The lithium effects on morphology and apoptosis in hepatocellular carcinoma cells

Poster (download) Iuliia Taskaeva1, Izabella Gogaeva2, Natalia Obanina3, Viktoriia Makarova4, Nataliya Bgatova51Laboratory of ultrastructural research, Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences; Laboratory of boron-neutron capture therapy, Department of Physics, Novosibirsk State University, inabrite@yandex.ru2Laboratory of ultrastructural research, Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences; Department of Natural Sciences, Novosibirsk State University, i.gogaeva@g.nsu.ru3Laboratory of ultrastructural research, Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences; Section of cytology and genetics, Department of Natural Sciences, Novosibirsk State University, n.obanina@g.nsu.ru4Laboratory of ultrastructural research, Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, shedina_vika@mail.ru5Laboratory of ultrastructural research, Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, n_bgatova@ngs.ru Hepatocellular carcinoma (HCC) is characterized dysregulation of cell death mechanisms, and the imbalance of pro- and anti-apoptotic signals. The development of HCC is accompanied by genetic mutations in the signaling pathways involved in the cell proliferation, growth and death. The molecular changes in apoptosis signaling in HCC determine the requirement for targeted chemotherapy to increasing apoptosis in HCC cells. The aim of this study was to assess the ability of lithium to influence on the hepatocellular carcinoma-29 (HCC-29) cells apoptosis in vivo. Light and transmission electron microscopy, and immunofluorescence staining were used to evaluate of apoptosis development in HCC-29 cells after administration of 20 mM lithium carbonate. It was revealed that lithium extremely increased the pro-apoptotic proteins Bad and caspase-3 expression, and decreased the anti-apoptotic protein Bcl-2 expression. These results indicate that lithium carbonate induces apoptosis pathways in HCC-29 cells. Lithium administration can enhance pro-apoptotic chemotherapeutic drugs potential and overcome the resistance of tumor cells to apoptosis in HCC.

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The effect of lithium carbonate on angiogenesis of hepatocellular carcinoma-29

Viktoriia Makarova1, Nataliya Bgatova2, Iuliia Taskaeva31Laboratory of ultrastructural research, Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, shedina_vika@mail.ru2Laboratory of ultrastructural research, Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, n_bgatova@ngs.ru3Laboratory of ultrastructural research, Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences, inabrite@yandex.ru Гепатоцеллюлярная карцинома является одной из самых агрессивных опухолей человека с высокой распространенностью и смертностью. В то же время существует проблема устойчивости ГЦК к стандартной терапии. Поиск лекарств, блокирующих рост и метастазирование опухоли, является актуальным. Имеются данные о противоопухолевых свойствах карбоната лития. Целью нашего исследования было определить влияние лития на развитие и структуру кровеносных сосудов экспериментальной гепатоцеллюлярной карциномы-29 (G-29). Исследование было выполнено на самцах мышей CBA. Клетки гепатокарциномы-29 использовали для индукции опухолевого процесса. Изучали экспрессию эндотелиального маркера кровеносных сосудов (CD-31) и ультраструктурную организацию опухолевых сосудов эндотелиальных клеток. Было показано, что карбонат лития уменьшает объемную плотность кровеносных сосудов G-29. Ультраструктурный анализ опухолевых сосудов выявил нетипичный характер их строения. Стенки сосудов были выстланы как эндотелиальными, так и опухолевыми клетками.

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The development of compensatory processes in the liver and kidney in conditions of distant tumor growth

Poster (download) Nataliya Bgatova1, Asel Rakhmetova2, Saule Bakhbaeva3, Viktoriia Makarova4, Iuliia Taskaeva51Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences,Novosibirsk, Russia, n_bgatova@ngs.ru2Pavlodar State University; Pavladar, Kazakhsta, asel-rakhmetova@mail.ru3Pavlodar State University; Pavladar, Kazakhstan, saule0577@mail.ru4Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences Novosibirsk, Russia, shedina_vika@mail.ru5Research Institute of Clinical and Experimental Lymphology – Branch of the Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences Novosibirsk, Russia, inabrite@yandex.ru Development of malignant tumor accompanied endogenous intoxication of an organism having a mixed nature, in particular due to dysfunction of organs detoxification and excretion damaging effect of tumor metabolism. The active process of moving toxic and biologically active substances formed during tumor progression from the primary focus by blood and lymph flow leads to damage of distant organ. The aim of this work was to identify structural changes in the liver and kidney under the conditions of modeling distant tumor growth. For modelingВ  tumor growth, hepatocarcinoma-29 (G-29) cells were used. G-29 cells were injected into the muscle of the right thigh of CBA mice [1]. The material for research was collected after 3, 7, 13, and 30 days of the experiment. The structure of the liver and kidney was studied by the method of light and electron microscopy. Both destructive and compensatory changes in the liver and kidney were revealed in conditions of distant tumor growth. In the liver, a decrease a size of hepatocytes and concentration of organelles, as well as development of autophagy, as a mechanism for maintaining intracellular homeostasis, were noted. In the kidney at the early stages of the development of the tumor growth, structural signs of filtration barrier disorde were shown. Subsequent development of compensatory hypertrophy of podocytes and glomerular capillary endothelium, as well as autophagy in the epithelium of the proximal nephron were noted.

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