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Breast cancer is the most prevalent type of cancer among women worldwide and it is characterized by a high morbidity. Curcumin is a naturally occurring compound derived from the rhizome of Curcuma longa and is known to have antioxidant and anticarcinogenic properties. Emerging evidence has indicated that microRNAs (miRNAs or miRs) function as oncogenes or tumor suppressor genes to control invasion and migration. The aim of this study was to evaluate the effects of curcumin on genes implicated in epithelial‑mesenchymal transition (EMT) and to examine the involvement of Rho‑A in the migration and invasion of MCF‑10F and MDA‑MB‑231 breast cell lines. Furthermore, to the best of our knowledge, this is the first study to examine the effects of curcumin on Rho‑A and on genes involved in EMT, such as Axl, Slug and CD24 in order to determine whether the compound is able to prevent migration and invasion by targeting miRNAs as a regulator of such genes. Specifically, we focused on miR‑34a which acts as a tumor suppressor gene in human breast cell lines. The present study demonstrated that the Axl, Slug and CD24 genes were implicated in EMT, and Rho‑A was also involved in the migration and invasion of MCF‑10F and MDA‑MB‑231 cell lines. Curcumin also acted upon the miRNA as a regulator of genes implicated in EMT and upon Rho‑A as well, affecting the migration and invasion of the cells. This occurred independently of their estrogen receptor (ER), progesterone receptor (PgR) and human epidermal growth factor receptor 2 (HER2) receptors in the non‑malignant MCF‑10F and malignant MDA‑MB‑231 breast cell lines, which are both negative for such receptors.

Breast cancer is a major health problem and accounted for 11.6% of all new cancer cases and 6.6% of all cancer deaths among women worldwide in 2018. However, its etiology has remained elusive. According to epidemiological studies, environmental factors are influencing the increase in the incidence of breast cancer risk. Components such as chemicals, including pesticides, are agents that produce deleterious effects on wildlife and humans. Among them, the organophosphorus pesticides, such as malathion, have largely been considered in this etiology. The epithelial-mesenchymal transition serves a key role in tumor progression and it is proposed that malathion is closely associated with the origin of this transition, among other causes. Moreover, proteins participating in this process are primordial in the transformation of a normal cell to a malignant tumor cell. The aim of the current study was to evaluate markers that indicated oncogenic properties. The results indicated greater expression levels of proteins associated with the epithelial-to-mesenchymal transition, including E-cadherin, Vimentin, Axl, and Slug in the rat mammary glands treated with malathion alone and combined with estrogen. Atropine was demonstrated to counteract the malathion effect as a muscarinic antagonist. The understanding of the use of markers in experimental models is crucial to identify different stages in the cancer process. The alteration of these markers may serve as a predicting factor that can be used to indicate whether a person has altered ducts or lobules in breast tissue within biopsies of individuals exposed to OPs or other environmental substances. [ABSTRACT FROM AUTHOR]