Anticancer Effects of Arsenic Compounds in Non-Small Cell Lung Cancer

Non-small cell lung cancer (NSCLC) is the most common and prevalent subtype of lung cancer and continues to be one of the leading causes of cancer-related deaths worldwide. Despite various treatment options, a majority of NSCLC patients continue to experience disease progression and associated side effects, which are largely attributed to drug resistance, indicating the need for alternative strategies to combat this deadly disease. Among various applicable alternative approaches, repurposed drugs such as arsenic compounds have been shown to exert anticarcinogenic properties against NSCLC and possess the ability to overcome drug resistance mechanisms. Notably, numerous studies have demonstrated that the antitumor effects of arsenic compounds such as arsenic trioxide, arsenic sulfide, and tetra arsenic hexoxide are mediated via their ability to target several oncogenic signaling pathways, including nuclear factor-kappa B (NF-kB), epidermal growth factor receptor (EGFR), and signal transducer and activator of transcription 3 (STAT3). Inhibition of such signaling cascades results in altered cellular activities, including cell cycle arrest, decreased proliferation, and increased apoptosis. Importantly, these arsenic compounds have also been shown to overcome tumor resistance mechanisms and/or exert synergy in combination with other therapeutic agents resulting in the augmentation of cancer cell cytotoxicity. This review highlights the anticarcinogenic mechanisms of arsenic compounds and their impact on the efficacy of therapeutic agents.