transcript of CCRL2 gene, CRAM-A, was specifically expressed in a transient fashion under the influence of IFN-gamma. CRAM-A expression was also positively correlated with the presence of IFN-gamma mRNA in patient samples. CCRL2-associated chemotactic molecules, chemerin, CCL19 and CCL5, were also detected in cancer tissues and CCL5 mRNA level was correlated with that of CRAM-A and IFN-gamma. Hence, in breast cancer, CRAM-A becomes specifically upregulated under inflammatory stimuli and may serve as a potential marker of immune response. (C) 2015 Elsevier Ltd. All rights reserved.