Sodium Selenite Enhanced the Anti-proliferative Effect of MEK-ERK Inhibitor in Thyroid Cancer Cells
- 주제(키워드) Selenium , thyroid cancer , MEK-ERK inhibitor , U0126 , ERK pathway
- 주제(기타) Medicine, Research & Experimental
- 설명문(일반) [Kim, Jong Bin; Yang, Eun Yeol; Woo, Joohyun; Kwon, Hyungju; Lim, Woosung; Moon, Byung-In] Ewha Womans Univ, Mokdong Hosp, Sch Med, Dept Surg, Seoul, South Korea
- 등재 SCIE, SCOPUS
- OA유형 Green Published, gold
- 발행기관 INT INST ANTICANCER RESEARCH
- 발행년도 2020
- 총서유형 Journal
- URI http://www.dcollection.net/handler/ewha/000000166078
- 본문언어 영어
- Published As http://dx.doi.org/10.21873/invivo.11760
- PubMed https://pubmed.ncbi.nlm.nih.gov/31882478
초록/요약
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 p90(RSK) was determined by western blot. Results: Treatment with U0126 inhibited proliferation of TPC1 and 8505C cells in a dose-dependent manner. When 5 mu M sodium selenite was added to 1 mu M U0126, relative cell survival further decreased. Decreased expression of p90(RSK) 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.
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