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ANTI-BREAST CANCER ACTIVITY OF PTEROSPERMUM DIVERSIFOLIUM: APOPTOSIS INDUCTION AND SELECTIVE SYNERGY WITH LAPATINIB
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Pterospermum diversifolium Blume, a Vietnamese indigenous medicinal plant, along with other species in the same genus, has been preliminarily reported to possess anti-cancer properties. However, its breast cancer subtype-specific effects and underlying mechanisms remain largely unexplored. In this study, we evaluated the effects of P. diversifolium ethanol extract (PDE) on cell viability, proliferation, and apoptosis in two breast cancer cell lines, including MCF-7 (ER-positive) and SKBR3 (HER2-positive). PDE inhibited the viability of both MCF-7 and SKBR3 cells, with IC₅₀ values of 38.09 µg/mL and 35.68 µg/mL, respectively. Moreover, PDE showed a remarkable degree of selective cytotoxicity, with a selectivity index (SI) ranging from 3.56 to 3.80 when compared to non-malignant HEK293 cells. Mechanistically, PDE suppressed the expression of the proliferation marker Ki67 at 40 µg/mL and induced apoptosis at concentrations as low as 20 µg/mL. Notably, PDE exhibited a synergistic cytotoxic effect with lapatinib against HER2-positive SKBR3 cells but showed no synergism with tamoxifen in ER-positive MCF-7 cells. These original findings warrant further investigation into the potential use of PDE as an adjuvant agent in breast cancer therapy.
National Institute of Medical Materials
Title: ANTI-BREAST CANCER ACTIVITY OF PTEROSPERMUM DIVERSIFOLIUM: APOPTOSIS INDUCTION AND SELECTIVE SYNERGY WITH LAPATINIB
Description:
Pterospermum diversifolium Blume, a Vietnamese indigenous medicinal plant, along with other species in the same genus, has been preliminarily reported to possess anti-cancer properties.
However, its breast cancer subtype-specific effects and underlying mechanisms remain largely unexplored.
In this study, we evaluated the effects of P.
diversifolium ethanol extract (PDE) on cell viability, proliferation, and apoptosis in two breast cancer cell lines, including MCF-7 (ER-positive) and SKBR3 (HER2-positive).
PDE inhibited the viability of both MCF-7 and SKBR3 cells, with IC₅₀ values of 38.
09 µg/mL and 35.
68 µg/mL, respectively.
Moreover, PDE showed a remarkable degree of selective cytotoxicity, with a selectivity index (SI) ranging from 3.
56 to 3.
80 when compared to non-malignant HEK293 cells.
Mechanistically, PDE suppressed the expression of the proliferation marker Ki67 at 40 µg/mL and induced apoptosis at concentrations as low as 20 µg/mL.
Notably, PDE exhibited a synergistic cytotoxic effect with lapatinib against HER2-positive SKBR3 cells but showed no synergism with tamoxifen in ER-positive MCF-7 cells.
These original findings warrant further investigation into the potential use of PDE as an adjuvant agent in breast cancer therapy.
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