The Effects of Cisplatin on MTOR, AKT, CCND1 and STAT3 mRNA Expressions on HeLa Cells
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Original Investigation
P: 5-9
January 2020

The Effects of Cisplatin on MTOR, AKT, CCND1 and STAT3 mRNA Expressions on HeLa Cells

GMJ 2020;31(1):5-9
1. Giresun Üniversitesi, Tıp Fakültesi, Tıbbi Biyoloji Anabilim Dalı, Giresun, Türkiye
2. Hitit Üniversitesi, Tıp Fakültesi, Tıbbi Biyoloji Anabilim Dalı, 19030, Corum, Türkiye
3. Gazi Üniversitesi, Tıp Fakültesi, Tıbbi Biyoloji ve Genetik Anabilim Dalı, 06510, Beşevler, Ankara, Türkiye
No information available.
No information available
Received Date: 30.06.2018
Accepted Date: 28.08.2019
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ABSTRACT

Objective:

Cervical cancer is one of the most tumors seen in womans and second leading cause of cancer death in women. Cisplatin (CDDP), a platin based compound, is the most important chemotherapeutic agent and effectively used for the treatment of sarcomas and solid tumors. It binds to the DNA with crosslinks and leads inhibition of replication, causing DNA damage. As a result of this action, apoptotic pathways are induced and cell death occurs. In our study, we aimed to investigate the effect of CDDP on relative mRNA expression of mTOR, AKT, Cyclin D1 (CCND1) ve STAT3 on cervical cancer cell line.

Method:

In this study, HeLa cells were treated with different concentrations of CDDP at 24 and 48 hours. Cell viability was determined by XTT method. Moreover, after treatment with selected doses of cisplatin, quantitative mRNA expression of mTOR, AKT, CCND1 and STAT-3 genes was analyzed using Real-Time PCR.

Results:

IC50 concentration of CDDP was found to be about 60 μM for 24h and 8 μM for 48h treatment. Moreover, all analyzed genes’ expression was shown to diminish only after 24 h treatment. On the other hand, no statistically significant change was found after 48 h cisplatin exposure with respect to quantitative mRNA expression.

Conclusion:

In summary, different mRNA expression pattern was found after CDDP treatment regarding to exposure time. Our study has been contributed the literature in terms of detecting the effect of conventional chemotherapeutic CDDP on cell survival pathways.