Abstract

The biological function of non-thermal atmospheric pressure plasma has been widely accepted in several types of cancer. We previously developed plasma-activated medium (PAM) for clinical use, and demonstrated that PAM exhibits a metastasis-inhibitory effect on ovarian cancer through reduced MMP-9 secretion. However, the anti-tumor effects of PAM on endometrial cancer remain unknown. In this study, we investigated the inhibitory effect of PAM on endometrial cancer cell viability in vitro. Our results demonstrated that AMEC and HEC50 cell viabilities were reduced by PAM at a certain PAM ratio, and PAM treatment effectively increased autophagic cell death in a concentration dependent manner. In addition, we evaluated the molecular mechanism of PAM activity and found that the mTOR pathway was inactivated by PAM. Moreover, our results demonstrated that the autophagy inhibitor MHY1485 partially inhibited the autophagic cell death induced by PAM treatment. These findings indicate that PAM decreases the viability of endometrial cancer cells along with alteration of the mTOR pathway, which is critical for cancer cell viability. Collectively, our data suggest that PAM inhibits cell viability while inducing autophagic cell death in endometrial cancer cells, representing a potential novel treatment for endometrial cancer.

Highlights

  • The biological function of non-thermal atmospheric pressure plasma has been widely accepted in several types of cancer

  • Our results demonstrated that AMEC and HEC50 cell viabilities were reduced by plasma-activated medium (PAM) at a certain PAM ratio, and PAM treatment effectively increased autophagic cell death in a concentration dependent manner

  • These findings indicate that PAM decreases the viability of endometrial cancer cells along with alteration of the mTOR pathway, which is critical for cancer cell viability

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Summary

Introduction

The biological function of non-thermal atmospheric pressure plasma has been widely accepted in several types of cancer. Our results demonstrated that the autophagy inhibitor MHY1485 partially inhibited the autophagic cell death induced by PAM treatment. These findings indicate that PAM decreases the viability of endometrial cancer cells along with alteration of the mTOR pathway, which is critical for cancer cell viability. Our colleagues reported that the intraperitoneal administration of PAM effectively inhibits the peritoneal dissemination of gastric cancer and ovarian cancer in a mouse model, which may be applicable in clinical situations[14]. Induction of autophagic cell death by small molecules contributes to the enhancement of anti-tumor activity of chemotherapy or radiation therapy, whereas autophagy-dependent anti-apoptotic responses induced by chemotherapy have negative impacts on anti-tumor treatment through inhibition of the mTOR pathway[17,18]. No association between anti-tumor effects of PAM and autophagy has been reported

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