Abstract
Endocrine disruptors (EDCs) can display estrogenic and androgenic effects, and their exposure has been linked to increased cancer risk. EDCs have been shown to directly affect cancer cell regulation and progression, but their influence on tumour microenvironment is still not completely elucidated. In this context, the signalling hub protein RACK1 (Receptor for Activated C Kinase 1) could represent a nexus between cancer and the immune system due to its roles in cancer progression and innate immune activation. Since RACK1 is a relevant EDCs target that responds to steroid-active compounds, it could be considered a molecular bridge between the endocrine-regulated tumour microenvironment and the innate immune system. We provide an analysis of immunomodulatory and cancer-promoting effects of different EDCs in shaping tumour microenvironment, with a final focus on the scaffold protein RACK1 as a pivotal molecular player due to its dual role in immune and cancer contexts.
Highlights
Steroid hormones can interact with specific receptors, orchestrating a vast set of physiological functions, including growth, development, reproduction, energy imbalance, metabolism, immunity and behaviour [1]
Since Receptor for Activated C Kinase 1 (RACK1) is a relevant Endocrine disruptors (EDCs) target that responds to steroid-active compounds, it could be considered a molecular bridge between the endocrine-regulated tumour microenvironment and the innate immune system
We provide an analysis of immunomodulatory and cancer-promoting effects of different EDCs in shaping tumour microenvironment, with a final focus on the scaffold protein RACK1 as a pivotal molecular player due to its dual role in immune and cancer contexts
Summary
Steroid hormones can interact with specific receptors, orchestrating a vast set of physiological functions, including growth, development, reproduction, energy imbalance, metabolism, immunity and behaviour [1]. EDCs are known to display hormonal features, including oestrogen and androgen activities, and they have been correlated with increased tumour risk considering their effects on cancer progression [11,12,13,14]. The role of EDCs in modulating the tumour microenvironment has not been elucidated, but is of pivotal interest In this regard, the scaffold protein Receptor for Activated C Kinase 1 (RACK1) is an EDC target in the immune context [17,18,19,20] and an important molecular player for cancer progression (reviewed in [21]). We discussed RACK1 dual role as a possible molecular bridge for cell response to EDCs in immune and cancer system
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