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@ARTICLE{Asokan:169931,
      author       = {S. Asokan$^*$ and O. R. Bandapalli$^*$},
      title        = {{CXCL}8 {S}ignaling in the {T}umor {M}icroenvironment.},
      journal      = {Advances in experimental medicine and biology},
      volume       = {1302},
      issn         = {0065-2598},
      address      = {[Heidelberg]},
      publisher    = {Springer},
      reportid     = {DKFZ-2021-01637},
      isbn         = {978-3-030-62657-0 (print)},
      pages        = {25-39},
      year         = {2021},
      note         = {#EA:W071#LA:B062#},
      abstract     = {The tumor microenvironment represents a dynamic and complex
                      cellular network involving intricate communications between
                      the tumor and highly heterogeneous groups of cells,
                      including tumor-supporting immune and inflammatory cells,
                      cancer-associated fibroblasts, endothelial cells,
                      tumor-associated macrophages, adipose cells, and pericytes.
                      Associated with a variety of growth factors, chemokines,
                      cytokines, and other signaling molecules, the interaction
                      between the tumor microenvironment and the tumor cells
                      empowers aggressiveness of tumor by enhancing its
                      survivability. CXCL8 (also known as Interleukin 8), a
                      multifunctional proinflammatory chemokine that was initially
                      classified as a neutrophil chemoattractant, recently has
                      been found to be a key contributor in tumorigenesis. The
                      upregulation of CXCL8 at the tumor invasion front in several
                      human cancers suggests its interplay between the tumor and
                      its microenvironment rendering tumor progression by
                      enhancing angiogenesis, tumor genetic diversity, survival,
                      proliferation, immune escape, metastasis, and multidrug
                      resistance. The autocrine and paracrine modulation of CXCL8
                      via the chemokine receptors CXCR1/2 promotes several
                      intracellular signaling cascades that fosters
                      tumor-associated inflammation, reprogramming,
                      epithelial-mesenchymal transition, and neovascularization.
                      Hence, decrypting the regulatory/signaling cascades of CXCL8
                      and its downstream effects may harbor prognostic clinical
                      prospects of a tumor microenvironment-oriented cancer
                      therapeutics.},
      keywords     = {Endothelial Cells / Humans / Interleukin-8 / Receptors,
                      Interleukin-8A / Receptors, Interleukin-8B / Tumor
                      Microenvironment / Angiogenesis (Other) / Angiogenic switch
                      (Other) / Autocrine signaling (Other) / CXCL8 (Other) /
                      CXCR1/2 (Other) / Cancer (Other) / Chemokines (Other) /
                      Epithelial-mesenchymal transition (Other) / Interleukin-8
                      (Other) / Intracellular signaling cascade (Other) / Invasion
                      front (Other) / Metastasis (Other) / Survival (Other) /
                      Tumor microenvironment (Other) / Tumor-related inflammation
                      (Other) / Interleukin-8 (NLM Chemicals) / Receptors,
                      Interleukin-8A (NLM Chemicals) / Receptors, Interleukin-8B
                      (NLM Chemicals)},
      cin          = {B062 / HD01},
      ddc          = {570},
      cid          = {I:(DE-He78)B062-20160331 / I:(DE-He78)HD01-20160331},
      pnm          = {312 - Funktionelle und strukturelle Genomforschung
                      (POF4-312)},
      pid          = {G:(DE-HGF)POF4-312},
      typ          = {PUB:(DE-HGF)3 / PUB:(DE-HGF)16},
      pubmed       = {pmid:34286439},
      doi          = {10.1007/978-3-030-62658-7_3},
      url          = {https://inrepo02.dkfz.de/record/169931},
}