Wang Wei, Yang Tao, Li Dongsheng, Huang Yinpeng, Bai Guang, Li Qing
Department of General Surgery, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, 121000, China.
Department of Nephrology, The Third Affiliated Hospital of Jinzhou Medical University, No. 2 Section 5 Heping Road, Jinzhou, 121000, China.
J Transl Med. 2021 Dec 7;19(1):504. doi: 10.1186/s12967-021-03139-z.
LINC00491 was involved in some tumors development, but its function in liver cancer has not been reported. This study aimed to investigate LINC00491 expression and function in liver cancer progression.
Sixty liver cancer cases were enrolled. LINC00491, miR-324-5p and rho-associated kinase 1 (ROCK1) expression in liver cancer patients and cells were detected by quantitative reverse transcription-polymerase chain reaction and Western blot. HUH-7 and SK-Hep-1 cells were transfected to modulate LINC00491, miR-324-5p and ROCK1 expression. Cell counting kit-8 assay, colony formation assay, wound healing assay, Transwell experiment, Tunel assay and flow cytometry were performed to detected HUH-7 and SK-Hep-1 cells proliferation, migration, invasion, apoptosis and cell cycle. Biotin-RNA pull-down assay and Dual-Luciferase Reporter Assay was performed to detect the binding among LINC00491, miR-324-5p and ROCK1. Xenograft tumor and lung metastasis was performed using nude mice. Xenograft tumor and lung tissues of mice were experienced immunohistochemistry and hematoxylin-eosin staining.
LINC00491 was highly expressed in liver cancer cases, associating with poor prognosis. si-LINC00491 inhibited proliferation, colony formation, invasion, migration, and induced cell cycle G1 arrest and apoptosis in HUH-7 and SK-Hep-1 cells. LINC00491 overexpression showed opposite effects. LINC00491 promoted ROCK1 expression by reducing miR-324-5p. miR-324-5p up-regulation or ROCK1 knockdown reversed LINC00491 promotion on liver SK-Hep-1 cells malignant phenotype. LINC00491 facilitated xenograft tumor growth and lung metastasis in mice.
LINC00491 was highly expressed in liver cancer patients, associating with poor prognosis. LINC00491 facilitated liver cancer progression by sponging miR-324-5p/ROCK1. LINC00491 might be a potential treatment target of liver cancer.
LINC00491参与了一些肿瘤的发展，但其在肝癌中的作用尚未见报道。本研究旨在探讨LINC00491在肝癌进展中的表达及功能。
纳入60例肝癌病例。采用定量逆转录-聚合酶链反应和蛋白质免疫印迹法检测肝癌患者及细胞中LINC00491、miR-324-5p和rho相关激酶1（ROCK1）的表达。转染HUH-7和SK-Hep-1细胞以调节LINC00491、miR-324-5p和ROCK1的表达。采用细胞计数试剂盒-8法、集落形成试验、伤口愈合试验、Transwell实验、Tunel试验和流式细胞术检测HUH-7和SK-Hep-1细胞的增殖、迁移、侵袭、凋亡和细胞周期。进行生物素RNA下拉试验和双荧光素酶报告基因试验以检测LINC00491、miR-324-5p和ROCK1之间的结合。使用裸鼠进行异种移植瘤和肺转移实验。对小鼠的异种移植瘤和肺组织进行免疫组织化学和苏木精-伊红染色。
LINC00491在肝癌病例中高表达，与预后不良相关。si-LINC00491抑制HUH-7和SK-Hep-1细胞的增殖、集落形成、侵袭、迁移，并诱导细胞周期G1期阻滞和凋亡。LINC00491过表达则表现出相反的作用。LINC00491通过降低miR-324-5p促进ROCK1表达。miR-324-5p上调或ROCK1敲低可逆转LINC00491对肝癌SK-Hep-1细胞恶性表型的促进作用。LINC00491促进小鼠异种移植瘤生长和肺转移。
LINC00491在肝癌患者中高表达，与预后不良相关。LINC00491通过吸附miR-324-5p/ROCK1促进肝癌进展。LINC00491可能是肝癌的一个潜在治疗靶点。
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