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11/19/2018 - 11:13 | Science External News

Korean publication appeared in the International Journal of Hyperthermia

To link to this article

Title: Combined treatment with modulated electrohyperthermia and an autophagy inhibitor effectively inhibit ovarian and cervical cancer growth

Authors: Wookyeom Yang, Gwan Hee Han, Ha-Yeon Shin, Eun-Ju Lee, Hanbyoul Cho, Doo Byung Chay & Jae-Hoon Kim

Published online: 14 Nov 2018., International Journal of Hyperthermia

 

ABSTRACT

Purpose:
Modulated electro-hyperthermia (mEHT), known as oncothermia, is an anticancer therapy that induces radiofrequency thermal damage to the cancer tissues. This study aimed to evaluate the potential effectiveness of mEHT as a therapeutic tool in ovarian and cervical cancer.

Materials and methods:
We used both tumor-bearing mice and ovarian and cervical OVCAR-3, SKOV-3, HeLa and SNU-17 cancer cell lines to investigate the effects of mEHT in vivo and in vitro, respectively, and determine whether it was enhanced by cotreatment with an autophagy inhibitor.

Results:
We discovered that phosphorylation of p38, a stress-dependent kinase, was induced at the Thr180/Tyr182 residue in cancer cells exposed to mEHT. Apoptotic markers such as cleaved caspase-3 and poly-ADP ribose polymerase (PARP) were increased in OVCAR-3 and SNU-17 cells. Fluorescenceactivated cell sorting (FACS) analysis showed a significant increase in the population of sub-G1 mEHTexposed cells, which are dying and apoptotic cells. mEHT also reduced both weight and volume of xenograft tumors in mice transplanted with ovarian and cervical cancer cells and patient-derived cancer tissues. We determined that mEHT-induced cellular damage recovery was mediated by autophagy
and, therefore, expectedly, cotreatment with mEHT and 3-methyladenine (3-MA), an autophagy inhibitor, more effectively inhibited cancer cell growth than individual treatment did.

Conclusions:
mEHT treatment alone was sufficient to inhibit cancer growth, while a combined treatment with mEHT and an autophagy inhibitor amplified this inhibition effect.