Anticancer opportunities at every stage of chemokine function

Zacarı́as, Natalia V. Ortiz; Bemelmans, Martijn P.; Handel, Tracy M.; Visser, Karin E. de; Heitman, Laura H.

doi:10.1016/j.tips.2021.08.001

Cited by 25 publications

(13 citation statements)

References 88 publications

(120 reference statements)

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“…Malfunctioning or overexpression of the chemokine receptor response has been linked to various inflammatory diseases, including rheumatoid arthritis (RA), 4 chronic obstructive pulmonary disease (COPD), 5 multiple sclerosis (MS) 6 and inflammatory bowel disease (IBD), 7 as well as cancer development, invasion and metastasis. 8,9 Hitherto, 48 distinct chemokines and 19 chemokine receptors have been discovered, forming an intricate and seemingly redundant network, since multiple chemokines can interact with a single receptor and vice versa. 10 Instinctively, chemokine system redundancy should pose a problem regarding drug efficacy: if a receptor-specific small-molecule antagonist inhibits the function of one chemokine receptor, another will adopt its duties, making single-chemokine receptor inhibition a never-ending battle in the treatment of inflammatory diseases.…”

Section: Dominique Scholsmentioning

confidence: 99%

Targeting chemokine receptors from the inside-out: discovery and development of small-molecule intracellular antagonists

2022

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Section: Dominique Scholsmentioning

confidence: 99%

Targeting chemokine receptors from the inside-out: discovery and development of small-molecule intracellular antagonists

2022

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“…The challenge in targeting chemokines lies in their pleiotropic action, most often mediated through several receptors, which can complicate the anticipation of the intervention's effects. Chemokines can act directly on cancer cells to promote their stemness, proliferation, survival, and metastasis [146,147]. Among the chemokines reported in oncovirus-associ-…”

Section: Clinical Trials and Promises In Targeting Chemokines In Onco...mentioning

confidence: 99%

“…Chemokines can act directly on cancer cells to promote their stemness, proliferation, survival, and metastasis [146,147]. Among the chemokines reported in oncovirus-associated cancers, CCL2 and CXCL12 are known to directly support cancer cell stemness, proliferation, and survival.…”

Section: Targeting Chemokines To Modulate Cancer Cell Functionsmentioning

confidence: 99%

“…Based on these reports, the use of inhibitors targeting EZH2 or DNMT has been tested and reported to increase the production of these chemokines in the tumor bed, thereby promoting T-cell trafficking into tumors [146]. Conversely, the detrimental effects of certain chemokines, including CCL2, CCL3, CCL5, CXCL8, and CXCL12, in shaping immunosuppressive TME may also be targeted directly using chemokine-directed monoclonal antibodies or nanobodies [145][146][147] or indirectly using glycomimetics aimed at disrupting chemokines/GAGs interaction, thereby interfering with the formation of local chemokine gradients and impacting on cell trafficking [12].…”

Section: Targeting Chemokines To Modulate Immune Cell Recruitment And...mentioning

confidence: 99%

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The Chemokine System in Oncogenic Pathways Driven by Viruses: Perspectives for Cancer Immunotherapy

Schlecht-Louf

Deback

Bachelerie

2022

Cancers

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Chemokines interact with glycosaminoglycans of the extracellular matrix and activate heptahelical cellular receptors that mainly consist of G Protein-Coupled Receptors and a few atypical receptors also with decoy activity. They are well-described targets of oncogenic pathways and key players in cancer development, invasiveness, and metastasis acting both at the level of cancer cells and cells of the tumor microenvironment. Hence, they can regulate cancer cell proliferation and survival and promote immune or endothelial cell migration into the tumor microenvironment. Additionally, oncogenic viruses display the potential of jeopardizing the chemokine system by encoding mimics of chemokines and receptors as well as several products such as oncogenic proteins or microRNAs that deregulate their human host transcriptome. Conversely, the chemokine system participates in the host responses that control the virus life cycle, knowing that most oncoviruses establish asymptomatic latent infections. Therefore, the deregulated expression and function of chemokines and receptors as a consequence of acquired or inherited mutations could bias oncovirus infection toward pro-oncogenic pathways. We here review these different processes and discuss the anticancer therapeutic potential of targeting chemokine availability or receptor activation, from signaling to decoy-associated functions, in combination with immunotherapies.

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“…Chemokines act as key determinants of disease progression, with a strong influence on patient prognosis and response to therapy. Due to their multifaceted role in the tumor immune response, the chemokine network has emerged as a new potential immunotherapy target [13,14]. It is now also evident that cancer initiation and progression require a metabolic reprogramming of cancer cells.…”

mentioning

confidence: 99%