scholarly journals Comparison of Cantharidin Toxicity in Breast Cancer Cells to Two Common Chemotherapeutics

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Katie M. Kern ◽  
Jennifer R. Schroeder
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Cell Viability Assay ◽  
Chemotherapy Drugs ◽  
Viability Assay ◽  
Systemic Side Effects ◽  
High Level ◽  
Cancerous Cells

As part of a larger study synthesizing a more directed form of chemotherapy, we have begun to assess the efficacy of different potential toxins that could be delivered locally rather than systemically. In doing so, we hope to reduce the systemic side effects commonly observed, while maintaining a high level of toxicity and eliminating the need for metabolic alterations. In a search for this more efficient method for killing cancerous cells, we have begun studying cantharidin, a toxin used in traditional Chinese medicine, as a potential chemotherapeutic. Using an MTT cell viability assay, the toxicity of cantharidin was compared to both cyclophosphamide and paclitaxel in three different breast cancer cell lines: MCF-7, MDA-MB-231, and SK-BR-3. Increasing the concentration of chemotherapy drugs did decrease cell viability in all cell lines when cantharidin and cyclophosphamide were applied; however differences for paclitaxel were cell-specific. Additionally, cantharidin exhibited the highest decrease in cell viability regardless of cell type, indicating it may be a much more potent and less specific chemotherapeutic. These results will help us move forward in developing a potentially more potent treatment for breast cancer that might eliminate the need for subtype-specific treatments.

Characteristics of the combination paclitaxel plus doxorubicin in breast cancer cell lines analyzed with the ATP-Cell Viability Assay

1993 ◽  
Vol 28 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Ossi R. Koechli ◽  
Bernd-Uwe Sevin ◽  
James P. Perras ◽  
Ting Chao Chou ◽  
Roberto Angioli ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Cell Viability Assay ◽  
Viability Assay

Comparative Chemosensitivity Profiles in Three Human Breast Cancer Cell Lines with the ATP-Cell Viability Assay

Oncology ◽  
1994 ◽  
Vol 51 (6) ◽  
pp. 552-558 ◽  
Author(s):  
Ossi R. Koechli ◽  
Bernd-Uwe Sevin ◽  
James P. Perras ◽  
Roberto Angioli ◽  
Michael Untch ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cell Lines ◽  
Breast Cancer Cell ◽  
Human Breast Cancer ◽  
Human Breast Cancer Cell ◽  
Breast Cancer Cell Lines ◽  
Human Breast ◽  
Cell Viability Assay ◽  
Viability Assay

Comparison of paclitaxel and docetaxel (Taxotere) in gynecologic and breast cancer cell lines with the ATP–cell viability assay

1994 ◽  
Vol 5 (1) ◽  
pp. 24-30 ◽  
Author(s):  
Michael Untch ◽  
Andrea Untch ◽  
Bernd-Uwe Sevin ◽  
Roberto Angioli ◽  
James P Perras ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines ◽  
Cell Viability Assay ◽  
Viability Assay

Synthesis and Antitumor Activity of Some N2-(Thien-3-yl)amidrazones

2014 ◽  
Vol 69 (7) ◽  
pp. 811-816 ◽  
Author(s):  
Mohammed M. Abadleh ◽  
Mustafa M. El-Abadelah ◽  
Salim S. Sabri ◽  
Hanan H. Mohammed ◽  
Malek A. Zihlif ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Antitumor Activity ◽  
Cell Viability ◽  
Cell Lines ◽  
K562 Cell ◽  
Cyclic Amine ◽  
Cell Viability Assay ◽  
Viability Assay ◽  
A Cell ◽  
Mcf 7

6aA set of new N2-(thien-3-yl)amidrazones (-h) incorporating N-piperazines and related congeners has been synthesized by reacting the hydrazonoyl chloride 4(derived from 3-aminothiophene- 2-carboxylate) with the appropriate sec-cyclic amine. The antitumor activity of these compounds was evaluated on breast cancer (MCF-7) and leukemic (K562) cell lines by a cell viability assay utilizing the tetrazolium dye (MTT). The amidrazone 6d encompassing the N-piperazine moiety, was the most active against MCF-7 and K562 with IC50 of 7.28 and 9:91 μM, respectively.

scholarly journals Effect of Astaxanthin on cell viability in T-47D and MDA-MB-231 Breast Cancer Cell Lines

2017 ◽  
Vol 1 (Supplementary 1) ◽  
pp. 0-0 ◽  
Author(s):  
Aida Karimian ◽  
Mohammad Hadi Bahadori ◽  
Akbar Hajizadeh Moghaddam ◽  
Fereshteh Mir Mohammadrezaei
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Cancer Cell Lines ◽  
Breast Cancer Cell Lines

scholarly journals Cisplatin-resistant HepG2 cell-derived exosomes transfer cisplatin resistance to cisplatin-sensitive cells in HCC

