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Author Notes:

Correspondence: Kazim Sahin, Firat University Veterinary Faculty, Elazıg 23119, Turkey. E-mail: nsahinkm@yahoo.com; ksahin@firat.edu.tr

The project was designed and implemented by Ulkan Kilic and Kazim Sahin.

Data were analyzed by Mehmet Tuzcu, Nazli Basak, Cemal Orhan, Birsen Elibol-Can, Ertugrul Kilic, Fikrettin Sahin, and Omer Kucuk.

Ulkan Kilic prepared the manuscript.

Ulkan Kilic and Kazim Sahin supervised overall project.

All authors read and approved the final version of manuscript.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

The reviewer Mustafa Ozen declares that, despite having collaborated with the author Fikrettin Sahin, the review process was handled objectively and no conflict of interest exists.


Research Funding:

This study was supported by grants from Turkish Academy of Sciences (TUBA).


  • HeLa cells
  • cisplatin
  • epigallocatechin gallate
  • human cervical cancer
  • sensitization

Enhancement of Cisplatin sensitivity in human cervical cancer: epigallocatechin-3-gallate.


Journal Title:

Frontiers in Nutrition


Volume 1


Type of Work:

Article | Final Publisher PDF


Cisplatin is one of the effective chemotherapeutics in the treatment of several types of cancers. However, in addition to the efforts against to its toxicity, the amelioration of cisplatin sensitivity is an important point in treatment of cervical cancer. To do so, additional substances such as epigallocatechin gallate (EGCG), a polyphenol in green tea, have been used in combination with chemotherapeutics. We aimed to investigate the possible molecular pathways to potentiate cervical cancer cell (HeLa) growth inhibition by combination therapy of cisplatin and EGCG. HeLa cells were treated with EGCG (25 μM), cisplatin (250 nM), and their combination for 24 h. Cell viability was determined by MTS Assay. We analyzed the expressions of NF-κB p65, COX-2, Nrf2, HO-1, p-mTOR, p-p70S6K1, p-4E-BP1, and p-Akt by Western blot analysis. Herein, we have demonstrated that EGCG works synergistic with cisplatin in inhibiting growth of cervical cancer cells. EGCG improved efficacy of cisplatin treatment in HeLa cells by regulating NFκB p65, COX-2, p-Akt, and p-mTOR pathways, whereas it increased the expression levels of Nrf2/HO-1 in combined therapy. Our observations revealed that EGCG increases the sensitization of cisplatin to cervical cancer cells by inhibiting cell survival and inducing apoptosis.

Copyright information:

© 2015 Kilic, Sahin, Tuzcu, Basak, Orhan, Elibol-Can, Kilic, Sahin and Kucuk.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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