Abstract

Previous studies have reported that 4,6′-Anhydrooxysporidinone (SSF2-2), isolated from Fusarium lateritium SSF2, has neuroprotective effects on the HT-22 hippocampal neuronal cell line. However, the anti-cancer effect of SSF2-2 remains unclear. Here, we examined the viability of MCF-7 human breast cancer cells treated with SSF2-2 or left untreated using a cell viability assay kit. The underlying molecular mechanism was further investigated by Western blotting and immunocytochemistry studies. The results demonstrated that SSF2-2 inhibited the viability of MCF-7 cells. Treatment with SSF2-2 increased the levels of cleaved caspase-9, cleaved caspase-7, poly (ADP-ribose) polymerase (PARP), and LC3B. Additionally, SSF2-2 significantly increased the conversion of LC3-I to LC3II and LC3-positive puncta in MCF-7 cells.

Highlights

  • Breast cancer is one of the leading causes of death among women worldwide [1].It is the most common type of malignant tumor that can be treated with chemotherapy, radiotherapy, and surgery [2]

  • We first evaluated the effects of SSF2-1, SSF2-2, and SSF2-3, isolated from the F. lateritium SSF2 cultures, on the viability of MCF-7 breast cancer cells

  • The results demonstrate that the protein levels of cleaved caspase-9 and caspase-7 and cleaved poly (ADP-ribose) polymerase (PARP) increased after treatment with 50 μM pf SSF2-2 for 24 h in MCF-7 cells (Figure 2A,B)

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Summary

Introduction

Breast cancer is one of the leading causes of death among women worldwide [1]. It is the most common type of malignant tumor that can be treated with chemotherapy, radiotherapy, and surgery [2]. These treatments have undesirable side effects, as they affect breast cancer cells but have undesirable effects on normal cells as well. We have continually studied the effects of natural products on the apoptotic cell death of breast cancer cells [4,5,6,7,8,9]. Accumulating studies on the identification of anticancer substances from natural products have reported that apoptosis and autophagy are important pathways in the death of cancer cells [10]

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