Expression analysis of TOP2A, MSH2 and MLH1 genes in MCF7 cells at different levels of etoposide resistance

Kaplan, Esra
Gündüz, Ufuk
Purpose: Development of resistance against anti-cancer drugs is one of the major obstacles of chemotherapy in the treatment of cancer. Etoposide is a topoisomerase II alpha (TOP2A) inhibitor, which is used in the treatment of breast cancer. Alterations in the expression of drug targets or DNA repair genes are among the important resistance mechanisms against TOP2A inhibitors. In this study, expression changes in TOP2A gene and two important mismatch repair (MMR) genes MSH2 and MLH1 were examined in order to understand the relationship between differential expression of these genes and drug resistance against etoposide.


Reversal of breast cancer resistance protein mediated multidrug resistance in MCF7 breast adenocarcinoma cell line
Urfalı, Çağrı; Gündüz, Ufuk; Department of Biology (2011)
Resistance to various chemotherapeutic agents is a major problem in success of cancer chemotherapy. One of the primary reasons of development of multidrug resistance (MDR) is the overexpression of ATP binding cassette (ABC) transporter proteins. Breast cancer resistance protein (BCRP) belongs to ABC transporter family and encoded by ABCG2 gene. BCRP is mainly expressed in MDR1 (P-glycoprotein) lacking breast cancer cells. Overexpression of BCRP leads to efflux of chemotherapeutic agents at higher rates, the...
Development and investigation of etoposide resistance in MCF-7 Breast cancer cell line
Kaplan, Esra; Gündüz, Ufuk; Department of Biology (2010)
Failure of chemotherapy in cancer patients because of development of drug resistance is a major problem. Alterations of DNA repair mechanisms and drug targets are among the important resistance mechanisms which are developed against topoisomerase II inhibitors etoposide and doxorubicin. Modifications in the expression levels of mismatch repair (MMR) genes due to resistance to topoisomerase II inhibitors are involved in breast cancer. In this study, etoposide resistant sublines were developed from MCF7 breas...
Synthesis of poly (dl-lactic-co-glycolic acid) coated magnetic nanoparticles for anti-cancer drug delivery
Tansık, Gülistan; Gündüz, Ufuk; Department of Biology (2012)
One of the main problems of current cancer chemotherapy is the lack of selectivity of anti-cancer drugs to tumor cells which leads to systemic toxicity and adverse side effects. In order to overcome these limitations, researches on controlled drug delivery systems have gained much attention. Nanoscale based drug delivery systems provide tumor targeting. Among many types of nanocarriers, superparamagnetic nanoparticles with their biocompatible polymer coatings can be targeted to an intented site by an extern...
Etoposide resistance in MCF-7 breast cancer cell line is marked by multiple mechanisms
Alpsoy, Aktan; Yasa, Seda; Gündüz, Ufuk (2014-04-01)
Purpose: Acquired or intrinsic drug resistance is one of the major handicaps in the success of chemotherapy. Etoposide is a topoisomerase II poison widely used in chemotherapy. Similar to other topoisomerase inhibitors and DNA damaging agents, resistance to etoposide may arise as a result of alterations in target expression and activity, increased drug efflux and alterations in DNA damage response mechanisms. Here, we tested the involvement of such mechanisms in etoposide-resistant MCF-7 breast cancer cells.
Role of ABCB1 and ABCC1 Gene Induction on Survival in Locally Advanced Breast Cancer
Atalay, C.; DEMİRKAZIK, AHMET; Gündüz, Ufuk (2008-12-01)
Drug resistance to chemotherapy in patients with locally advanced breast cancer results in a decrease in treatment efficacy and in patient survival. This study aimed to evaluate the impact of ABCB1 and ABCC1 gene induction during chemotherapy on disease-free and overall survival of breast cancer patients.
Citation Formats
E. Kaplan and U. Gündüz, “Expression analysis of TOP2A, MSH2 and MLH1 genes in MCF7 cells at different levels of etoposide resistance,” BIOMEDICINE & PHARMACOTHERAPY, pp. 29–35, 2012, Accessed: 00, 2020. [Online]. Available: