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Eun Hye Kim [1] and Seungho Baek [2] and Daiha Shin [1] and Jaewang Lee [1] and Jong-Lyel Roh [1]

Academic Editor: Kum Kum Khanna

1, Department of Otolaryngology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Republic of Korea, ulsan.ac.kr

2, Department of Pathology, College of Korean Medicine, Woosuk University, Jeonju-si, Jeollabuk-do, Republic of Korea, woosuk.ac.kr

Received Aug 6, 2017; Revised Oct 19, 2017; Accepted Oct 23, 2017

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

1. Introduction

Resistance to chemotherapy is a major obstacle to treating human cancer. Cisplatin is one of the most widely used chemotherapeutic agents in the treatment of various types of solid neoplasms [1]. Cisplatin is currently used as a first-line agent for the treatment of various cancers, including head and neck cancer (HNC), in combination with other anticancer chemotherapeutic agents and/or radiation therapy [1, 2]. However, cisplatin is commonly associated with acquired resistance and increased toxicity, leading to poor tolerance and treatment outcomes [3, 4]. HNC, the eighth most common cancer globally, typically manifests in the oral/nasal cavity, pharynx, and larynx of the upper aerodigestive tract [5, 6]. A combined approach of surgery, radiotherapy, and chemotherapy is commonly used to treat HNC. Nonsurgical chemoradiotherapy has increasingly been used as an organ-preserving treatment for patients with HNC [7, 8]. Recent advances in cancer therapy have improved treatment outcomes; however, survival outcomes in patients with treatment-resistant HNC remain poor. Therefore, improving HNC treatment outcomes requires the development of novel approaches to treat chemotherapy-resistant cancers and identify more effective anticancer agents [7, 9].

Transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2) plays a key role in regulating cellular redox homeostasis because its promoter binds to target genes containing the antioxidant response element (ARE) [10]. Cancer cells buffer cellular reactive oxygen species (ROS) levels by actively upregulating antioxidant pathways, including the Nrf2 pathway, that contribute to cancer therapy resistance [11, 12]. Cellular metabolic pathways and antioxidant defense systems are commonly altered in treatment-resistant cancer cells exposed to high levels of oxidative stress [12, 13]. This metabolic alteration might represent a critical weakness that can be used as a...

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