排序方式： 共有12条查询结果，搜索用时 46 毫秒
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N. V. Koroban A. V. Kudryavtseva G. S. Krasnov A. F. Sadritdinova M. S. Fedorova A. V. Snezhkina N. L. Bolsheva O. V. Muravenko A. A. Dmitriev N. V. Melnikova 《Molecular Biology》2016,50(3):337-343
Regulation of gene expression via microRNA is the key mechanism of response to biotic and abiotic stresses in plants. There are a lot of experimental data on the biological function of microRNAs in response to different stresses in various plant species. This review contains up-to-date information on molecular mechanisms of microRNA action in plants in response to abiotic stresses, including drought, salinity, mineral nutrient deficiency or imbalance. 相似文献
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Dmitriev Alexey A. Kudryavtseva Anna V. Krasnov George S. Koroban Nadezhda V. Speranskaya Anna S. Krinitsina Anastasia A. Belenikin Maxim S. Snezhkina Anastasiya V. Sadritdinova Asiya F. Kishlyan Natalya V. Rozhmina Tatiana A. Yurkevich Olga Yu. Muravenko Olga V. Bolsheva Nadezhda L. Melnikova Nataliya V. 《BMC plant biology》2016,16(3):139-146
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Alexey A. Dmitriev Anna V. Kudryavtseva George S. Krasnov Nadezhda V. Koroban Anna S. Speranskaya Anastasia A. Krinitsina Maxim S. Belenikin Anastasiya V. Snezhkina Asiya F. Sadritdinova Natalya V. Kishlyan Tatiana A. Rozhmina Olga Yu. Yurkevich Olga V. Muravenko Nadezhda L. Bolsheva Nataliya V. Melnikova 《BMC plant biology》2016,16(3):237
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Downregulation of OGDHL expression is associated with promoter hypermethylation in colorectal cancer
Fedorova M. S. Kudryavtseva A. V. Lakunina V. A. Snezhkina A. V. Volchenko N. N. Slavnova E. N. Danilova T. V. Sadritdinova A. F. Melnikova N. V. Belova A. A. Klimina K. M. Sidorov D. V. Alekseev B. Ya. Kaprin A. D. Dmitriev A. A. Krasnov G. S. 《Molecular Biology》2015,49(4):608-617
Molecular Biology - Cell metabolic reprogramming is one of the cancer hallmarks. Glycolysis activation, along with suppression of oxidative phosphorylation and, to a lower extent, the TCA cycle,... 相似文献
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Anna V. Kudryavtseva Maria S. Fedorova Alex Zhavoronkov Alexey A. Moskalev Alexander S. Zasedatelev Alexey A. Dmitriev Asiya F. Sadritdinova Irina Y. Karpova Kirill M. Nyushko Dmitry V. Kalinin Nadezhda N. Volchenko Nataliya V. Melnikova Kseniya M. Klimina Dmitry V. Sidorov Anatoly Y. Popov Tatiana V. Nasedkina Andrey D. Kaprin Boris Y. Alekseev George S. Krasnov Anastasiya V. Snezhkina 《BMC genetics》2016,17(3):156
Background
The switch from oxidative phosphorylation to glycolysis in proliferating cancer cells, even under aerobic conditions, has been shown first in 1926 by Otto Warburg. Today this phenomenon is known as the “Warburg effect” and recognized as a hallmark of cancer. The metabolic shift to glycolysis is associated with the alterations in signaling pathways involved in energy metabolism, including glucose uptake and fermentation, and regulation of mitochondrial functions. Hexokinases (HKs), which catalyze the first step of glycolysis, have been identified to play a role in tumorigenesis of human colorectal cancer (CRC) and melanoma. However, the mechanism of action of HKs in the promotion of tumor growth remains unclear.Results
The purpose of the present study was to investigate the effect of silencing of hexokinase genes (HK1, HK2, and HK3) in colorectal cancer (HT-29, SW 480, HCT-15, RKO, and HCT 116) and melanoma (MDA-MB-435S and SK-MEL-28) cell lines using short hairpin RNA (shRNA) lentiviral vectors. shRNA lentiviral plasmid vectors pLSLP-HK1, pLSLP-HK2, and pLSLP-HK3 were constructed and then transfected separately or co-transfected into the cells. HK2 inactivation was associated with increased expression of HK1 in colorectal cancer cell lines pointing to the compensation effect. Simultaneous attenuation of HK1 and HK2 levels led to decreased cell viability. Co-transfection with shRNA vectors against HK1, HK2, and HK3 mRNAs resulted in a rapid cell death via apoptosis.Conclusions
We have demonstrated that simultaneous inactivation of HK1 and HK2 was sufficient to decrease proliferation and viability of melanoma and colorectal cancer cells. Our results suggest that HK1 and HK2 could be the key therapeutic targets for reducing aerobic glycolysis in examined cancers.7.
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