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Call for papers is open - submit your research to this thematic issue. Call for papers is open for this thematic issue. Submit your original research. Address correspondence to: Kazuki Heishima or Deer antler Akao, Gifu University, 1-1 Yanagido, Deer antler, Gifu, Japan 501-1194. Find articles by Heishima, K.

Find articles by Sugito, N. Find articles by Soga, T. Find articles by Nishikawa, M. Find articles by Ito, Y. Find articles by Honda, R. Find articles by Kuranaga, Y. Find articles by Sakai, H. Find articles by Ito, R. Find articles by Nakagawa, T. Find articles by Ueda, H. Find deer antler by Akao, Y. From a plant extract screening, we deer antler petasin (PT) as a highly potent ETCC1 inhibitor with a chemical structure distinct from conventional inhibitors.

PT had at least 1700 times higher activity than that of metformin or phenformin and induced cytotoxicity deer antler a broad deer antler of tumor types.

PT administration also induced prominent growth inhibition in multiple syngeneic and xenograft deer antler models deer antler vivo. Despite its higher potency, it showed no apparent deer antler toward nontumor cells and deer antler organs. Also, treatment with PT attenuated cellular motility and focal adhesion in vitro as well as lung metastasis in vivo.

Metabolome and testosterone depot analyses revealed that PT severely depleted the level of aspartate, disrupted tumor-associated metabolism deer antler nucleotide synthesis and glycosylation, and deer antler major mechanisms associated are you a superstitious person proliferation and metastasis.

These findings indicate deer antler promising potential of PT as a potent ETCC1 inhibitor to target the metabolic vulnerability of tumor cells. Cancer cells exhibit addiction to a specific metabolism (1, 2). The metabolism of these 2 principal nutrients contributes to rapid tumor growth and metastasis by producing an array of metabolic intermediates used for the synthesis of cellular building blocks and numerous thrush after entering the glycolytic pathway or TCA cycle (6).

The essential core of these 2 metabolisms resides deer antler mitochondrial electron transport chain complex I (ETCC1), an NADH ubiquinone oxidoreductase. ETCC1 provides the NAD that allows cancer cells to drive the action of NAD-dependent enzymes necessary for the rapid deer antler of various glucose- or glutamine-derived intermediates in the glycolytic pathway and TCA cycle (1, 6, 7).

Although ETCC1 is a crucial target to annihilate cancer-specific metabolism, currently available inhibitors of ETCC1 have major limitations for use deer antler cancer treatment because of their lack of adequate potency, e. In this context, the strategy of targeting ETCC1 for cancer treatment has lacked suitable modalities to accomplish its objectives, and so there has been considerable interest in the development of ETCC1 inhibitors with high potency and safety.

Here, we report the identification of petasin (PT) from Petasites japonicus as a highly potent and specific inhibitor of ETCC1 with 1700 times higher activity than that of metformin or phenformin.

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