Jong Bin Kim1, Eun Yeol Yang1, Joohyun Woo1, Hyungju Kwon2, Woosung Lim1, Byung-In Moon1. 1. Department of Surgery, Ewha Womans University School of Medicine, Ewha Womans University Mokdong Hospital, Ewha Womans University, Seoul, Republic of Korea. 2. Department of Surgery, Ewha Womans University School of Medicine, Ewha Womans University Mokdong Hospital, Ewha Womans University, Seoul, Republic of Korea hkwon@ewha.ac.kr.
Abstract
BACKGROUND/AIM: MEK-ERK pathway plays major roles in the progression of thyroid cancer, while the use of MEK-ERK inhibitors has been limited by its toxicity. We investigated the effect of sodium selenite as an adjunct for MEK-ERK inhibitors to avoid the toxicity of ERK inhibitors. MATERIALS AND METHODS: TPC1, 8505C and HTori-3 cells were treated with U0126 (MEK-ERK inhibitor) and cell viability was counted in the Neubauer chamber. The synergistic effects of sodium selenite and U0126 were also measured. The expression of ERK, p-ERK, and p90RSK was determined by western blot. RESULTS: Treatment with U0126 inhibited proliferation of TPC1 and 8505C cells in a dose-dependent manner. When 5 μM sodium selenite was added to 1 μM U0126, relative cell survival further decreased. Decreased expression of p90RSK indicated that sodium selenite down-regulated ERK signaling in thyroid cancer cells. CONCLUSION: The combination of U0126 and sodium selenite inhibited proliferation of thyroid cancer cells through ERK inhibition. Copyright
BACKGROUND/AIM: MEK-ERK pathway plays major roles in the progression of thyroid cancer, while the use of MEK-ERK inhibitors has been limited by its toxicity. We investigated the effect of sodium selenite as an adjunct for MEK-ERK inhibitors to avoid the toxicity of ERK inhibitors. MATERIALS AND METHODS:TPC1, 8505C and HTori-3 cells were treated with U0126 (MEK-ERK inhibitor) and cell viability was counted in the Neubauer chamber. The synergistic effects of sodium selenite and U0126 were also measured. The expression of ERK, p-ERK, and p90RSK was determined by western blot. RESULTS: Treatment with U0126 inhibited proliferation of TPC1 and 8505C cells in a dose-dependent manner. When 5 μM sodium selenite was added to 1 μM U0126, relative cell survival further decreased. Decreased expression of p90RSK indicated that sodium selenite down-regulated ERK signaling in thyroid cancer cells. CONCLUSION: The combination of U0126 and sodium selenite inhibited proliferation of thyroid cancer cells through ERK inhibition. Copyright
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