Cited by 47Immune cells in cancerCytokine Signaling Pathways and InteractionsCancer, Stress, Anesthesia, and Immune Response

Regulation of immunophenotype modulation of monocytes-macrophages from M1 into M2 by prostate cancer cell-culture supernatant via transcription factor STAT3

Solís-Martínez, R., Cancino-Marentes, M., Hernández-Flores, G., Ortiz-Lazareno, P., Mandujano-Álvarez, G., Cruz-Gálvez, C., Sierra-Díaz, E., Rodríguez-Padilla, C. +3 more·2018·Immunology Letters

Abstract

Background Transcription factor STAT3 has a prominent innate immunity effect on cancer progression. We determined the regulation of STAT3 in the immunophenotype modulation of macrophages from M1 into M2 induced by the cell-culture supernatant of the Prostate-Cancer line PC3. Methods Monocytes-macrophages from healthy donors were cultured in the supernatant of PC3 cells, membrane proteins, and intracytoplasmic and phosphorylated STAT3 were measured using flow cytometry, while cytokines and growth factors were studied using luminescence. Cytotoxicity and nitric oxide were evaluated via colorimetric assays. Results The supernatant of PC3 prostate-tumor cells effectively induced macrophages toward an M2 profile, and the expression of phosphorylated STAT3 in the monocytes-macrophages notably increased, and mainly related to IL-10. In the group of monocytes-macrophages treated with a STAT3 inhibitor, the macrophages were induced toward an M1 phenotype. Conclusions In this study, we showed that the secretion profile of PC3 prostate-cancer cells induces a change in macrophage phenotype from M1 into M2, and that the phenomenon is related to phosphorylation of transcription factor STAT3 and IL-10.

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Crossref · 10.1016/j.imlet.2018.02.009

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  • IL-6 and IL-10 are abundant in tumor microenvironments originated from myeloid cells, fibroblasts and tumor cells, and they further induce M2 macrophage differentiation through STAT3.

    “IL-6 and IL-10 are abundant in tumor microenvironments originated from myeloid cells, fibroblasts and tumor cells, and they further induce M2 macrophage differentiation through STAT3 (215, 216).”

    From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [215]

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Authors
Solís-Martínez, R., Cancino-Marentes, M., Hernández-Flores, G., Ortiz-Lazareno, P., Mandujano-Álvarez, G., Cruz-Gálvez, C., Sierra-Díaz, E., Rodríguez-Padilla, C., Jave-Suárez, L. F., Aguilar-Lemarroy, A., & Bravo-Cuellar, A.
Affiliations
  • Universidad de Guadalajara (MX)
  • Universidad Juárez Autónoma de Tabasco (MX)
Venue
Immunology Letters
Publisher
Elsevier BV
Published
2018-04
Volume
196
Pages
140-148
ISSN
0165-2478 (ISSN-L)
OpenAlex
W2794377359
Cited by
47
References
46
Citations by year
2026: 2 · 2025: 3 · 2024: 5 · 2023: 9 · 2022: 11 · 2021: 6 · 2020: 5 · 2019: 4 · 2018: 2
FWCI
1.82
Type
journal article
Language
en
Open access
closed
Locations
  • Immunology Letters (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune cells in cancer
  • Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
  • Health Sciences › Medicine › Psychiatry and Mental health › Cancer, Stress, Anesthesia, and Immune Response
Keywords
STAT3, M2 macrophages, M1 macrophages, macrophage polarization, prostate cancer, PC-3 cells, tumor cell supernatant, IL-10, STAT3 phosphorylation, monocytes, STAT3 inhibitor, nitric oxide, cytokines
MeSH terms
PC-3 Cells, Cells, Cultured, Humans, Macrophages, Male, Monocytes, Phosphorylation, Prostatic Neoplasms, Immunophenotyping, Interleukin-10, Culture Media, Conditioned, STAT3 Transcription Factor

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