Butanol Fraction Inhibits MCF-7 Breast Cancer Cell Migration, Adhesion, and Invasiveness

In this study, the potential of an n-butanol fraction from Ricinus communis to prevent metastasis in MCF-7 breast cancer cells was investigated. The effect of the fraction on BUD-8 and MCF-7 cell viability was assessed using the MTT assay. Apoptotic cell death was analyzed by Hoechst staining assay....

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Main Authors: Rixile Mabasa MSc, Kholofelo Malemela MSc, Karabo Serala MSc, Mante Kgakishe BSc (Hons.), Thabe Matsebatlela PhD, Matlou Mokgotho PhD, Vusi Mbazima PhD
Format: Article
Language:English
Published: SAGE Publishing 2021-02-01
Series:Integrative Cancer Therapies
Online Access:https://doi.org/10.1177/1534735420977684
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author Rixile Mabasa MSc
Kholofelo Malemela MSc
Karabo Serala MSc
Mante Kgakishe BSc (Hons.)
Thabe Matsebatlela PhD
Matlou Mokgotho PhD
Vusi Mbazima PhD
author_facet Rixile Mabasa MSc
Kholofelo Malemela MSc
Karabo Serala MSc
Mante Kgakishe BSc (Hons.)
Thabe Matsebatlela PhD
Matlou Mokgotho PhD
Vusi Mbazima PhD
author_sort Rixile Mabasa MSc
collection DOAJ
description In this study, the potential of an n-butanol fraction from Ricinus communis to prevent metastasis in MCF-7 breast cancer cells was investigated. The effect of the fraction on BUD-8 and MCF-7 cell viability was assessed using the MTT assay. Apoptotic cell death was analyzed by Hoechst staining assay. The antimetastatic effect of the fraction on MCF-7 cell was evaluated using the wound healing, adhesion and Boyden chamber invasion assays. Gelatin-zymography was used to assess the effect of the fraction on MMP-2 and MMP-9 activity. The expression profile of proteins implicated in metastasis and angiogenesis was determined using the human angiogenesis antibody array kit, following treatment with the fraction. BUD-8 cell viability was significantly reduced at concentrations between 300 and 500 µg/ml of the extract. In contrast, a significant reduction in cell viability was seen in MCF-7 cells treated with 400 to 500 µg/ml of the fraction. At sub-lethal concentrations (100 and 200 µg/ml) of the fraction, no nuclei morphological changes associated with apoptotic cell death were observed in MCF-7 cells. In addition, the fraction showed to have an inhibitory effect on MCF-7 cell migration, adhesion, invasiveness, and MMP-2 activity. Moreover, the fraction was seen to modulate the expression of several proteins, such as MMP-9, uPA, VEGF, and TGF-β1, playing a role in the metastasis process. This study demonstrates that the n -butanol fraction of R. communis can inhibit major steps of the metastatic cascade and modulate metastasis regulatory proteins. Thus, the fraction can be considered a potential source of antimetastatic agents that could be useful in the treatment of malignant cancers.
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spelling doaj.art-5e1209f1c9784e73b851bfce579786502022-12-21T17:44:12ZengSAGE PublishingIntegrative Cancer Therapies1534-73541552-695X2021-02-012010.1177/1534735420977684Butanol Fraction Inhibits MCF-7 Breast Cancer Cell Migration, Adhesion, and InvasivenessRixile Mabasa MSc0Kholofelo Malemela MSc1Karabo Serala MSc2Mante Kgakishe BSc (Hons.)3Thabe Matsebatlela PhD4Matlou Mokgotho PhD5Vusi Mbazima PhD6University of Limpopo, Sovenga, South AfricaUniversity of Limpopo, Sovenga, South AfricaUniversity of Limpopo, Sovenga, South AfricaUniversity of Limpopo, Sovenga, South AfricaUniversity of Limpopo, Sovenga, South AfricaUniversity of Limpopo, Sovenga, South AfricaUniversity of Limpopo, Sovenga, South AfricaIn this study, the potential of an n-butanol fraction from Ricinus communis to prevent metastasis in MCF-7 breast cancer cells was investigated. The effect of the fraction on BUD-8 and MCF-7 cell viability was assessed using the MTT assay. Apoptotic cell death was analyzed by Hoechst staining assay. The antimetastatic effect of the fraction on MCF-7 cell was evaluated using the wound healing, adhesion and Boyden chamber invasion assays. Gelatin-zymography was used to assess the effect of the fraction on MMP-2 and MMP-9 activity. The expression profile of proteins implicated in metastasis and angiogenesis was determined using the human angiogenesis antibody array kit, following treatment with the fraction. BUD-8 cell viability was significantly reduced at concentrations between 300 and 500 µg/ml of the extract. In contrast, a significant reduction in cell viability was seen in MCF-7 cells treated with 400 to 500 µg/ml of the fraction. At sub-lethal concentrations (100 and 200 µg/ml) of the fraction, no nuclei morphological changes associated with apoptotic cell death were observed in MCF-7 cells. In addition, the fraction showed to have an inhibitory effect on MCF-7 cell migration, adhesion, invasiveness, and MMP-2 activity. Moreover, the fraction was seen to modulate the expression of several proteins, such as MMP-9, uPA, VEGF, and TGF-β1, playing a role in the metastasis process. This study demonstrates that the n -butanol fraction of R. communis can inhibit major steps of the metastatic cascade and modulate metastasis regulatory proteins. Thus, the fraction can be considered a potential source of antimetastatic agents that could be useful in the treatment of malignant cancers.https://doi.org/10.1177/1534735420977684
spellingShingle Rixile Mabasa MSc
Kholofelo Malemela MSc
Karabo Serala MSc
Mante Kgakishe BSc (Hons.)
Thabe Matsebatlela PhD
Matlou Mokgotho PhD
Vusi Mbazima PhD
Butanol Fraction Inhibits MCF-7 Breast Cancer Cell Migration, Adhesion, and Invasiveness
Integrative Cancer Therapies
title Butanol Fraction Inhibits MCF-7 Breast Cancer Cell Migration, Adhesion, and Invasiveness
title_full Butanol Fraction Inhibits MCF-7 Breast Cancer Cell Migration, Adhesion, and Invasiveness
title_fullStr Butanol Fraction Inhibits MCF-7 Breast Cancer Cell Migration, Adhesion, and Invasiveness
title_full_unstemmed Butanol Fraction Inhibits MCF-7 Breast Cancer Cell Migration, Adhesion, and Invasiveness
title_short Butanol Fraction Inhibits MCF-7 Breast Cancer Cell Migration, Adhesion, and Invasiveness
title_sort butanol fraction inhibits mcf 7 breast cancer cell migration adhesion and invasiveness
url https://doi.org/10.1177/1534735420977684
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