Selective anti-CXCR2 receptor blockade by AZD5069 inhibits CXCL8-mediated pro-tumorigenic activity in human thyroid cancer cells in vitro.

AZD5069 CXCL8 CXCR2 receptor Thyroid cancer

Journal

Journal of endocrinological investigation
ISSN: 1720-8386
Titre abrégé: J Endocrinol Invest
Pays: Italy
ID NLM: 7806594

Informations de publication

Date de publication:
20 Jun 2024
Historique:
received: 30 04 2024
accepted: 06 06 2024
medline: 20 6 2024
pubmed: 20 6 2024
entrez: 20 6 2024
Statut: aheadofprint

Résumé

Thyroid cancer is the most common endocrine malignancy. Current therapies are successful, however some patients progress to therapeutically refractive disease. The immunotherapeutic potential of the CXCL8-chemokine/CXCR2-chemokine-receptor system is currently being explored in numerous human cancers. This study aimed to evaluate if the targeting of CXCR2 by its selective antagonist, AZD5069, could modulate CXCL8-mediated pro-tumorigenic effects in thyroid-cancer (TC) cells in vitro. Normal human primary thyroid cells (NHT) and TC cell lines TPC-1 (RET/PTC), BCPAP, 8505C and 8305C (BRAFV600e) were treated with AZD5069 (100 pM-10 µM) over a time-course. Viability and proliferation were assessed by WST-1 and crystal violet assays. CXCL8 and CXCR2 mRNA were evaluated by RT-PCR. CXCL8-protein concentrations were measured in cell culture supernatants by ELISA. CXCR2 on cell surface was evaluated by flow-cytometry. Cell-migration was assessed by trans-well-migration chamber-system. AZD5069 exerted negligible effects on cell proliferation or viability. AZD5069 significantly reduced CXCR2, (but not CXCL8) mRNAs in all cell types. CXCR2 was reduced on the membrane of some TC cell lines. A significant reduction of the CXCL8 secretion was found in TPC-1 cells (basal-secretion) and NHT (TNFα-induced secretion). AZD5069 significantly reduced basal and CXCL8-induced migration in NHT and different TC cells. Our findings confirm the involvement of the CXCL8/CXCR2-axis in promoting pro-tumorigenic effects in TC cells, further demonstrating its immunotherapeutic significance in human cancer.

Sections du résumé

BACKGROUND BACKGROUND
Thyroid cancer is the most common endocrine malignancy. Current therapies are successful, however some patients progress to therapeutically refractive disease. The immunotherapeutic potential of the CXCL8-chemokine/CXCR2-chemokine-receptor system is currently being explored in numerous human cancers. This study aimed to evaluate if the targeting of CXCR2 by its selective antagonist, AZD5069, could modulate CXCL8-mediated pro-tumorigenic effects in thyroid-cancer (TC) cells in vitro.
METHODS METHODS
Normal human primary thyroid cells (NHT) and TC cell lines TPC-1 (RET/PTC), BCPAP, 8505C and 8305C (BRAFV600e) were treated with AZD5069 (100 pM-10 µM) over a time-course. Viability and proliferation were assessed by WST-1 and crystal violet assays. CXCL8 and CXCR2 mRNA were evaluated by RT-PCR. CXCL8-protein concentrations were measured in cell culture supernatants by ELISA. CXCR2 on cell surface was evaluated by flow-cytometry. Cell-migration was assessed by trans-well-migration chamber-system.
RESULTS RESULTS
AZD5069 exerted negligible effects on cell proliferation or viability. AZD5069 significantly reduced CXCR2, (but not CXCL8) mRNAs in all cell types. CXCR2 was reduced on the membrane of some TC cell lines. A significant reduction of the CXCL8 secretion was found in TPC-1 cells (basal-secretion) and NHT (TNFα-induced secretion). AZD5069 significantly reduced basal and CXCL8-induced migration in NHT and different TC cells.
CONCLUSIONS CONCLUSIONS
Our findings confirm the involvement of the CXCL8/CXCR2-axis in promoting pro-tumorigenic effects in TC cells, further demonstrating its immunotherapeutic significance in human cancer.

Identifiants

pubmed: 38900374
doi: 10.1007/s40618-024-02410-6
pii: 10.1007/s40618-024-02410-6
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Ministero della Salute
ID : Ricerca Corrente

Informations de copyright

© 2024. The Author(s).

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Auteurs

F Coperchini (F)

Department of Internal Medicine and Therapeutics, University of Pavia, Via S. Maugeri 4, 27100, Pavia, Italy.

A Greco (A)

Department of Internal Medicine and Therapeutics, University of Pavia, Via S. Maugeri 4, 27100, Pavia, Italy.

E Petrosino (E)

Department of Internal Medicine and Therapeutics, University of Pavia, Via S. Maugeri 4, 27100, Pavia, Italy.

L Croce (L)

Department of Internal Medicine and Therapeutics, University of Pavia, Via S. Maugeri 4, 27100, Pavia, Italy.
Unit of Endocrinology and Metabolism, Laboratory for Endocrine Disruptors, Istituti Clinici Scientifici Maugeri IRCCS, 27100, Pavia, Italy.

M Teliti (M)

Department of Internal Medicine and Therapeutics, University of Pavia, Via S. Maugeri 4, 27100, Pavia, Italy.
Unit of Endocrinology and Metabolism, Laboratory for Endocrine Disruptors, Istituti Clinici Scientifici Maugeri IRCCS, 27100, Pavia, Italy.

N Marchesi (N)

Unit of Pharmacology, Department of Drug Sciences, University of Pavia, 27100, Pavia, Italy.

A Pascale (A)

Unit of Pharmacology, Department of Drug Sciences, University of Pavia, 27100, Pavia, Italy.

B Calì (B)

Department of General and Minimally Invasive Surgery, Istituti Clinici Scientifici Maugeri IRCCS, 27100, Pavia (PV), Italy.

P Pignatti (P)

Allergy and Immunology Unit, Istituti Clinici Scientifici Maugeri IRCCS, 27100, Pavia, Italy.

F Magri (F)

Department of Internal Medicine and Therapeutics, University of Pavia, Via S. Maugeri 4, 27100, Pavia, Italy.
Unit of Endocrinology and Metabolism, Laboratory for Endocrine Disruptors, Istituti Clinici Scientifici Maugeri IRCCS, 27100, Pavia, Italy.

M Uddin (M)

AstraZeneca Gothenburg, Biopharmaceuticals R&D, Mӧlndal, Sweden.

M Rotondi (M)

Department of Internal Medicine and Therapeutics, University of Pavia, Via S. Maugeri 4, 27100, Pavia, Italy. mario.rotondi@icsmaugeri.it.
Unit of Endocrinology and Metabolism, Laboratory for Endocrine Disruptors, Istituti Clinici Scientifici Maugeri IRCCS, 27100, Pavia, Italy. mario.rotondi@icsmaugeri.it.

Classifications MeSH