TERT attenuated ER stress-induced cell death.
TERT attenuated ER stress-induced cell death.
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DOI：
10.1016/j.bbrc.2014.04.034
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发表时间：
2014-05
影响因子：
3.1
通讯作者：
Toru Hosoi;Yuki Inoue;Kanako Nakatsu;Naomi Matsushima;Noriko Kiyose;A. Shimamoto;H. Tahara;K. Ozawa
中科院分区：
文献类型：
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作者：
Toru Hosoi;Yuki Inoue;Kanako Nakatsu;Naomi Matsushima;Noriko Kiyose;A. Shimamoto;H. Tahara;K. Ozawa
肿瘤细胞经常出现在营养缺乏的地区，尽管其生存机制尚不清楚。在本研究中，我们发现，剥夺细胞的葡萄糖引起内质网应激（ER应力）在乳腺癌细胞系，MCF-7，和ER应力的特异性激活增加端粒酶逆转录酶（TERT）的表达。TERT的过度表达可减少内质网应激诱导的细胞死亡，从而起到对抗应激的作用。因此，结果为应激条件下肿瘤进展的潜在机制提供了证据，突出了ER应激诱导TERT表达以耐受环境应激，我们称之为“ER应激-TERT轴”的机制。
Tumor cells are frequently encountered in nutrient-deprived areas, though the mechanisms underlying their survival are unclear. In the present study, we found that depriving cells of glucose caused endoplasmic reticulum stress (ER stress) in a breast cancer cells line, MCF-7, and that specific activation of ER stress increased telomerase reverse transcriptase (TERT) expression. TERT expression would function in counteracting against the stress because over-expression of TERT diminished ER stress-induced cell death. Therefore, the results provide evidence for the underlying mechanisms of tumor progression in stressed conditions, highlighting that ER stress induces TERT expression to withstand environmental stress, a mechanism which we termed the “ER stress-TERT axis”.