ArticleInternational journal of cancer2010
BRAF mutation-selective inhibition of thyroid cancer cells by the novel MEK inhibitor RDEA119 and genetic-potentiated synergism with the mTOR inhibitor temsirolimus.
Article in International journal of cancer, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 60 citations in OpenAlex.
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- The potential role of reprogrammed glucose metabolism: an emerging actionable codependent target in thyroid cancer.Journal of translational medicine · 2023Review
- Integrated pan-cancer analysis of centromere protein F and experimental verification of its role and clinical significance in cholangiocarcinoma.Functional & integrative genomics · 2023Article
- State of the Art in the Current Management and Future Directions of Targeted Therapy for Differentiated Thyroid Cancer.International journal of molecular sciences · 2022Review
- Combinatorial Therapies in Thyroid Cancer: An Overview of Preclinical and Clinical Progresses.Cells · 2020Review
- Poorly Differentiated Carcinoma of the Thyroid Gland: Current Status and Future Prospects.Thyroid : official journal of the American Thyroid Association · 2019Review
- Metformin inhibits thyroid cancer cell growth, migration, and EMT through the mTOR pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
- Defining a rational step-care algorithm for managing thyroid carcinoma patients with elevated thyroglobulin and negative on radioiodine scintigraphy (TENIS): considerations and challenges towards developing an appropriate roadmap.European journal of nuclear medicine and molecular imaging · 2015Article
- A novel dual AMPK activator/mTOR inhibitor inhibits thyroid cancer cell growth.The Journal of clinical endocrinology and metabolism · 2015Article
- New therapies for dedifferentiated papillary thyroid cancer.International journal of molecular sciences · 2015Review
- BRAF inhibitor dabrafenib in patients with metastatic BRAF-mutant thyroid cancer.Thyroid : official journal of the American Thyroid Association · 2015Article
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- Switch in signaling control of mTORC1 activity after oncoprotein expression in thyroid cancer cell lines.The Journal of clinical endocrinology and metabolism · 2014Article
- Accelerated disease progression after discontinuation of sorafenib in a patient with metastatic papillary thyroid cancer.Endocrinology and metabolism (Seoul, Korea) · 2014Article
- BRAF V600E and TERT promoter mutations cooperatively identify the most aggressive papillary thyroid cancer with highest recurrence.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We examined the therapeutic potential of a novel MEK inhibitor, RDEA119, and its synergism with the mTOR inhibitor, temsirolimus, in thyroid cancer cell lines. RDEA119 potently inhibited the proliferation of the 4 cell lines that harbored BRAF mutation but had no or modest effects on the other 4 cells that harbored wild-type BRAF (IC(50) of 0.034-0.217 μM vs. 1.413-34.120 μM). This inhibitory effect of RDEA119 in selected cell lines OCUT1 (BRAF V600E(+), PIK3CA H1047R(+)) and SW1376 (BRAF V600E(+)) was enhanced by combination with the mTOR inhibitor, temsirolimus. The PTEN-deficient cell FTC133 was highly sensitive to temsirolimus but insensitive to RDEA119, and simultaneous treatment with the latter enhanced the sensitivity of the cell to the former. The KAT18 (wild-type) cell was not sensitive to either drug alone but became sensitive to the combination of the 2 drugs. The drug synergy was confirmed by combination index and isobologram analyses. RDEA119 and temsirolimus also showed synergistic effects on autophagic death of OCUT1 and KAT18 cells selectively tested. Dramatic synergistic effects of the 2 drugs were also seen on the growth of FTC133 xenograft tumors in nude mice. Overall, the effects of the 2 drugs on cell proliferation or autophagic death, either alone or in combination, were more pronounced in cells that harbored genetic alterations in the MAP kinase and PI3K/Akt pathways. Thus, these results demonstrated the important therapeutic potential of the novel MEK inhibitor RDEA119 and its synergism with temsirolimus in thyroid cancer.
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