Immune response to supernatant of ferroptotic breast cancer cells: from inflammation to immunomodulation
- 1Reproductive Immunology Research Center, Shahid Sadoughi University of Medical Sciences
Abstract
Ferroptosis is an iron-dependent, lipid peroxidation–driven form of regulated cell death with emerging relevance to tumor–immune interactions. This study examined whether soluble factors from ferroptotic breast cancer cells alter transcriptional responses in primary human peripheral blood mononuclear cells (PBMCs). Human Michigan Cancer Foundation-7 (MCF-7) cells were treated with ferroptosis inducer 56 (FIN56), and loss of viability, intracellular reactive oxygen species (ROS), and lactate dehydrogenase (LDH) release were monitored as indicators associated with ferroptotic cell death. Conditioned medium (CM, 50%) from treated or control cells was applied to PBMCs from healthy donors for 24–72 h, and interleukin 10 (IL10), interferon gamma (IFNG), tumor necrosis factor alpha (TNFA), transforming growth factor beta 1 (TGFB1), and forkhead box P3 (FOXP3) transcripts were quantified by quantitative polymerase chain reaction (qPCR). The CM from FIN56-treated MCF-7 cells significantly increased IL10 at all time points, as well as a short-term increase in IFNG expression at 24 h. The FOXP3 gene exhibited a mild increase at early times but returned to baseline levels later. No significant differences were detected for TNFA and TGFB1 expression. Factors released from tumor cells undergoing ferroptosis-associated stress shifted PBMC gene expression toward a regulatory and anti-inflammatory pattern, characterized by strong IL10 induction and short IFNG activation.
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BibTeX
@article{meshkin2026immune,
title = {{Immune response to supernatant of ferroptotic breast cancer cells: from inflammation to immunomodulation}},
author = {Ahmad Meshkin and Mohammad Masoud Khodaei and Farzaneh Fesahat and Fateme Zare},
journal = {Scientific Reports},
year = {2026},
month = jul,
doi = {10.1038/s41598-026-63328-y},
url = {https://doi.org/10.1038/s41598-026-63328-y},
note = {CC BY},
}
RIS
TY - JOUR
TI - Immune response to supernatant of ferroptotic breast cancer cells: from inflammation to immunomodulation
AU - Ahmad Meshkin
AU - Mohammad Masoud Khodaei
AU - Farzaneh Fesahat
AU - Fateme Zare
PY - 2026
DA - 2026/07/01
JO - Scientific Reports
DO - 10.1038/s41598-026-63328-y
UR - https://doi.org/10.1038/s41598-026-63328-y
AB - Ferroptosis is an iron-dependent, lipid peroxidation–driven form of regulated cell death with emerging relevance to tumor–immune interactions. This study examined whether soluble factors from ferroptotic breast cancer cells alter transcriptional responses in primary human peripheral blood mononuclear cells (PBMCs). Human Michigan Cancer Foundation-7 (MCF-7) cells were treated with ferroptosis inducer 56 (FIN56), and loss of viability, intracellular reactive oxygen species (ROS), and lactate dehydrogenase (LDH) release were monitored as indicators associated with ferroptotic cell death. Conditioned medium (CM, 50%) from treated or control cells was applied to PBMCs from healthy donors for 24–72 h, and interleukin 10 (IL10), interferon gamma (IFNG), tumor necrosis factor alpha (TNFA), transforming growth factor beta 1 (TGFB1), and forkhead box P3 (FOXP3) transcripts were quantified by quantitative polymerase chain reaction (qPCR). The CM from FIN56-treated MCF-7 cells significantly increased IL10 at all time points, as well as a short-term increase in IFNG expression at 24 h. The FOXP3 gene exhibited a mild increase at early times but returned to baseline levels later. No significant differences were detected for TNFA and TGFB1 expression. Factors released from tumor cells undergoing ferroptosis-associated stress shifted PBMC gene expression toward a regulatory and anti-inflammatory pattern, characterized by strong IL10 induction and short IFNG activation.
SN - 2045-2322
ER -