Home > Institute Collections > W500 > Beyond Cell Motility: The Expanding Roles of Chemokines and Their Receptors in Malignancy. > print

001     306232
005     20251118111148.0
024 7 _ |a 10.3389/fimmu.2020.00952
|2 doi
024 7 _ |a pmid:32582148
|2 pmid
024 7 _ |a pmc:PMC7287041
|2 pmc
037 _ _ |a DKFZ-2025-02461
041 _ _ |a English
082 _ _ |a 610
100 1 _ |a Morein, Dina
|b 0
245 _ _ |a Beyond Cell Motility: The Expanding Roles of Chemokines and Their Receptors in Malignancy.
260 _ _ |a Lausanne
|c 2020
|b Frontiers Media
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1763460675_1939190
|2 PUB:(DE-HGF)
|x Review Article
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
500 _ _ |a #DKFZ-MOST-Ca187#
520 _ _ |a The anti-tumor activities of some members of the chemokine family are often overcome by the functions of many chemokines that are strongly and causatively linked with increased tumor progression. Being key leukocyte attractants, chemokines promote the presence of inflammatory pro-tumor myeloid cells and immune-suppressive cells in tumors and metastases. In parallel, chemokines elevate additional pro-cancerous processes that depend on cell motility: endothelial cell migration (angiogenesis), recruitment of mesenchymal stem cells (MSCs) and site-specific metastasis. However, the array of chemokine activities in cancer expands beyond such 'typical' migration-related processes and includes chemokine-induced/mediated atypical functions that do not activate directly motility processes; these non-conventional chemokine functions provide the tumor cells with new sets of detrimental tools. Within this scope, this review article addresses the roles of chemokines and their receptors at atypical levels that are exerted on the cancer cell themselves: promoting tumor cell proliferation and survival; controlling tumor cell senescence; enriching tumors with cancer stem cells; inducing metastasis-related functions such as epithelial-to-mesenchymal transition (EMT) and elevated expression of matrix metalloproteinases (MMPs); and promoting resistance to chemotherapy and to endocrine therapy. The review also describes atypical effects of chemokines at the tumor microenvironment: their ability to up-regulate/stabilize the expression of inhibitory immune checkpoints and to reduce the efficacy of their blockade; to induce bone remodeling and elevate osteoclastogenesis/bone resorption; and to mediate tumor-stromal interactions that promote cancer progression. To illustrate this expanding array of atypical chemokine activities at the cancer setting, the review focuses on major metastasis-promoting inflammatory chemokines-including CXCL8 (IL-8), CCL2 (MCP-1), and CCL5 (RANTES)-and their receptors. In addition, non-conventional activities of CXCL12 which is a key regulator of tumor progression, and its CXCR4 receptor are described, alongside with the other CXCL12-binding receptor CXCR7 (RDC1). CXCR7, a member of the subgroup of atypical chemokine receptors (ACKRs) known also as ACKR3, opens the gate for discussion of atypical activities of additional ACKRs in cancer: ACKR1 (DARC, Duffy), ACKR2 (D6), and ACKR4 (CCRL1). The mechanisms involved in chemokine activities and the signals delivered by their receptors are described, and the clinical implications of these findings are discussed.
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: inrepo02.dkfz.de
650 _ 7 |a atypical chemokine activities in cancer
|2 Other
650 _ 7 |a atypical chemokine receptors
|2 Other
650 _ 7 |a breast cancer
|2 Other
650 _ 7 |a chemokines
|2 Other
650 _ 7 |a classical chemokine receptors
|2 Other
650 _ 7 |a Antineoplastic Agents
|2 NLM Chemicals
650 _ 7 |a Chemokines
|2 NLM Chemicals
650 _ 7 |a Receptors, Chemokine
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Antineoplastic Agents: therapeutic use
|2 MeSH
650 _ 2 |a Cell Movement: drug effects
|2 MeSH
650 _ 2 |a Chemokines: metabolism
|2 MeSH
650 _ 2 |a Drug Resistance, Neoplasm
|2 MeSH
650 _ 2 |a Epithelial-Mesenchymal Transition
|2 MeSH
650 _ 2 |a Humans
|2 MeSH
650 _ 2 |a Neoplasms: drug therapy
|2 MeSH
650 _ 2 |a Neoplasms: immunology
|2 MeSH
650 _ 2 |a Neoplasms: metabolism
|2 MeSH
650 _ 2 |a Neoplasms: pathology
|2 MeSH
650 _ 2 |a Neoplastic Stem Cells: immunology
|2 MeSH
650 _ 2 |a Neoplastic Stem Cells: metabolism
|2 MeSH
650 _ 2 |a Neoplastic Stem Cells: pathology
|2 MeSH
650 _ 2 |a Receptors, Chemokine: metabolism
|2 MeSH
650 _ 2 |a Signal Transduction
|2 MeSH
650 _ 2 |a Tumor Microenvironment
|2 MeSH
700 1 _ |a Erlichman, Nofar
|b 1
700 1 _ |a Ben-Baruch, Adit
|b 2
773 _ _ |a 10.3389/fimmu.2020.00952
|g Vol. 11, p. 952
|0 PERI:(DE-600)2606827-8
|p 952
|t Frontiers in immunology
|v 11
|y 2020
|x 1664-3224
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b FRONT IMMUNOL : 2022
|d 2024-12-28
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2024-12-28
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2024-12-28
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
|d 2023-12-29T15:23:07Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
|d 2023-12-29T15:23:07Z
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b DOAJ : Anonymous peer review
|d 2023-12-29T15:23:07Z
915 _ _ |a Creative Commons Attribution CC BY (No Version)
|0 LIC:(DE-HGF)CCBYNV
|2 V:(DE-HGF)
|b DOAJ
|d 2023-12-29T15:23:07Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2024-12-28
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0160
|2 StatID
|b Essential Science Indicators
|d 2024-12-28
915 _ _ |a WoS
|0 StatID:(DE-HGF)0113
|2 StatID
|b Science Citation Index Expanded
|d 2024-12-28
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2024-12-28
915 _ _ |a IF >= 5
|0 StatID:(DE-HGF)9905
|2 StatID
|b FRONT IMMUNOL : 2022
|d 2024-12-28
915 _ _ |a Article Processing Charges
|0 StatID:(DE-HGF)0561
|2 StatID
|d 2024-12-28
915 _ _ |a Fees
|0 StatID:(DE-HGF)0700
|2 StatID
|d 2024-12-28
980 _ _ |a journal
980 _ _ |a I:(DE-He78)W500-20160331
980 _ _ |a I:(DE-He78)W510-20160331
980 1 _ |a EXTERN4COORD

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21