Cited by 161Chemokine receptors and signalingConnective Tissue Growth Factor ResearchGalectins and Cancer Biology

The Role of CXCL16 in the Pathogenesis of Cancer and Other Diseases

Open access
Korbecki, Jan, Bajdak-Rusinek, Karolina, Kupnicka, Patrycja, Kapczuk, Patrycja, Simińska, Donata, Chlubek, Dariusz, Baranowska-Bosiacka, Irena·2021·International Journal of Molecular Sciences

Abstract

CXCL16 is a chemotactic cytokine belonging to the α-chemokine subfamily. It plays a significant role in the progression of cancer, as well as the course of atherosclerosis, renal fibrosis, and non-alcoholic fatty liver disease (NAFLD). Since there has been no review paper discussing the importance of this chemokine in various diseases, we have collected all available knowledge about CXCL16 in this review. In the first part of the paper, we discuss background information about CXCL16 and its receptor, CXCR6. Next, we focus on the importance of CXCL16 in a variety of diseases, with an emphasis on cancer. We discuss the role of CXCL16 in tumor cell proliferation, migration, invasion, and metastasis. Next, we describe the role of CXCL16 in the tumor microenvironment, including involvement in angiogenesis, and its significance in tumor-associated cells (cancer associated fibroblasts (CAF), microglia, tumor-associated macrophages (TAM), tumor-associated neutrophils (TAN), mesenchymal stem cells (MSC), myeloid suppressor cells (MDSC), and regulatory T cells (Treg)). Finally, we focus on the antitumor properties of CXCL16, which are mainly caused by natural killer T (NKT) cells. At the end of the article, we summarize the importance of CXCL16 in cancer therapy.

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Crossref · 10.3390/ijms22073490

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  • Upregulation of SOS1, SOS2 and RTKs (ERBB2 and ERBB3), as well as CXCL16 and PDGFA, was observed as early as 4 h post-last dose of combination treatment.

    “On the molecular level, upregulation of SOS1, SOS2 and RTKs (for example ERBB2 and ERBB3), as well as CXCL16 and PDGFA, both associated with activation of the MAPK and/or PI3K signaling32,33, was observed as early as 4 h post-last dose of combination treatment (Fig. 5b).”

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Authors
Korbecki, J., Bajdak-Rusinek, K., Kupnicka, P., Kapczuk, P., Simińska, D., Chlubek, D., & Baranowska-Bosiacka, I.
Affiliations
  • Pomeranian Medical University (PL)
  • Medical University of Silesia (PL)
  • Department of Biochemistry and Medical Chemistry, Powstańców Wielkopolskich 72 Av., Pomeranian Medical University in Szczecin, 70-111 Szczecin, Poland
Venue
International Journal of Molecular Sciences
Publisher
MDPI AG
Published
2021-03-28
Volume
22
Issue
7
Pages
3490
ISSN
1422-0067 (ISSN-L)
OpenAlex
W3139615586
Cited by
161
References
196
Citations by year
2026: 22 · 2025: 40 · 2024: 43 · 2023: 26 · 2022: 26 · 2021: 4
FWCI
3.00
Type
journal article
Language
en
Open access
Locations
  • International Journal of Molecular Sciences (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Topics
  • Health Sciences › Medicine › Oncology › Chemokine receptors and signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Connective Tissue Growth Factor Research
  • Life Sciences › Immunology and Microbiology › Immunology › Galectins and Cancer Biology
Keywords
CXCL16, CXCR6, CXC chemokines, tumor progression, tumor microenvironment, tumor angiogenesis, cancer-associated fibroblasts, tumor-associated macrophages, tumor-associated neutrophils, mesenchymal stem cells, myeloid-derived suppressor cells, regulatory T cells, NKT cells, antitumor immunity, metastasis, atherosclerosis, renal fibrosis, non-alcoholic fatty liver disease
MeSH terms
ADAM10 Protein, Chemokine CXCL16, Receptors, CXCR6, Animals, Cell Movement, Humans, Inflammation, Membrane Proteins, Neoplasm Invasiveness, Neoplasm Metastasis, Neoplasms, Gene Expression Regulation, Neoplastic, Lymphocytes, Tumor-Infiltrating, Chemokines, Endothelial Cells, Cell Proliferation, Mice, Amyloid Precursor Protein Secretases, Tumor Microenvironment, Mesenchymal Stem Cells

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