Yuan Zhi-Jun, Yu Can, Hu Xiao-Fang, He Yi, Chen Po, Ouyang Sha-Xi
Department of Medical Oncology, Hunan Cancer Hospital, The Affiliated Cancer Hospital of Xiangya School of Medicine, Central South University Changsha 410013, Hunan Province, P. R China.
Department of Hepatobiliary Pancreatic Surgery, Xiangya Third Hospital, Central South University Changsha 410013, Hunan Province, P. R. China.
Am J Transl Res. 2020 May 15;12(5):2241-2256. eCollection 2020.
Pancreatic cancer (PC) is one of the top deaths causing cancers with low 5-year survival rate. Long non-coding RNAs (lncRNAs) are recognized as a crucial type of nonprotein-coding transcripts implicated in tumorigenesis. Emerging evidence has implied that LINC00152 exerts the potential oncogenic functions in various cancers. Nevertheless, the role of LINC00152 in PC remains elusive. In the present study, we found that LINC00152 was significantly up-regulated while miR-150 was down-regulated both in tissues and cell lines of PC, indicating their negative correlation in PC progression. Functionally, overexpression of LINC00152 promoted cell proliferation, migration and invasion, while LINC00152 knockdown reversed these effects. Mechanistic experiments reveal that miR-150 acted as a target of LINC00152 confirmed by luciferase reporter assay. Moreover, inhibition of miR-150 could markedly attenuate the suppression of cell proliferation, migration and invasion by knocking down LINC00152. Altogether, our findings concluded that LINC00152 facilitated PC progression through inhibiting miR-150 expression, indicating an innovative therapeutic target for PC.
胰腺癌（PC）是导致死亡的主要癌症之一，5年生存率较低。长链非编码RNA（lncRNAs）被认为是一类与肿瘤发生相关的关键非蛋白质编码转录本。新出现的证据表明，LINC00152在多种癌症中发挥潜在的致癌作用。然而，LINC00152在胰腺癌中的作用仍不清楚。在本研究中，我们发现LINC00152在胰腺癌组织和细胞系中均显著上调，而miR-150则下调，表明它们在胰腺癌进展中呈负相关。在功能上，LINC00152的过表达促进细胞增殖、迁移和侵袭，而敲低LINC00152则逆转了这些作用。机制实验表明，荧光素酶报告基因检测证实miR-150是LINC00152的靶点。此外，抑制miR-150可显著减弱敲低LINC00152对细胞增殖、迁移和侵袭的抑制作用。总之，我们的研究结果表明，LINC00152通过抑制miR-150表达促进胰腺癌进展，这为胰腺癌提供了一个新的治疗靶点。
