J. Zafari , F. Javani Jouni , M. Satari Keykaleh , P. Abdolmaleki , M.j. Khodayar , A. Jalali ,
Volume 9, Issue 4 (12-2018)
Abstract
Aims: Regarding the treatment of cancer, due to the limitation in the use of high dose and resistance of cancer cells, it is necessary to use optimal methods that have high therapeutic efficacy and reduce the dose of radiation and medicine. The aim of the present research was to investigate toxicity of cisplatin under the influence of static magnetic field in susceptible and drug-resistant cell.
Materials and Methods: In the present experimental study, A2780-CP resistant cell classes and susceptible to A2780 cisplatin were investigated in the field and drug-treated cell groups compared to the drug-receiving group alone, and to determine the effect of static magnetic field and concentration of drug, 10mT for 24 hours and logarithmic drug concentration (1, 10, 50, 100, and 500mcg/ml) were used. Inhibitory concentration of 50% cell growth (IC50) was obtained for the cells in the absence and presence of the magnetic field after conversion of the absorption obtained in the ELISA from the MTT test to cytotoxicity percentage. Data were analyzed with Prism software using two-way ANOVA and T-test.
Findings: In the presence of a static magnetic field and different drug concentrations, a greater reduction in the percentage of In vivo cells was observed. IC50 values for A2780 cells in the absence and presence of magnetic fields were 27.69±9.58 and 8.96±1.48μg/ml for A2780-CP, and 61.61±8.03 and 9.58±3.13μg/ml, respectively.
Conclusion: The mortality rate of the cells treated with cisplatin under the influence of the magnetic field is more in susceptible and drug-resistant cells than that of only drug use. Drug-resistance decreases in the drug-resistant cell class in the presence of a magnetic field.
Zeinab Karbalaei Pazoki, Amir Reza Javanmard, Sayed Mostafa Hosseini, Shiva Irani, Bahram Mohammad Soltani,
Volume 14, Issue 1 (3-2023)
Abstract
Resistance to chemotherapy drugs always has been an obstacle in the definitive treatment of cancers. Therefore, the discovery of molecular events leading to drug resistance improves therapeutic methods. Non-coding RNAs (ncRNAs) are a group of molecules that regulate intracellular events, including carcinogenesis and drug resistance pathways. For example, the competitive network of endogenous ncRNAs (ceRNA) regulates the mRNA expression of target genes by binding to miRNAs and limiting their regulatory effect. So far, limited studies have been reported on the role of ceRNA in drug resistance in ovarian cancer. In this study, large-scale RNAseq sequencing data obtained from cisplatin-resistant and sensitive cells were used to search for ceRNAs that are possible regulators of drug resistance in ovarian cancer. For this purpose, the A2780 sensitive and resistant cisplatin ovarian cancer cell line was selected, and the SRA data prepared by RNAseq method was screened. During this process, lncRNAs, microRNAs and mRNAs with expression changes were separated and classified. In the bioinformatic analysis of resistant and sensitive cells, 16 mRNAs, 10 lncRNAs, and 149 miRNAs were overexpressed, and 622 mRNAs, 263 lncRNAs, and 177 miRNAs were underexpressed. These genes were involved in 57 cellular pathways, and by mapping the regulatory ceRNA network, ZNRF3-AS1-miR-33-DUSP1 and ZNRF3-AS1-miR33-HSPA2 axes were identified as potential ceRNA networks involved in cisplatin-resistant ovarian cancer.
Volume 15, Issue 4 (2-2013)
Abstract
Objective: Breast cancer is the second leading cause of cancer death in women. Cisplatin is a traditional cancer drug commonly used in chemotherapy for killing cancer cells. Modulation at the mRNA levels of apoptotic related genes often correlate with the sensitivity of various types of cancer cells to chemotherapeutic agents. Nanoparticulate drug delivery systems are being developed to effectively deliver smaller doses of chemotherapeutic agents and control drug distribution in the body. In this study, we evaluate the expressions of BCL2 and BAX genes in T47D treated with cisplatin and cisplatin nanoparticles, which can result in a new approach to breast cancer therapy.
Methods: In this study, we treated T47D cells with different concentrations of cisplatin and cisplatin nanoparticles at 48 h. The IC50 was determined. We extracted RNA by using RNX solution, after which cDNA was synthesized. The precise primers for the BCL2, BAX and TBP genes were designed by specific software. The quantity of BCL2 and BAX gene expression compared to TBP gene (reference gene) was analyzed using real-time PCR.
Results: BCL2 and BAX gene expression levels in T47D cells treated by cisplatin were 0.7 (BCL2) and 1.48 (BAX); in T47D cells treated with cisplatin-loaded nanoparticles, the gene expressions were 0.03 (BCL2) and 2.41 (BAX).
Conclusion: In this study, the results have shown that cisplatin-loaded nanoparticles are effective anticancer agents. Cisplatin nanoparticles induce apoptosis in human breast cancer cell lines. We have shown that cisplatin nanoparticles strongly increased cytotoxicity in comparison to the free drug in the T47D cell line.
