Wu Dianchao, Li Hui, Wang Junfeng, Li Hua, Xiao Qihai, Zhao Xiaofeng, Huo Zhibin
Department of Surgical Oncology, Xingtai People's Hospital, No.16, Hongxing Street, Xingtai, 054031, Hebei, China.
Department of Colorectal Surgery, Tianjin Medical University Cancer Institute and Hospital, Tianjin, China.
Open Med (Wars). 2020 Oct 9;15(1):1028-1038. doi: 10.1515/med-2020-0218. eCollection 2020.
Long non-coding RNAs (lncRNAs) were reported to promote the development of gastric cancer (GC). Nuclear-enriched abundant transcript 1 (NEAT1) played a great role in diverse cancers, but the mechanism of NEAT1 in GC remains indistinct. NEAT1 and AKT1 were distinctly up-regulated and miR-1294 was down-regulated in GC tissues and cells. Cell proliferation and metastasis were refrained but apoptosis was promoted in GC cells after knockdown of NEAT1. NEAT1 negatively regulated miR-1294 expression, and the miR-1294 inhibitor reverted the si-NEAT1-induced effect on GC cells. NEAT1 modulated AKT1 expression through miR-1294, and the si-NEAT1-induced effect was relieved by AKT1. NEAT1 affected phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway via regulating miR-1294 and AKT1. NEAT1 could modulate cell proliferation, apoptosis, and metastasis in GC cells by regulating the PI3K/AKT/mTOR signaling pathway via the miR-1294/AKT1 axis, showing the great potential for NEAT1 as a valid biomarker in the progression and treatment of GC.
据报道，长链非编码RNA（lncRNAs）可促进胃癌（GC）的发展。核富集丰富转录本1（NEAT1）在多种癌症中发挥重要作用，但NEAT1在GC中的作用机制仍不清楚。在GC组织和细胞中，NEAT1和AKT1明显上调，而miR-1294下调。敲低NEAT1后，GC细胞的增殖和转移受到抑制，但细胞凋亡增加。NEAT1负向调节miR-1294的表达，miR-1294抑制剂可逆转si-NEAT1对GC细胞的诱导作用。NEAT1通过miR-1294调节AKT1的表达，AKT1可缓解si-NEAT1的诱导作用。NEAT1通过调节miR-1294和AKT1影响磷脂酰肌醇3激酶（PI3K）/AKT/雷帕霉素哺乳动物靶蛋白（mTOR）信号通路。NEAT1可通过miR-1294/AKT1轴调节PI3K/AKT/mTOR信号通路，从而调节GC细胞的增殖、凋亡和转移，这表明NEAT1作为GC进展和治疗中有效的生物标志物具有巨大潜力。
