Митохондриальные изменения в канцерогенезе как цель противоопухолевой терапии (обзор)
Аннотация
Причины и механизмы развития рака в настоящее время являются одной из актуальных проблем медицины. Основным вариантом на сегодняшний день является мутационная теория. Выявление системы генных мутаций, в том числе и в митохондриях, приводящих к тому или иному виду опухолей, сделали возможным разработку персонализированной так называемой таргетной терапии злокачественных опухолей.
Об авторах
Т. Е. Потемина
ФГБОУ ВО «Приволжский исследовательский медицинский университет» Министерства здравоохранения Российской Федерации
Россия
Россия
Потемина Татьяна Евгеньевна - доктор медицинских наук, профессор, заведующий кафедрой патологической физиологии
Нижний Новгород
Э. В. Гузиков
ФГБОУ ВО «Приволжский исследовательский медицинский университет» Министерства здравоохранения Российской Федерации; ГБУЗ НО «Нижегородская областная детская клиническая больница»
Россия
Россия
Гузиков Эдуард Валерьевич - ассистент кафедры патологической физиологии; врач анестезиолог реаниматолог отделения реанимации и интенсивной терапии для новорожденных
Нижний Новгород
Список литературы
1. Porporato PE et al. Mitochondrial metabolism and cancer // Cell Res. – 2018. – № 28 (3). – P. 265–280.
2. Senft D., Ronai Z.A. Regulators of mitochondrial dynamics in cancer. Curr. Opin. // Cell Biol. – 2016. – Vol. 39. – P. 43–52.
3. Warburg O. On the origin of cancer cells / O. Warburg // Science. – 1956. – Vol. 123, № 3191. – P. 309–314.
4. Taganovich A.D. Patologicheskaya bioximiya. – M.: BINOM, 2013. – 448 s.
5. Isidoro A. et al. breast carcinomas funfill the Warburg hypothesis and providt metabolic markers of cancerprognosis // Cfncerogenesis. – 2005. – Vol. 26, № 12. – P. 2095–2104.
6. Guezva M. et al. The bioenergeticsignature of cancer: a marker of tumor pro-gression // Cancer. Res. – 2002. – Vol. 62, № 22. – P. 6674–6681.
7. Lopez-Rios F. Loss of the mitochondrial bioenergetic capacity underlies the glucose avidity of carcinomas // Cancer Res. – 2007. – Vol. 67, № 19. – P. 9013–9017.
8. M. Wu Neilson A et al. Multiparameter metabolic analysis reveals a close link between attenuated mitochondrial bioenergetic function and enhanced glycoly-sis dependency in human tumor cells // Am. J. Physiol. Cell. Physiol. – 2007 – Vol. 292, № 1. – P. C125–136.
9. Schulz TJ et al. Induction of oxidative metabolism by mitochondrial frataxin inhibits cancer growth: Otto Warburg revisited // J. Biol. Chem. – 2006. – Vol. 281, № 2. – P. 977–981.
10. Gaude, E., Frezza С. Defects in mitochondrial metabolism and cancer // Can-cer. Metab. – 2014. – Vol. 2. – P. 10.
11. Morin A, Letouzé E, Gimenez-Roqueplo AP, Favier J. Oncometabolites-driven tu-morigenesis: From genetics to targeted therapy // Int. J. Cancer. – 2014. – Vol. 135, № 10. – P. 2237–2248.
12. Kiebish MA et al. Cardiolipin and electron transport chain abnormalities in mouse brain tumor mitochondria: lipidomic evidence supporting the Warburg theory of cancer // J. Lipid. Res. – 2008. – Vol. 49, № 12. –
13. P. 2545–2556.
14. Samudio I., Fiegl M, Andreeff M. Mitochondrial uncoupling and the Warburg ef-fect: molecular basis for the reprogramming of cancer cell metabolism // Can-cer Res. – 2009. – Vol. 69, № 6. – P. 2163–2166.
15. Ayyasamy V et al. Cellular model of Warburg effect identifies tumor promoting function of UCP2 in breast cancer and its suppression by genipin // PLoS One. – 2011. – Vol. 6 (9). – Р. e24792.
16. Ibsen K.H. The Crabtree effect: a review // Cancer Res. – 1961. – Vol. 21. – P. 829–841.
17. Eakin RT et al. Carbon-13 nuclear magnetic resonance spectroscopy of living cells and their metabolism of a specifically labeled 13C substrate // FEBS Lett. – 1972. – Vol. 28(3). – Р. 259–264.
18. Weinhouse S., Krebsforsch Z. The Warburg hypothesis fifty years later // Klin. Onkol. Cancer Res. Clin. Oncol. – 1976. – Vol. 87, № 2. – Р. 115–126.
