Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Effects of Molecular Iodine/Chemotherapy in the Immune Component of Breast Cancer Tumoral Microenvironment

Version 1 : Received: 8 September 2021 / Approved: 9 September 2021 / Online: 9 September 2021 (10:45:34 CEST)

A peer-reviewed article of this Preprint also exists.

Cuenca-Micó, O.; Delgado-González, E.; Anguiano, B.; Vaca-Paniagua, F.; Medina-Rivera, A.; Rodríguez-Dorantes, M.; Aceves, C. Effects of Molecular Iodine/Chemotherapy in the Immune Component of Breast Cancer Tumoral Microenvironment. Biomolecules 2021, 11, 1501. Cuenca-Micó, O.; Delgado-González, E.; Anguiano, B.; Vaca-Paniagua, F.; Medina-Rivera, A.; Rodríguez-Dorantes, M.; Aceves, C. Effects of Molecular Iodine/Chemotherapy in the Immune Component of Breast Cancer Tumoral Microenvironment. Biomolecules 2021, 11, 1501.

Journal reference: Biomolecules 2021, 11, 1501
DOI: 10.3390/biom11101501

Abstract

Molecular iodine (I2) induces apoptotic, antiangiogenic, and antiproliferative effects in breast cancer cells. Little is known about its effects on the tumor immune microenvironment. We studied the effect of oral (5 mg/day) I2 supplementation alone (I2) or together with conventional chemotherapy (Cht+I2) on the im-mune component of breast cancer tumors from a previously published pilot study conducted in Mexico. RNA-seq, I2 and Cht+I2 samples showed significant increases in expression of Th1 and Th17 pathways. Tumor immune composition determined by deconvolution analysis revealed significant increases in M0 macrophages and B lymphocytes in both I2 groups. Real-time RT-PCR showed that I2 tumors overexpress T-BET (p = 0.019) and interferon-gamma (IFNγ; p = 0.020) and silence tumor growth factor-beta (TGFβ; p = 0.049); whereas in Cht+I2 tumors, GATA3 is silenced (p = 0.014). Preliminary methylation analysis shows that I2 activates IFNγ gene promoter (by increasing its unmethylated form) and silences TGFβ in Cht+I2. In conclusion, our data showed that I2 supplements induce the activation of the immune response and that when combined with Cht, the Th1 pathways are stimulated. The molecular mechanisms involved in these responses are being analyzed, but preliminary data suggest that methylation/demethylation mechanisms could also participate.

Keywords

molecular iodine; immune response; breast cancer

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