Krętowski Rafał, Borzym-Kluczyk Małgorzata, Stypułkowska Anna, Brańska-Januszewska Justyna, Ostrowska Halina, Cechowska-Pasko Marzanna
Department of Pharmaceutical Biochemistry, Medical University of Białystok, Mickiewicza 2A, 15-222, Białystok, Poland.
Department of Biology, Medical University of Białystok, Białystok, Poland.
Mol Cell Biochem. 2016 Jun;417(1-2):35-47. doi: 10.1007/s11010-016-2711-4. Epub 2016 May 9.
Cancer cells have developed a number of adaptation mechanisms involving the signal activation of the transduction pathways, which promotes the progression and metastasis. Our results showed that the percentage of apoptotic MCF-7 cells incubated in the low glucose medium for 48 h was lower in comparison to those cultured in the high glucose medium, despite the high expression of the proapoptotic transcription factor-CHOP. Furthermore, the MCF-7 cells incubated in the low glucose medium for 48 h showed a higher expression of NF-κB p100/p52 subunits compared to cells incubated in the high glucose medium. Moreover, our findings demonstrated that the shortage of glucose strongly induces autophagy in MCF-7 cells. The activation of this process is not associated with the changes in the expression of mTOR kinase. We suggest, that the antiapoptotic chaperone ORP150 induction, transcription factor NF-κB2 activation, and increased autophagy constitute mechanisms protecting the MCF-7 cells against apoptosis.
癌细胞已经形成了许多涉及信号转导通路激活的适应机制，这促进了肿瘤的进展和转移。我们的结果表明，尽管促凋亡转录因子CHOP高表达，但在低葡萄糖培养基中培养48小时的凋亡MCF-7细胞百分比低于在高葡萄糖培养基中培养的细胞。此外，与在高葡萄糖培养基中培养的细胞相比，在低葡萄糖培养基中培养48小时的MCF-7细胞显示出更高的NF-κB p100/p52亚基表达。此外，我们的研究结果表明，葡萄糖缺乏强烈诱导MCF-7细胞自噬。这一过程的激活与mTOR激酶表达的变化无关。我们认为，抗凋亡伴侣蛋白ORP150的诱导、转录因子NF-κB2的激活以及自噬增加构成了保护MCF-7细胞免受凋亡的机制。