19. Pedersen P.L. Tumor mitochondria and the bioenergetics of cancer cells // Prog. Exp. Tumor Res. – 1978. – Vol. 22. – P. 190–274.
20. Mishra P., Chan D.C. Metabolic regulation of mitochondrial dynamics // J. Cell Biol. – 2016. – № 12. –
21. P. 379–387.
22. Wallace DC. Mitochondria and cancer: Warburg addressed // Cold Spring Harb Symp Quant Biol. – 2005. –Vol. 70. – P. 363–374.
23. Ishikawa K et al. ROS-generating mitochondrial DNA mutations can regulate tu-mor cell metastasis // Science. – 2008. – Vol. 320 (5876). – P. 661–664.
24. Wang Y, Xia Y, Lu Z. Metabolic features of cancer cells // Cancer Commun. – 2018. – Vol. 38 (1). – Р. 65. –URL:http://www.cancercommun.biomedcentral.com/articles/10.1186/s40880-018-0335-7
25. Roth KG, Mambetsariev I, Kulkarni P, Salgia R. The mitochondrion as an emerg-ing therapeutic target in cancer // Trends Mol Med. – 2019. – № 26 (1). – Р.119–134.
26. Khutornenko AA et al. Pyrimidine biosynthesis links mitochondrial respiration to the p53 pathway // Proc Natl Acad Sci USA. – 2010. – № 107 (29). – P. 12828–33.
27. Dong L.F. et al. Horizontal transfer of whole mitochondria restores tumor-igenic potential in mitochondrial DNA-deficient cancer cells // Cancer Com-mun. – 2019. – Р. 39–63. – URL: http://www.cancercommun.
28. biomedcentral.com/track/pdf/10.1186/s40880-019-0412-6
29. Tan A.S. et al. Mitochondrial genome acquisition restores respiratory func-tion and tumorogenic potential of cancer cells without mitochondrial DNA // Cell Metab. – 2015. – № 21 (1). – P. 81–94.
30. Hu Y.L. et al. Hypoxia-induced autophagy promotes tumor cell survival and ad-aptation to antiangiogenic treatment in glioblastoma // Cancer Res. – 2012. – Vol. 72. – P. 1773–1783.
31. Kulikov V.A., Belyaeva L.E. Metabolicheskoe pereprogrammirovanie rakovy`x kletok // Vestnik Vi-tebskogo gosudarstvennogo medicinskogo universiteta. – 2013. – № 2. – Tom 12. – C. 6–12.
32. Dang C.V., Kim J.W., Gao P., Yustein J. The interplay between MYC and HIF in cancer // Nat. Rev. Cancer. – 2008. – Vol. 8. – Р. 51–56.
33. Kulikov V.A. Signal'nye kaskady, onkogeny, geny-onkosupressory i metabolizm rakovoj kletki // Vestn. VGMU. – 2014. – T. 13, № 5. – S. 6-15.
34. Kumykova Z.Yu. Rol' gena r53 i kodiruemogo im belka v kancerogeneze cheloveka i zhivotnyh // Vestnik magistratury. - 2014.- № 5-1 (32). - S. 18–20.
35. Bell E.L., Emerlin, B.M., Ricoul S.J., Guarente L. SirT3 suppresses hypoxia inducible factor 1a and tumor growth by inhibiting mitochondrial ROS produc-tion. // Oncogene. – 2011. – Vol. 30. – Р. 2986–2996.
36. Chen W. et al. Tumor protein translationally controlled 1 is a p53 target gene that promotes cell survival // Cell Cycle. – 2013. – Vol. 12. – № 14. – P. 617–633.
37. Martinou J.C., Youle R.J. Mitochondria in apoptosis: Bcl-2 family members and mitochondrial dynamics // Dev. Cell. – 2011. – № 21. – P. 92–101.
38. Tan Z. et al. The Role of PGC1a in Cancer Metabolism and its Therapeutic Im-plications // Mol. Cancer Ther. – 2016. – Vol. 15. – P. 774–782.
39. La Gory E.L. et al. Suppression of PGC-1a Is Critical for Reprogramming Oxi-dative Metabolism in Renal Cell Carcinoma // Cell Rep. – 2015. – № 12. – P. 116–127.
40. Lamb R. et al. Mitochondria as new therapeutic targets for eradicating cancer stem cells: Quantitative proteomics and functional validation via MCT1/2 in-hibition // Oncotarget. – 2014. – Vol. 5. – P. 11029–11037.
41. De Luca, A. et al. Mitochondrial biogenesis is required for the anchorage-independent survival and propagation of stem-like cancer cells // Oncotarget. – 2015. – Vol. 6. – P. 14777–14795.
