Fujian Cancer Hospital & Institute, No 420 Fuma Road, Fuzhou, Fujian, 350014, China.
Fujian Cancer Hospital & Institute, No 420 Fuma Road, Fuzhou, Fujian, 350014, China.
Pathol Res Pract. 2021 Aug;224:153521. doi: 10.1016/j.prp.2021.153521. Epub 2021 Jun 8.
Colorectal cancer (CRC) is considered as one of the commonest tumors and is the major reason of cancer-related deaths around the world. Plentiful evidences have validated that long non-coding RNAs (lncRNAs) play a significant part in various cancers, including CRC. LINC01559 is implicated in the development of various cancers. However, the detailed function of LINC01559 in CRC has not been illustrated.
LINC01559 expression was examined via RT-qPCR, and a series of functional experiments were conducted to explore the role of LINC01559 in CRC progression. Mechanism experiments were carried out to examine the underlying mechanism of LINC01559.
LINC01559 expression was increased in CRC cells and tissues, and LINC01559 depletion restrained the biological behaviors of CRC cells. Also, LINC01559 sponged miR-1343-3p in CRC, and PARP1 was the target of miR-1343-3p. Besides, miR-1343-3p overexpression or PARP1 down-regulation affected the biological behaviors of CRC cells. In addition, up-regulation of PARP1 or adding SC79 (AKT pathway activator) could remedy the repressive effects of LINC01559 silencing on CRC cell biological behaviors.
LINC01559 promotes CRC through sponging miR-1343-3p to modulate PARP1/PTEN/AKT pathway, which may be conducive to offering a new idea for CRC therapeutic treatment.
结直肠癌(CRC)被认为是最常见的肿瘤之一,也是全球癌症相关死亡的主要原因。大量证据表明,长非编码 RNA(lncRNA)在包括 CRC 在内的各种癌症中发挥着重要作用。LINC01559 参与了各种癌症的发展。然而,LINC01559 在 CRC 中的详细功能尚未阐明。
通过 RT-qPCR 检测 LINC01559 的表达,并进行一系列功能实验以探讨 LINC01559 在 CRC 进展中的作用。通过机制实验来检验 LINC01559 的潜在作用机制。
LINC01559 在 CRC 细胞和组织中表达增加,LINC01559 耗竭抑制了 CRC 细胞的生物学行为。此外,LINC01559 在 CRC 中海绵吸附 miR-1343-3p,PARP1 是 miR-1343-3p 的靶基因。此外,miR-1343-3p 的过表达或 PARP1 的下调影响了 CRC 细胞的生物学行为。另外,PARP1 的上调或添加 SC79(AKT 通路激活剂)可以弥补 LINC01559 沉默对 CRC 细胞生物学行为的抑制作用。
LINC01559 通过海绵吸附 miR-1343-3p 来调节 PARP1/PTEN/AKT 通路促进 CRC 的发生,这可能有助于为 CRC 的治疗提供新的思路。