Effet radiosensibilisateur de l'acide linoléique conjugué chez les cellules cancéreuses du sein MCF-7 et MDA-MB-231

2004 ◽  
Vol 82 (2) ◽  
pp. 94-102 ◽  
Author(s):  
Geneviève Drouin ◽  
Annie Douillette ◽  
Pierre Lacasse ◽  
Benoit Paquette
Keyword(s):  
Breast Cancer ◽  
Linoleic Acid ◽  
Cancer Cells ◽  
Conjugated Linoleic Acid ◽  
Breast Cancer Cells ◽  
Fold Increase ◽  
Breast Cancer Cell Lines ◽  
Apoptotic Pathways ◽  
Induced Apoptosis ◽  
Mcf 7

Apoptotic pathways in breast cancer cells are frequently altered, reducing the efficiency of radiotherapy. Conjugated linoleic acid (CLA), known to trigger apoptosis, was tested as radiosensitizer in breast cancer cells MCF-7 and MDA-MB-231. The CLA-mix, made up of the isomers CLA-9cis 11trans and CLA-10trans 12cis, was compared to three purified isomers, i.e., the CLA-9cis 11cis, CLA-9cis 11trans, and CLA-10trans 12cis. Using the apoptotic marker YO-PRO®-1, the CLA-9cis 11cis at 50 µmol/L turned out to be the best apoptotic inducer leading to a 10-fold increase in MCF-7 cells and a 2,5-fold increase in MDA-MB-231 cells, comparatively to the CLA-mix. Contrary to previous studies on colorectal and prostate cancer cells, CLA-10trans 12cis does not lead to an apoptotic response on breast cancer cell lines MCF-7 and MDA-MB-231. Our results also suggest that the main components of the CLA-mix (CLA-9cis 11trans and CLA-10trans 12cis) are not involved in the induction of apoptosis in the breast cancer cells studied. A dose of 5 Gy did not induce apoptosis in MCF-7 and MDA-MB-231 cells. The addition of CLA-9cis 11cis or CLA-mix has allowed us to observe a radiation-induced apoptosis, with the CLA-9cis 11cis being about 8-fold better than the CLA-mix. CLA-9cis 11cis turned out to be the best radiosensitizer, although the isomers CLA-9cis 11trans and CLA-10trans 12cis have also reduced the cell survival following irradiation, but using a mechanism not related to apoptosis. In conclusion, the radiosensitizing property of CLA-9cis 11cis supports its potential as an agent to improve radiotherapy against breast carcinoma.Key words: breast cancer, conjugated linoleic acid (CLA), radiotherapy, apoptosis.

Role of specific apoptotic pathways in the restoration of paclitaxel-induced apoptosis by valspodar in doxorubicin-resistant MCF-7 breast cancer cells

2000 ◽  
Vol 59 (3) ◽  
pp. 231-244 ◽  
Author(s):  
Antony Chadderton ◽  
David J. Villeneuve ◽  
Stefan Gluck ◽  
Angie F. Kirwan-Rhude ◽  
Brian R. Gannon ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Apoptotic Pathways ◽  
Induced Apoptosis ◽  
Mcf 7

Enhanced anticancer effect of conjugated linoleic acid by conjugation with Pluronic F127 on MCF-7 breast cancer cells

2007 ◽  
Vol 254 (2) ◽  
pp. 244-254 ◽  
Author(s):  
Ding-Ding Guo ◽  
Hyun-Seuk Moon ◽  
Rohidas Arote ◽  
Ji-Hye Seo ◽  
Ji-Shan Quan ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Linoleic Acid ◽  
Cancer Cells ◽  
Conjugated Linoleic Acid ◽  
Breast Cancer Cells ◽  
Pluronic F127 ◽  
Anticancer Effect ◽  
Mcf 7

scholarly journals Conjugated Linoleic Acid Induces Apoptosis by Activating AMPK in MCF-7 Breast Cancer Cells

2008 ◽  
Vol 18 (12) ◽  
pp. 1679-1685
Author(s):  
Sun-Kyo Lin ◽  
Hyun-Sook Kim ◽  
Ock-Jin Park ◽  
Young-Min Kim
Keyword(s):  
Breast Cancer ◽  
Linoleic Acid ◽  
Cancer Cells ◽  
Conjugated Linoleic Acid ◽  
Breast Cancer Cells ◽  
Mcf 7

