Luffa cylindrica flower extract induces apoptosis and autophagy in breast cancer cells.
Luffa cylindrica flower has been used to treat haemorrhoids and breast hyperplasia, but the mechanism is unclear.
In this study, the antiproliferation activity of L. cylindrica flower extract (LCFE) was tested in breast cancer cells.
Following LCFE treatment, the CCK-8 assay, Hoechst staining and wound healing assay were used to evaluate cell proliferation, apoptotic cell morphology, and cell migration, respectively. qRT-PCR and western blot were used to analyze the expression of genes and proteins involved in the apoptosis and autophagy pathways. LC-MS was performed to characterize chemical constituents of LCFE.
CCK-8 and wound healing assays revealed that LCFE suppressed the proliferation and migration of MCF-7 and MDA-MB-231 cells. In these two breast cancer cells, the extract treatment induced apoptotic morphological changes. LCFE treatment induced apoptosis by upregulating ZFP36 and BNIP3 expression, while downregulating Bcl-2 expression in MCF-7 cells. LCFE increases ZFP36 expression while decreasing BMP4 expression in MDA-MB-231 cells, promoting apoptosis. Meanwhile, LCFE treatment induced autophagy by increasing VMP1 expression and activating LC3 in MCF-7 cells. It also triggered autophagy by decreasing TBC1D14 expression, increasing ATG5 and VAMP8 expression, and activating LC3 in MDA-MB-231 cells.
LCFE exerts an anti-tumor effect by activating apoptosis and autophagy processes in breast cancer cells, while having low cytotoxicity for normal breast cells, highlighting the potential of LCFE as a natural agent for cancer treatment.
In this study, the antiproliferation activity of L. cylindrica flower extract (LCFE) was tested in breast cancer cells.
Following LCFE treatment, the CCK-8 assay, Hoechst staining and wound healing assay were used to evaluate cell proliferation, apoptotic cell morphology, and cell migration, respectively. qRT-PCR and western blot were used to analyze the expression of genes and proteins involved in the apoptosis and autophagy pathways. LC-MS was performed to characterize chemical constituents of LCFE.
CCK-8 and wound healing assays revealed that LCFE suppressed the proliferation and migration of MCF-7 and MDA-MB-231 cells. In these two breast cancer cells, the extract treatment induced apoptotic morphological changes. LCFE treatment induced apoptosis by upregulating ZFP36 and BNIP3 expression, while downregulating Bcl-2 expression in MCF-7 cells. LCFE increases ZFP36 expression while decreasing BMP4 expression in MDA-MB-231 cells, promoting apoptosis. Meanwhile, LCFE treatment induced autophagy by increasing VMP1 expression and activating LC3 in MCF-7 cells. It also triggered autophagy by decreasing TBC1D14 expression, increasing ATG5 and VAMP8 expression, and activating LC3 in MDA-MB-231 cells.
LCFE exerts an anti-tumor effect by activating apoptosis and autophagy processes in breast cancer cells, while having low cytotoxicity for normal breast cells, highlighting the potential of LCFE as a natural agent for cancer treatment.