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11200
Author(s):  
Zuxiong Tang ◽  
Jun He ◽  
Jiayue Zou ◽  
Shufei Yu ◽  
Xiaoming Sun ◽  
...  
Keyword(s):  
Treatment Group ◽  
Cell Viability ◽  
Hepg2 Cells ◽  
Cisplatin Resistance ◽  
Resistant Cell ◽  
Resistant Cell Line ◽  
Cell Viability Assay ◽  
Chemotherapy Drugs ◽  
Viability Assay ◽  
Huh7 Cells

Backgrounds Cancer cell resistance to chemotherapy drugs such as Gemcitabine, Oxaliplatin, Cisplatin, Doxorubicin, and 5-fluorouracil account for the main reason of chemotherapy failure for HCC patients, especially for those with advanced HCC or metastasis patients. This emerging resistance limits the effectiveness and clinical application of these chemotherapy drugs. Previous studies reported that drug-resistant tumor cell-derived exosomes could transfer their resistance property to tumor sensitive cells in some cancer, including lung and gastric cancer. This study sought to explore whether HepG2/DDP cell-derived exosomes transmit cisplatin (DDP) resistance to HepG2 and other HCC sensitive cells, and provide considerable guidance for HCC nursing with Cisplatin DDP clinically. Methods The HepG2 DDP-resistant cell line (HepG2/DDP) was established, and the exosomes from both HepG2/DDP and HepG2 cells were isolated and named ES-2, ES-1, respectively. HepG2 or SMMC-7721 or Huh7 cells were treated with DDP or DDP + ES-2, and HepG2/DDP cells were treated with ES-1. Then, the activation of drug resistance via HepG2/DDP exosomes transfer to HepG2, SMMC-7721 and Huh7 cells were assessed by cell viability assay and ROS formation. Moreover, the relative expression of P-glycoprotein (P-gp) was measured by western blot analysis. Results HepG2/DDP cell-derived exosomes were successfully isolated from cisplatin-resistant HepG2 cells, and named ES-2. Cell viability of HepG2 or SMMC-7721 or Huh7 cells treated with DDP + ES-2 was enhanced compared with that of DDP treatment group. Also, the concentration of ROS generated in cells under DDP or DDP + ES-2 treatment was strongly increased compared with that of control, although the concentration of ROS was clearly smaller in DDP + ES-2 treatment group compared with DDP treatment. At the same time, the expression of P-gp was upregulated on the ES-2 surface. Conclusion The results mentioned above clarified that HepG2/DDP cell-derived exosomes conferred cisplatin resistance to HepG2 and other HCC cell lines, and provided a new significance for improving the effectiveness of DDP in treating HCC.

Determination of Vulpinic Acid Effect on Apoptosis and mRNA Expression Levels in Breast Cancer Cell Lines

2019 ◽  
Vol 18 (14) ◽  
pp. 2032-2041 ◽  
Author(s):  
Nil Kılıç ◽  
Sümer Aras ◽  
Demet Cansaran-Duman
Keyword(s):  
Breast Cancer ◽  
Cell Viability ◽  
Cancer Cells ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Breast Cancer Cell ◽  
Breast Cancer Cells ◽  
Breast Cancer Cell Lines ◽  
Human Breast

Objective: Breast cancer is one of the most common diseases among women worldwide and it is characterized by a high ratio of malignancy and metastasis and low rate of survival of patients. Due to limited treatment options, the discovery of alternative therapeutic agents and clarifying the molecular mechanism of breast cancer development may offer new hope for its treatment. Lichen secondary metabolites may be one of these therapeutic agents. Methods: In this study, the effects of Vulpinic Acid (VA) lichen secondary metabolite on the cell viability and apoptosis of breast cancer cells and non-cancerous cell line were investigated. Quantitative polymerase chain reaction was also performed to determine changes in the expression of apoptosis-related genes at a molecular level. Results: The results demonstrated that VA significantly inhibited the cell viability and induced apoptosis of human breast cancer cells. The highest rates of decreased growth were determined using the IC50 value of VA for 48h on MCF-7 breast cancer cell. Interestingly, VA treatment significantly reduced cell viability in all examined breast cancer cell lines compared to their non-cancerous human breast epithelial cell line. This is the first study on the investigation of the effects of VA on the molecular mechanisms associated with the expression of apoptosis-related genes in breast cancer cell lines. Results demonstrated that the gene expression of P53 genes was altered up to fourteen-fold levels in SK-BR-3 cell lines whereas it reached 2.5-fold in the MCF-12A cell line after treatment with VA. These observations support that VA induces apoptosis on the breast cancer cells compared with the non-cancerous human breast epithelial cell line. Conclusion: It is implicated that VA may be a promising novel molecule for the induction of apoptosis on breast cancer cells.

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