ROR1-AS1 knockdown inhibits growth and invasion and promotes apoptosis in NSCLC cells by suppression of the PI3K/Akt/mTOR pathway
ROR1-AS1 knockdown inhibits growth and invasion and promotes apoptosis in NSCLC cells by suppression of the PI3K/Akt/mTOR pathway
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DOI：
10.1002/jbt.22726
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发表时间：
2021-01-24
影响因子：
3.6
通讯作者：
Zhu, Xuezhuan
中科院分区：
文献类型：
--
作者：
Li, Fengbo;Gu, Fengming;Zhu, Xuezhuan
ROR 1-AS 1在非小细胞肺癌（NSCLC）中的作用尚不清楚。因此，我们的目的是研究ROR 1-AS 1在NSCLC中的功能作用，并探讨其潜在的机制。进行3-（4，5-二甲基噻唑-2-基）-2，5-二苯基-溴化四唑测定以检测细胞增殖。Transwell法检测细胞侵袭能力。通过检测细胞凋亡率和caspase-3/7活性来评价细胞凋亡。Western blot检测PI 3 K/Akt/mTOR通路相关蛋白的表达水平。结果显示，ROR 1-AS 1在NSCLC样品中表达上调。ROR 1-AS 1的敲低抑制了NSCLC细胞的生存力和侵袭能力。ROR 1-AS 1的敲低诱导凋亡率和半胱天冬酶-3/7活性，并抑制异种移植NSCLC肿瘤生长。此外，ROR 1-AS 1敲低抑制NSCLC细胞中PI 3 K/Akt/mTOR通路的激活。然而，用740 Y-P处理阻止了si-ROR 1-AS 1对NSCLC细胞的存活力、侵袭能力和凋亡的影响。提示ROR 1-AS 1可能通过调节PI 3 K/Akt/mTOR通路在NSCLC中发挥致癌作用。
The role of ROR1-AS1 in non-small-cell lung cancer (NSCLC) remains unclear. Therefore, we aimed to investigate the functional role of ROR1-AS1 in NSCLC and to explore the underlying mechanisms. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay was performed to detect cell proliferation. Transwell assay was performed to evaluate cell invasive ability. Cell apoptotic rates and caspase-3/7 activity were determined to evaluate apoptosis. The expression levels of PI3K/Akt/mTOR pathway-related proteins were measured using Western blot analysis. Results showed that ROR1-AS1 expression was upregulated in NSCLC samples. Knockdown of ROR1-AS1 inhibited the viability and invasive ability of NSCLC cells. Knockdown of ROR1-AS1 induced apoptotic rate and caspase-3/7 activity and suppressed xenograft NSCLC tumor growth. In addition, ROR1-AS1 knockdown inhibited the activation of the PI3K/Akt/mTOR pathway in NSCLC cells. However, treatment with 740Y-P prevented the effects of si-ROR1-AS1 on viability, invasive ability, and apoptosis of NSCLC cells. These findings implied that ROR1-AS1 played an oncogenic role in NSCLC via regulating the PI3K/Akt/mTOR pathway.