Retinoids and breast cancer: new clues to increase their activity and selectivity

Enrico Garattini,Mineko Terao,Gabriela Paroni

doi:10.1186/bcr3245

Enrico Garattini, Mineko Terao + Show 1 more

Open Access

https://doi.org/10.1186/bcr3245

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Abstract

All-trans retinoic acid and derivatives (retinoids) are promising agents in the management of certain hematologic malignancies and solid tumors, including breast cancer. Retinoids are endowed with anti-proliferative, cyto-differentiating and apoptotic effects that are largely mediated by activation of the nuclear hormone retinoic acid receptors RARα, RARβ and RARγ. These are ligand-dependent transcriptional factors controlling the expression of numerous genes. The relative importance of each receptor subtype for the anti-tumor activity of retinoids is largely unknown. Clarification of this point is of fundamental importance for the rational design of retinoid-based therapeutic approaches aimed at controlling a heterogeneous type of tumors, like breast cancer.

Highlights

All-trans retinoic acid and derivatives are promising agents in the management of certain hematologic malignancies and solid tumors, including breast cancer
The results presented by Bosch and colleagues [1] in the previous issue of Breast Cancer Research are a major step towards the identification of the critical determinants controlling the responses of breast tumor cells to alltrans-retinoic acid (ATRA), the prototype of retinoids, a promising class of anti-cancer agents
The idea is supported by the observation that estrogen receptor-positive breast carcinoma cell lines are sensitive to ATRA, while estrogen receptornegative ones are not [11]

Summary

Introduction

All-trans retinoic acid and derivatives (retinoids) are promising agents in the management of certain hematologic malignancies and solid tumors, including breast cancer. The authors demonstrate that the two retinoid nuclear receptors RARα and RARγ play opposite roles in controlling the growth of breast cancer cells [1]. Retinoid-dependent activation of RARα arrests the growth, while activation of the other receptor favors the proliferation of the neoplastic cell.

Results

Conclusion