PhD Scientific Days 2020

Budapest, 31 August-1 September 2020

Molecular Sciences III. Posters

The Killing Effect of Modulated Electro-hyperthermia on B16F10 Melanoma Cells

Előadó neve

Dr. Major, Enikő

Előadó munkahelye

Institute of Translational Medicine, Semmelweis University, Budapest, Hungary

Előadó telefonszáma

+36305342593

Előadó e-mail címe

major.eniko@med.semmelweis-univ.hu

Az előadás címe

The Killing Effect of Modulated Electro-hyperthermia on B16F10 Melanoma Cells

Szerző(k) neve és munkahelye

Enikő Major1, Anett Benedek1, Balázs Besztercei1, Zoltán Benyó1, Andrea Balogh1
1 Institute of Translational Medicine, Semmelweis University, Budapest, Hungary

Szekció

Molecular Sciences III. Posters

Language of the presentation

Hungarian

Section, first choice

Molecular Sciences

Section, second choice

Pathology and Oncology

Összefoglaló szövege

Introduction and aims: Modulated electro-hyperthermia (mEHT) is a novel adjuvant, non- invasive form of tumor treatment which induces tumor-selective heat shock at 42 ºC. The objective of the present study was to examine the effect of mEHT on B16F10 mouse melanoma cell line in vitro. Our aim was to detect the effect of mEHT on cell viability and to examine if hyperthermia can augment the cell killing effect of various chemotherapeutic agents.
Methods: B16F10 melanoma cells were grown on coverslips, treated with mEHT using LabEHY 100 (Oncotherm Ltd.) at 42ºC. To define the optimal dose of hyperthermia the cells were treated for 30, 60, 90 or 120 minutes. Cell viability was measured by cell titer blue and apoptosis by Annexin-V/ 7-AAD staining using flow cytometry 24 hours post-treatment. For analyzing gene expression cells were harvested 1, 3, 9, 24 hours after 60 minutes mEHT. In combined protocols, after 60 minutes mEHT cells were treated with dacarbazine (40 µM), paclitaxel (40 nM) or nutlin-3a (10 µM). Cell viability as well as cleaved caspase-3 as an indicator of apoptosis were detected by flow cytometry 48 hours after mEHT.
Results: Three hours after the treatment the peak levels of HSPA2 expression were 3 times higher as compared to the untreated control in a time-matched experiment. Next, we showed that in parallel to the upregulation of pro-apoptotic genes Puma, Bak-1, Bax, and downregulation of pro-survival genes XIAP, Bcl-2, Bcl-XL were induced by mEHT. In combination with chemotherapy, mEHT augmented the cell killing effect of dacarbazine or nutlin-3a but it had no effect on paclitaxel- induced cell death 48 hours post-treatment.
Conclusion: mEHT induced nuclear translocation of p53 which in turn regulates pro- and anti-apoptotic gene expression accounting for the upregulation of apoptotic genes and decreased cell viability. The sensitizing effect on chemotherapeutics demonstrate the efficiency as an adjuvant modality in cancer treatment.
Grants: This study was supported by NVKP 16-1-2016-0042 grant and by the Richter Gedeon Talentum Foundation.

Additional Information

Supervisor: Zoltán Benyó
E-mail address: benyo.zoltan@med.semmelweis-univ.hu

Bemutatás módja

Poszter

Kind

Szabad

Status

elfogadva

Accepted presentation method

poszter

Előadás fájl jóváhagyás

nem rendelkezett róla

Előadó

4810

Start

11:13

End

11:16

Authors (legacy)

Enikő Major1, Anett Benedek1, Balázs Besztercei1, Zoltán Benyó1, Andrea Balogh1
1 Institute of Translational Medicine, Semmelweis University, Budapest, Hungary