ArticleAnnals of surgical oncology2013
MK-2206 causes growth suppression and reduces neuroendocrine tumor marker production in medullary thyroid cancer through Akt inhibition.
Article in Annals of surgical oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Integrated transcriptome and single-cell RNA sequencing analysis revealed the prognostic significance of GBP4 in pancreatic adenocarcinoma.Translational oncology · 2025Article
- Akt inhibitor MK-2206 reduces pancreatic cancer cell viability and increases the efficacy of gemcitabine.Oncology letters · 2020Article
- Silencing of zinc finger protein 703 inhibits medullary thyroid carcinoma cell proliferationOncology letters · 2020Article
- Inhibition of esophageal cancer growth through the suppression of PI3K/AKT/mTOR signaling pathway.OncoTargets and therapy · 2019Article
- Reduced USP39 expression inhibits malignant proliferation of medullary thyroid carcinoma in vitro.World journal of surgical oncology · 2015Article
- PI3K/Akt/mTOR signaling in medullary thyroid cancer: a promising molecular target for cancer therapy.Endocrine · 2015Review
- Inhibition of the AKT pathway in cholangiocarcinoma by MK2206 reduces cellular viability via induction of apoptosis.Cancer cell international · 2015Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDevelopment of targeted therapies for medullary thyroid cancer (MTC) has focused on inhibition of the rearranged during transfection (RET) proto-oncogene. Akt has been demonstrated to be a downstream target of RET via the key mediator phosphoinositide-3-kinase. MK-2206 is an orally administered allosteric Akt inhibitor that has exhibited minimal toxicity in phase I trials. We explored the antitumor effects of this compound in MTC.
methodsHuman MTC-TT cells were treated with MK-2206 (0-20 μM) for 8 days. Assays for cell viability were performed at multiple time points with MTT (3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide). The mechanism of action, mechanism of growth inhibition, and production of neuroendocrine tumor markers were assessed with Western blot analysis.
resultsMK-2206 suppressed MTC cell proliferation in a dose-dependent manner (p ≤ 0.001). Levels of Akt phosphorylated at serine 473 declined with increasing doses of MK-2206, indicating successful Akt inhibition. The apoptotic proteins cleaved poly (ADP-ribose) polymerase and cleaved caspase-3 increased in a dose-dependent manner with MK-2206, while the apoptosis inhibitor survivin was markedly reduced. Importantly, the antitumor effects of MK-2206 were independent of RET inhibition, as the levels of RET protein were not blocked.
conclusionsMK-2206 significantly suppresses MTC proliferation without RET inhibition. Given its high oral bioavailability and low toxicity profile, phase II studies with this drug alone or in combination with RET inhibitors are warranted.
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