scholarly journals Ricinus communis Butanol Fraction Inhibits MCF-7 Breast Cancer Cell Migration, Adhesion, and Invasiveness

2021 ◽  
Vol 20 ◽  
pp. 153473542097768
Author(s):  
Rixile Mabasa ◽  
Kholofelo Malemela ◽  
Karabo Serala ◽  
Mante Kgakishe ◽  
Thabe Matsebatlela ◽  
...  

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.

2018 ◽  
Vol 105 ◽  
pp. 320-325 ◽  
Author(s):  
Guo-Dong Yao ◽  
Meng-Yao Ge ◽  
Dan-Qi Li ◽  
Ling Chen ◽  
Toshihiko Hayashi ◽  
...  

MedChemComm ◽  
2015 ◽  
Vol 6 (4) ◽  
pp. 702-707 ◽  
Author(s):  
Debanjana Chakraborty ◽  
Arindam Maity ◽  
Chetan K. Jain ◽  
Abhijit Hazra ◽  
Yogesh P. Bharitkar ◽  
...  

Dispiro andrographolides induce a caspase-dependent apoptotic cell death pathway in breast cancer (MCF-7) cells.


2013 ◽  
Vol 121 ◽  
pp. 100-107 ◽  
Author(s):  
Savvas Petanidis ◽  
Margarita Hadzopoulou-Cladaras ◽  
Athanasios Salifoglou

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Prema Robinson ◽  
Moses Kasembeli ◽  
Uddalak Bharadwaj ◽  
Nikita Engineer ◽  
Kris T. Eckols ◽  
...  

Doxorubicin (DOX), an anthracycline, is broadly considered the most active single agent available for treating breast cancer but has been known to induce cardiotoxicity. Although DOX is highly effective in treating triple-negative breast cancer (TNBC), DOX can have poor outcomes owing to induction of chemoresistance. There is an urgent need to develop new therapies for TNBC aimed at improving DOX outcome and DOX-induced cardiotoxicity. Substance P (SP), a neuropeptide involved in pain transmission is known to stimulate production of reactive oxygen species (ROS). Elevated cardiac ROS is linked with heart injury and failure. We investigated the role of SP in chemotherapy-associated death of cardiomyocytes and chemoresistance. We showed that pretreating a cardiomyocyte cell line (H9C2) and a TNBC cell line (MDA-MB 231) with aprepitant, a SP receptor antagonist that is routinely used to treat chemotherapy-associated associated nausea, decreased DOX-induced reduction of cell viability, apoptotic cell death, and ROS production in cardiomyocytes and increased DOX-induced reduction of cell viability, apoptotic cell death, and ROS production in TNBC cells compared with cells treated with DOX alone. Our findings demonstrate the ability of aprepitant to decrease DOX-induced killing of cardiomyocytes and to increase cancer cell sensitivity to DOX, which has tremendous clinical significance.


APOPTOSIS ◽  
2009 ◽  
Vol 14 (7) ◽  
pp. 913-922 ◽  
Author(s):  
A-Mi Seo ◽  
Seung-Woo Hong ◽  
Jae-Sik Shin ◽  
In-Chul Park ◽  
Nam-Joo Hong ◽  
...  

Proceedings ◽  
2019 ◽  
Vol 40 (1) ◽  
pp. 9
Author(s):  
Amani Abdulmunem ◽  
Pınar Obakan-Yerlikaya ◽  
Elif-Damla Arisan ◽  
Ajda Coker-Gurkan

Breast cancer is the most common cancer in women worldwide and the second most common cancer overall. Autocrine growth hormone (GH) expression induced cell proliferation, growth, invasion-metastasis in vitro and in vivo breast cancer models. Moreover, forced GH signaling acts as a drug resistance profile in breast cancer cell lines against chemotherapeutic drugs such as tamoxifen, mitomycin C, doxorubicin and curcumin. Triptolide, an active plant extract from Tripterygium wilfordii, has been shown to induce apoptotic cell death in various cancer cells such a prostate, colon, breast cancer. Metformin, a common therapeutic agent for type II Diabetes mellitus, has been shown to induce autophagy, endoplasmic reticulum (ER) stress and apoptotic cell death in cancer cells. Our aim is to demonstrate the potential effect of metformin on triptolide-mediated drug resistance in autocrine GH expressing MDA-MB-231 breast cancer cells through Endoplasmic reticulum (ER) stress. Autocrine GH-mediated triptolide (20 nM) resistance overcame by metformin (2 mM) co-teatment in MDA-MB231 breast cancer cells through accelerating cell viability loss, growth inhibition compared to alone triptolide treatment. Combined treatment increased apoptotic cell death via CHOP activation, IRE1α upregulation. Consequently, we suggest that triptolide can be more effective with metformin combination in MDA-MB-231 GH+ drug resistant breast cancer cells.


Author(s):  
Deepa Priya Ramadoss ◽  
Nageswaran Sivalingam

Objective: The main aim of the study was to investigate the bioactive compound vanillin extracted from proso millet (compound 1), and barnyard millet (compound 2) induces apoptotic cell death and whether it is mediated through mitochondrial pathway in HT-29 and MCF-7 cell line.Methods: The cells were treated with 250 μg/ml and 1000 μg/ml concentration of extracted vanillin for 48 hrs. Cytochrome c release and expression level of pro-apoptotic protein Bax and caspase-9 were detected by western blot analysis.Results: The results reveal that extracted compounds increased the release of cytochrome c and upregulating the expression of Bax and caspase-9 as concentration increases in a dose-dependent manner.Conclusion: The study suggests that the vanillin compound extracted from these millets induces apoptotic cell death through a mitochondria-dependent pathway.


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