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Prolonged estrogen ...
Prolonged estrogen deprivation triggers a broad immunosuppressive phenotype in breast cancer cells
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- Hühn, Daniela (författare)
- Karolinska Institutet
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- Martí‐Rodrigo, Pablo (författare)
- Science for Life Laboratory Division of Genome Biology Department of Medical Biochemistry and Biophysics Karolinska Institute Stockholm Sweden
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- Mouron, Silvana (författare)
- Breast Cancer Clinical Research Unit Spanish National Cancer Research Centre (CNIO) Madrid Spain
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- Hansel, Catherine (författare)
- Science for Life Laboratory Division of Genome Biology Department of Medical Biochemistry and Biophysics Karolinska Institute Stockholm Sweden
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- Tschapalda, Kirsten (författare)
- Science for Life Laboratory Division of Genome Biology Department of Medical Biochemistry and Biophysics Karolinska Institute Stockholm Sweden
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- Porebski, Bartlomiej (författare)
- Karolinska Institutet
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- Häggblad, Maria (författare)
- Karolinska Institutet
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- Lidemalm, Louise (författare)
- Karolinska Institutet
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- Quintela‐Fandino, Miguel (författare)
- Breast Cancer Clinical Research Unit Spanish National Cancer Research Centre (CNIO) Madrid Spain
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- Carreras-Puigvert, Jordi (författare)
- Karolinska Institutet
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- Fernandez‐Capetillo, Oscar (författare)
- Karolinska Institutet
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(creator_code:org_t)
- 2021-08-29
- 2021
- Engelska.
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Ingår i: Molecular Oncology. - : John Wiley & Sons. - 1574-7891 .- 1878-0261. ; 16:1, s. 148-165
- Relaterad länk:
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Abstract
Ämnesord
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- Among others, expression levels of programmed cell death 1 ligand 1 (PD-L1) have been explored as biomarkers of the response to immune checkpoint inhibitors in cancer therapy. Here, we present the results of a chemical screen that interrogated how medically approved drugs influence PD-L1 expression. As expected, corticosteroids and inhibitors of Janus kinases were among the top PD-L1 downregulators. In addition, we identified that PD-L1 expression is induced by antiestrogenic compounds. Transcriptomic analyses indicate that chronic estrogen receptor alpha (ER alpha) inhibition triggers a broad immunosuppressive program in ER-positive breast cancer cells, which is subsequent to their growth arrest and involves the activation of multiple immune checkpoints together with the silencing of the antigen-presenting machinery. Accordingly, estrogen-deprived MCF7 cells are resistant to T-cell-mediated cell killing, in a manner that is independent of PD-L1, but which is reverted by estradiol. Our study reveals that while antiestrogen therapies efficiently limit the growth of ER-positive breast cancer cells, they concomitantly trigger a transcriptional program that favors their immune evasion.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cancer and Oncology (hsv//eng)
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