Fatemeh Valinezhad Sani, Safa Kamalian, Hakim H Abdi, Shiva Ghofrani, Arad Boustan, F. Mosaffa
{"title":"Fucoxanthin inhibits the proliferation of ABCC2-over expressing cisplatin-resistance ovarian cancer cells via inducing apoptosis","authors":"Fatemeh Valinezhad Sani, Safa Kamalian, Hakim H Abdi, Shiva Ghofrani, Arad Boustan, F. Mosaffa","doi":"10.34172/ps.2022.44","DOIUrl":null,"url":null,"abstract":"Background: The development of multidrug resistance (MDR) is a major barrier to achieving effective chemotherapy in cancer. Studies have shown that epithelial ovarian cancer initially responds to platinum-based therapy, however, the recurrent type is often resistant to treatment and is associated with high mortality. Fucoxanthin, a natural component found in marine algae, possesses various pharmacologic properties. This study evaluated the cytotoxicity and resistance reversal activity of fucoxanthin on multidrug resistance-associated protein 2 (MRP2)-overexpressing, cisplatin-resistant ovarian cancer cells (A2780RCIS) and their parental cells (A2780). Methods: Cell viability was evaluated in the presence of different concentrations of fucoxanthin or cisplatin or fucoxanthin/cisplatin combination using the MTT assay. Propidium iodide staining and sub-G1 analysis were used to evaluate fucoxanthin potential for cell cycle modification and apoptosis induction in cancer cell lines. Results: The results showed that fucoxanthin was able to cause similar cell toxicity in both cell lines via apoptosis induction. Co-treatment of cells with cisplatin (3.125 to 100 µM) and nontoxic concentrations of fucoxanthin (1 and 2.5 µM) did not reverse resistance to cisplatin in A2780RCIS cells. Conclusion: Although fucoxanthin was not able to modify cisplatin-resistance in ovarian cancer cells, it was equally effective in inducing apoptosis and death in both A2780 and A2780RCIS cells indicating it is not an MRP2 substrate.","PeriodicalId":31004,"journal":{"name":"Infarma Pharmaceutical Sciences","volume":"5 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Infarma Pharmaceutical Sciences","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.34172/ps.2022.44","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"Pharmacology, Toxicology and Pharmaceutics","Score":null,"Total":0}
引用次数: 0
Abstract
Background: The development of multidrug resistance (MDR) is a major barrier to achieving effective chemotherapy in cancer. Studies have shown that epithelial ovarian cancer initially responds to platinum-based therapy, however, the recurrent type is often resistant to treatment and is associated with high mortality. Fucoxanthin, a natural component found in marine algae, possesses various pharmacologic properties. This study evaluated the cytotoxicity and resistance reversal activity of fucoxanthin on multidrug resistance-associated protein 2 (MRP2)-overexpressing, cisplatin-resistant ovarian cancer cells (A2780RCIS) and their parental cells (A2780). Methods: Cell viability was evaluated in the presence of different concentrations of fucoxanthin or cisplatin or fucoxanthin/cisplatin combination using the MTT assay. Propidium iodide staining and sub-G1 analysis were used to evaluate fucoxanthin potential for cell cycle modification and apoptosis induction in cancer cell lines. Results: The results showed that fucoxanthin was able to cause similar cell toxicity in both cell lines via apoptosis induction. Co-treatment of cells with cisplatin (3.125 to 100 µM) and nontoxic concentrations of fucoxanthin (1 and 2.5 µM) did not reverse resistance to cisplatin in A2780RCIS cells. Conclusion: Although fucoxanthin was not able to modify cisplatin-resistance in ovarian cancer cells, it was equally effective in inducing apoptosis and death in both A2780 and A2780RCIS cells indicating it is not an MRP2 substrate.