ECE2017 Oral Communications Thyroid Cancer (5 abstracts)
Suppression of heme oxygenase-1 inhibits growth and invasion of thyroid cancer
Shih-Ping Cheng 1, , Jie-Jen Lee 1, , Ming-Jen Chen 1, , Chien-Liang Liu 1, , Po-Sheng Yang 1, & Yi-Chiung Hsu 3
1MacKay Memorial Hospital, Taipei, Taiwan; 2Mackay Medical College, Taipei, Taiwan; 3National Central University, Taoyuan City, Taiwan.
Oxidative stress generated in the process of iodide metabolism and thyroid hormone synthesis may play a role in thyroid tumorigenesis and progression of thyroid cancer. The transcription factor Nrf2 is the most important regulator of antioxidant responses. It has been shown that Nrf2 expression is upregulated in papillary thyroid cancer. In response to oxidative stress, nuclear Nrf2 activates antioxidant-responsive elements and induces the expression of stress-responsive genes, including heme oxygenase-1 (HO-1). Previously we have demonstrated that HO-1 overexpression was associated with advanced tumor stage in thyroid cancer. Therefore, we hypothesize that HO-1 may represent a potential target for cancer therapy. HO-1 inhibitors have been clinically used in patients with hyperbilirubinemia and hereditary porphyria. In the present study, thyroid cancer cells were treated with two different classes of HO-1 inhibitors: metalloporphyrin and imidazole–dioxolane compound. We found that treatment with HO-1 inhibitors suppressed cell growth, colony formation, cell migration, and invasion of thyroid cancer cells in a dose-dependent manner. Cell cycle analysis by flow cytometry revealed that growth arrest in the G0/G1 phase. However, there was no synergistic effect of HO-1 inhibitors in combination with doxorubicin or sorafenib. Our results suggest a modest susceptibility of thyroid cancer cells to HO-1 inhibitors. Nonetheless, HO-1 inhibition may not act as a sensitizer to chemotherapy in thyroid cancer.
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Endocrine Abstracts
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