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. 2023 May 23;21:345. doi: 10.1186/s12967-023-04200-9

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© The Author(s) 2023

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 3 — The relationship between the occurrence and development of melanoma cells and mitochondria. Activation and mutation of NRAS or BRAF genes in MAPK and PI3K signaling pathways in melanoma cells can inhibit mitochondrial function and promote glycolysis. The increase of intracellular calcium concentration in melanoma cells can inhibit the function of mitochondria. In addition, some miRNAs may also affect the function of mitochondria. PI3K: Phosphatidylinositol 3-kinase; MAPK: Mitogen-activated protein kinases; NADH: Nicotinamide adenine dinucleotide; HIF1α: Hypoxia inducible factor-1α; mTOR: mammalian Target of rapamycin; PDK1: Phosphoinositide-dependent protein kinase 1; PTEN: Phosphatase and tensin homolog; NRAS: Neuroblastoma RAS; MAPK: Mitogen-activated protein kinase; MITF: Microphthalmia-associated transcription factor; NRF1: Nuclar respiratory factor-1; TFAM: Mitochondrial transcription factor A; MYC: Myelocytomatosis viral oncogene; Drp1: Dynamin-related protein 1; MDIVI-1: Mitochondrial division inhibitor 1