Lejeunea Cancellata as a modulating agent in breast cancer (MCF-7) tumor cell lines and human colostrum

Abstract

Breast cancer is a multifactorial disease resulting from genetic, immunological, and environmental interactions. Among environmental factors, it is known that diet plays a key role in cancer etiology. In addition, there is evidence that human milk may confer long-term benefits, such as reducing the risk of developing cancer. In breast cancer, macrophages represent one of the main components of the immune infiltrate. These cells contribute to the progression and spread of tumors, but studies suggest that these cells can be reprogrammed to act as a potent antitumor immune response. In addition to the mechanisms involved in the interaction between immune system cells and tumor progression, studies have related the use of plants as an alternative for tumor immunotherapy, among which the Cerrado bryophytes stand out. Thus, this study aimed to evaluate Lejeunea cancellata extract as a modulating agent in breast cancer (MCF-7) tumor cell lines and human colostrum. Therefore, the natural extract of Lejeunea cancellata was prepared, and from this, immunophenotyping assays, cytokine dosage, and data analysis were performed. There was an increase in the secretion of the inflammatory cytokines IL-1 and IL-8 in the groups cocultured with MCF-7 in the presence of Lejeunea cancellata. Furthermore, a decrease in the expression of CD14 (macrophages), CD163, CD197+ and CD86+ (M1 macrophages), and CD197- and CD86+ (M2 macrophages) is observed in colostrum cells when they were treated with Lejeunea cancellata in coculture with MCF-7 cells. These findings indicate that colostrum macrophages differentiate into two phenotypes, M1 and M2. When cocultured with MCF-7 breast tumor cells, the bryophyte Lejeunea cancellata reduces the percentage of both macrophage phenotypes. This data suggests that the bryophyte can inhibit the formation of inflammatory infiltrates caused by M1 macrophages in the tumor microenvironment and the progression of M2 macrophages that promote tumorigenesis.