Effect of aloin on some gene biomarkers for epithelial-mesenchymal transition in breast cancer in vitro compared to an anthracycline analog (Doxorubicin)

Abstract

Article history: Received 19 July 2020 Accepted 19 August 2020 Epithelial-mesenchymal transition (EMT) is a biologic process that permits an epithelial cell to undergo multiple biochemical changes that enable it to assume a mesenchymal cell phenotype with enhanced migratory capacity and invasiveness. In the present study, the cytotoxic activity of aloin, a natural anthraquinone glycoside, was assessed against a breast cancer cell line (T47D) using MTT and clonogenic assays, compared to doxorubicin, an anthracycline analog. The effects of exposure of T47D tumor cells to IC50 values of aloin and doxorubicin (181.5 and 0.17 μM, respectively) for 72 h on the mRNA expression levels of a nonreceptor tyrosine kinase (JAK2), a transcription factor (STAT5a) and some biomarkers for EMT were evaluated to provide new prognostic and therapeutic markers for estrogen receptor-positive breast cancer progression. Exposure to aloin down-regulated the expression levels of JAK2, STAT5a and vimentin mRNA in T47D cells, while the expression levels of E-cadherin and ZO-1 mRNA were not significantly changed. On the other hand, exposure of breast tumor cells to doxorubicin up-regulated the expression of E-cadherin mRNA, whereas the expression levels of JAK2, STAT5a, ZO-1 and vimentin mRNA were not affected. In conclusion, the chemosensitivity of aloin towards breast tumor cells is due to inhibition of JAK2/STAT5a signaling, which results in the inhibition of vimentin expression as a mesenchymal marker of EMT.