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.

中文翻译：

---

ROR1-AS1组合式抑制PI3K / Akt / mTOR途径抑制NSCLC细胞的生长和侵袭并促进其凋亡

ROR1-AS1在非小细胞肺癌（NSCLC）中的作用尚不清楚。因此，我们旨在研究ROR1-AS1在NSCLC中的功能，并探讨其潜在机制。进行3-（4,5-二甲基噻唑-2-基）-2-，5-二苯基四唑鎓溴化物测定以检测细胞增殖。进行Transwell测定以评估细胞侵袭能力。确定细胞凋亡率和caspase-3 / 7活性以评估细胞凋亡。使用蛋白质印迹分析测量PI3K / Akt / mTOR途径相关蛋白的表达水平。结果表明，NSCLC样品中ROR1-AS1表达上调。抑制ROR1-AS1抑制了NSCLC细胞的活力和侵袭能力。抑制ROR1-AS1诱导细胞凋亡率和caspase-3 / 7活性并抑制异种移植NSCLC肿瘤的生长。此外，ROR1-AS1抑制可抑制NSCLC细胞中PI3K / Akt / mTOR途径的激活。但是，用740Y-P处理可防止si-ROR1-AS1对NSCLC细胞活力，侵袭能力和细胞凋亡的影响。这些发现表明，ROR1-AS1通过调节PI3K / Akt / mTOR途径在NSCLC中发挥致癌作用。