42. Le Bleu V.S. et al. Pgc-1alpha Mediates Mitochondrial Biogenesis and Oxida-tive Phosphorylation in Cancer Cells to Promote Metastasis // Nat. Cell. Bi-ol. – 2016. – Vol. 16. – P. 992–1003, 1001–1015.
43. Lee J.V. et al. Akt-dependent metabolic reprogramming regulates tumor cell histone acetylation // Cell Metab. – 2014. – Vol. 20. – P. 306–319.
44. Morita M. et al. mTOR coordinates protein synthesis, mitochondrial activity and proliferation // Cell Cycle. – 2015. – Vol. 14. – P. 473–480.
45. Sancho P. et al. MYC/PGC-1a Balance Determines the Metabolic Phenotype and Plasticity of Pancreatic Cancer Stem Cells // Cell Metab. – 2015. – Vol. 22. – P. 590–605.
46. Guo J.Y. et al. Autophagy suppresses progression of K-ras-induced lung tumors to oncocytomas and maintains lipid homeostasis // Genes Dev. – 2013. – Vol. 27. – P. 1461–1463.
47. Hu Y.L. et al. Hypoxia-induced autophagy promotes tumor cell survival and ad-aptation to antiangiogenic treatment in glioblastoma // Cancer Res. – 2012. – Vol. 72. – P. 1773–1783.
48. Mancias J.D., Kimmelman A.C. Mechanisms of Selective Autophagy in Normal Physiology and Cancer //
49. J. Mol. Biol. – 2016. – Vol. 428. – P. 1659–1680.
50. Chourasia A.H., Boland M.L., Macleod K.F. Mitophagy and cancer // Cancer Metab. – 2014. – № 6. –
51. P. 329–339.
52. Ortega A.D. et al. Glucose avidity of carcinomas // Cancer Lett. – 2009. – Vol. 276. – № 2. – P. 125–135.
53. Ju Y.S. et al. Origins and functional consequences of somatic mitochondrial DNA mutations in human cancer. // eLife. – 2014. – № 3. – P. 2-28.
54. Porporato P.E. et al. A mitochondrial switch promotes tumor metastasis // Cell Rep. – 2014. – Vol. 8. –
55. P. 754–766.
56. Cui Q, Wen S, Huang P. Targeting cancer cell mitochondria as a therapeutic approach: recent updates // Future Med Chem. – 2017. – Vol 9 (9). – P. 929–949.
57. Kalyanaraman B et al. A review of the basics of mitochondrial bioenergetics, metabolism, and related signaling pathways in cancer cells: therapeutic tar-geting of tumor mitochondria with lipophilic cationic compounds // Redox Bi-ol. – 2018. – Vol. 14. – P. 316–327.
58. Ghosh J.C. et al. Adaptive mitochondrial reprogramming and resistance to PI3K therapy // J. Natl. Cancer Inst. – 2015. – Vol. 107 (3).
59. Du X, Zhang P, Fu H, Ahsan HM, Gao J, Chen Q. Smart mitochondrial-targeted cancer therapy: subcellular distribution, selective TrxR2 inhibition accompa-ny with declined antioxidant capacity // Int J Pharm. – 2019. –Vol. 555. – Р. 346–355.
60. Lei Y et al. Metformin targets multiple signaling pathways in cancer // Chin J Cancer. – 2017. – Vol. 6 (1). – Р. 17.
61. The 150 most important questions in cancer research and clinical oncology se-ries: questions 94–101: edited by Cancer Communications // Cancer Commun. – 2018. – Vol. 38 (1). – Р. 69.
62. Cheng G et al. Mitochondria-targeted drugs synergize with 2-deoxyglucose to trigger breast cancer cell death // Cancer Res. – 2012. – Vol. 72 (10). – Р. 2634–2644.
63. Vyas, S., and Chang, P. New PARP targets for cancer therapy // Nat. Rev. Can-cer. – 2014. – Vol. 14. –
64. P. 502–509.
65. Dong L. Neuzil J Тargeting mitochondria as an anticancer strategy // Cancer Communications. – 2019. – Vol. 39. – Р. 63.
Для цитирования:
Потемина Т.Е., Гузиков Э.В. Митохондриальные изменения в канцерогенезе как цель противоопухолевой терапии (обзор). Вестник медицинского института «РЕАВИЗ». Реабилитация, Врач и Здоровье. 2020;(4):65-73. https://doi.org/10.20340/vmi-rvz.2020.4.8
For citation:
Potemina T.E., Guzikov E.V. Mitochondrial changes in carcinogenesis as a goal of antitumor therapy (review). Bulletin of the Medical Institute "REAVIZ" (REHABILITATION, DOCTOR AND HEALTH). 2020;(4):65-73. (In Russ.) https://doi.org/10.20340/vmi-rvz.2020.4.8
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