PEGylation of Conjugated Linoleic Acid and its Application as an Anti-Cancer Prodrug

2007 ◽  
Vol 342-343 ◽  
pp. 441-444 ◽  
Author(s):  
Ji Hye Seo ◽  
Hyun Seuk Moon ◽  
Ding Ding Guo ◽  
Hong Gu Lee ◽  
Yun Jaie Choi ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Linoleic Acid ◽  
Cancer Cells ◽  
Conjugated Linoleic Acid ◽  
Breast Cancer Cells ◽  
Cancer Cell Proliferation ◽  
Anti Cancer ◽  
Ester Linkage ◽  
Poly Ethylene ◽  
Mcf 7

The objective of this study is to investigate whether the PEGylated conjugated linoleic acid (PCLA) as an anti-cancer prodrug can have favorable stability, biological activity, and prevention of proliferation in MCF-7 breast cancer cells for anti-cancer when compared with conjugated linoleic acid (CLA) itself. The CLA was simply coupled to poly(ethylene glycol) (PEG) at melting state without solvent or catalyst through ester linkage between carboxylic group of CLA and hydroxyl one of PEG. The results showed that the half life of PCLA was 55h in cell culture medium at pH 7.4 and 37°C. Apoptosis of MCF-7 breast cancer cells were induced by not only CLA- but PCLA-treatment with increasing concentrations whereas PCLA increased cell viability when compared with CLA itself. These results indicate that the PCLA is a more stable and valuable prodrug in that it has good stability and inhibition of cancer cell proliferation.

scholarly journals ARTEMISININ MODULATING EFFECT ON HUMAN BREAST CANCER CELL LINES WITH DIFFERENT SENSITIVITY TO CYTOSTATICS

2017 ◽  
Vol 39 (1) ◽  
pp. 25-29 ◽  
Author(s):  
V F Chekhun ◽  
N Yu Lukianova ◽  
T Borikun ◽  
T Zadvornyi ◽  
A Mokhir
Keyword(s):  
Breast Cancer ◽  
Drug Resistance ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Iron Homeostasis ◽  
Chemotherapeutic Agents ◽  
Fold Change ◽  
Breast Cancer Cell Lines ◽  
Cellular Iron ◽  
Mcf 7

Aim: To explore effects of Artemisinin on a series of breast cancer cells with different sensitivity to typical cytotoxic drugs (doxorubicin — Dox; cisplatin — DDP) and to investigate possible artemisinin-induced modification of the mechanisms of drug resistance. Materials and Methods: The study was performed on wild-type breast cancer MCF-7 cell line (MCF-7/S) and its two sublines MCF-7/Dox and MCF-7/DDP resistant to Dox and DDP, respectively. The cells were treated with artemisinin and iron-containing magnetic fluid. The latter was added to modulate iron levels in the cells and explore its role in artemisinin-induced effects. The MTT assay was used to monitor cell viability, whereas changes of expression of selected proteins participating in regulation of cellular iron homeostasis were estimated using immunocytochemical methods. Finally, relative expression levels of miRNA-200b, -320a, and -34a were examined by using qRT-PCR. Results: Artemisinin affects mechanisms of the resistance of breast cancer cells towards both Dox and DDP at sub-toxic doses. The former drug induces changes of expression of iron-regulating proteins via different mechanisms, including epigenetic regulation. Particularly, the disturbances in ferritin heavy chain 1, lactoferrin, hepcidin (decrease) and ferroportin (increase) expression (р ≤ 0.05) were established. The most enhanced increase of miRNA expression under artemisinin influence were found for miRNA-200b in MCF-7/DDP cells (7.1 ± 0.98 fold change), miRNA-320a in MCF-7/Dox cells (2.9 ± 0.45 fold change) and miRNA-34a (1.7 ± 0.15 fold change) in MCF-7/S cells. It was observed that the sensitivity to artemisinin can be influenced by changing iron levels in cells. Conclusions: Artemisinin can modify iron metabolism of breast cancer cells by its cytotoxic effect, but also by inducing changes in expression of iron-regulating proteins and microRNAs (miRNAs), involved in their regulation. This modification affects the mechanisms that are implicated in drug-resistance, that makes artemisinin a perspective modulator of cell sensitivity towards chemotherapeutic agents in cancer treatment.

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