THE TREATMENT OF BREAST CANCER CELLS WITH ERUFOSINE LEADS TO ACTIN CYTOSKELETON REORGANIZATION, INHIBITION OF CELL MOTILITY, CELL CYCLE ARREST AND APOPTOSIS

We investigated the effect of erufosine on actin cytoskeleton organization, inhibition of cell motility cell cycle and cell death on triple negative breast cancer cell line MDA-MB-231. Here we used actin staining to monitor cytoskeleton reorganization after erufosine treatment. The effect on cell motility was evaluated by wound-healing assay. The induction of cell cycle arrest and apoptosis were determined by flow cytometry of DNA content in different phases of cell cycle and DAPI contra staining of the nuclei, respectively. We found an increase of apoptotic cells and cell cycle arrest after treatment with erufosine. The low doses (IC25) of erufosine caused adhesive cell phenotype, but the higher doses (IC50 and IC75) led to actin fibre destruction and a decrease of cell motility, which is manifested as a slower closure of wound comparing to the untreated control cells. Taken together, our results strongly suggest that erufosine causes induction of apoptosis, G2/M cell cycle arrest, actin cytoskeleton destruction and inhibition of cell motility in a dose-dependent manner. Erufosine may be effective as anti-tumour agent against breast cancer.

Automated summary

Erufosine treatment induces apoptosis, G2/M cell cycle arrest, actin cytoskeleton destruction, and inhibition of cell motility in a dose-dependent manner in triple negative breast cancer cells. Erufosine may be effective as an anti-tumour agent against breast cancer.