ArticleEndocrinology and metabolism (Seoul, Korea)2015
Selective Mitochondrial Uptake of MKT-077 Can Suppress Medullary Thyroid Carcinoma Cell Survival In Vitro and In Vivo.
Article in Endocrinology and metabolism (Seoul, Korea), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Nicotinamide phosphoribosyltransferase activates the mitochondrial unfolded protein response to promote pulmonary arterial endothelial cell proliferation.bioRxiv : the preprint server for biology · 2026Article
- The dual-function of HSP70 in immune response and tumor immunity: from molecular regulation to therapeutic innovations.Frontiers in immunology · 2025Review
- Analogs of the Heat Shock Protein 70 Inhibitor MKT-077 Suppress Medullary Thyroid Carcinoma Cells.International journal of molecular sciences · 2022Article
- Effect of F16-Betulin Conjugate on Mitochondrial Membranes and Its Role in Cell Death Initiation.Membranes · 2021Article
- Emerging insights into mitochondria-specific targeting and drug delivering strategies: Recent milestones and therapeutic implications.Saudi journal of biological sciences · 2020Review
- Growth Inhibitory Signaling of the Raf/MEK/ERK Pathway.International journal of molecular sciences · 2020Review
- Resveratrol Reduces Kidney Injury in a Rat Model of Uremia and is Associated with Increased Expression of Heat Shock Protein 70 (Hsp70).Medical science monitor : international medical journal of experimental and clinical research · 2020Article
- Subcellular Performance of Nanoparticles in Cancer Therapy.International journal of nanomedicine · 2020Review
- Mortalin (GRP75/HSPA9) Promotes Survival and Proliferation of Thyroid Carcinoma Cells.International journal of molecular sciences · 2019Article
- Article
- Vandetanib and cabozantinib potentiate mitochondria-targeted agents to suppress medullary thyroid carcinoma cells.Cancer biology & therapy · 2017Article
- Suppression of B-RafCancer biology & therapy · 2017Article
- Targeted Therapy for Medullary Thyroid Cancer: A Review.Frontiers in oncology · 2017Review
- Mitochondrial autophagosomes as a mechanism of drug resistance in breast carcinoma.Ultrastructural pathologyArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundMedullary thyroid carcinoma (MTC) is a neuroendocrine tumor mainly caused by mutations in the rearranged during transfection (RET) proto-oncogene. Not all patients with progressive MTC respond to current therapy inhibiting RET, demanding additional therapeutic strategies. We recently demonstrated that disrupting mitochondrial metabolism using a mitochondria-targeted agent or by depleting a mitochondrial chaperone effectively suppressed human MTC cells in culture and in mouse xenografts by inducing apoptosis and RET downregulation. These observations led us to hypothesize that mitochondria are potential therapeutic targets for MTC. This study further tests this hypothesis using1-ethyl-2-[[3-ethyl-5-(3-methylbenzothiazolin-2-yliden)]-4-oxothiazolidin-2-ylidenemethyl] pyridinium chloride (MKT-077), a water-soluble rhodocyanine dye analogue, which can selectively accumulate in mitochondria.
methodsThe effects of MKT-077 on cell proliferation, survival, expression of RET and tumor protein 53 (TP53), and mitochondrial activity were determined in the human MTC lines in culture and in mouse xenografts.
resultsMKT-077 induced cell cycle arrest in TT and MZ-CRC-1. Intriguingly, MKT-077 also induced RET downregulation and strong cell death responses in TT cells, but not in MZ-CRC-1 cells. This discrepancy was mainly due to the difference between the capacities of these cell lines to retain MKT-077 in mitochondria. The cytotoxicity of MKT-077 in TT cells was mainly attributed to oxidative stress while being independent of TP53. MKT-077 also effectively suppressed tumor growth of TT xenografts.
conclusionMKT-077 can suppress cell survival of certain MTC subtypes by accumulating in mitochondria and interfering with mitochondrial activity although it can also suppress cell proliferation via other mechanisms. These results consistently support the hypothesis that mitochondrial targeting has therapeutic potential for MTC.
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