The Infectious Disease Center, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang 830054, P.R. China.
Oncol Rep. 2019 Mar;41(3):1669-1677. doi: 10.3892/or.2019.6971. Epub 2019 Jan 16.
microRNAs (miRNAs) play critical roles in hepatocellular carcinoma (HCC). However, the expression and biological function of miR‑3653 in HCC remain unknown. The present study demonstrated that miR‑3653 expression was significantly decreased in HCC tissues and cells using qRT‑PCR. A decreased miR‑3653 level was associated with unfavorable clinical features and poor prognosis of HCC patients. MTT, BrdU, Transwell and western blot assays showed that miR‑3653 overexpression inhibited the growth, migration, invasion and epithelial‑mesenchymal transition (EMT) of HCCLM3 cells while its knockdown promoted the growth and metastatic ability of Hep3B cells. In vivo experiments showed that miR‑3653 overexpression inhibited the subcutaneous and the lung metastasis of HCCLM3 cells in nude mice. Mechanistically, integrin‑β1 (ITGB1) was identified to be the downstream target of miR‑3653 in HCC. ITGB1 overexpression reversed the inhibitory effects of miR‑3653 on the growth, metastasis and EMT of HCCLM3 cells.
微小 RNA(miRNAs)在肝细胞癌(HCC)中发挥着关键作用。然而,miR-3653 在 HCC 中的表达和生物学功能仍不清楚。本研究通过 qRT-PCR 证明了 miR-3653 在 HCC 组织和细胞中的表达显著降低。miR-3653 水平的降低与 HCC 患者不良的临床特征和预后相关。MTT、BrdU、Transwell 和 Western blot 检测表明,miR-3653 过表达抑制 HCCLM3 细胞的生长、迁移、侵袭和上皮间质转化(EMT),而其敲低则促进 Hep3B 细胞的生长和转移能力。体内实验表明,miR-3653 过表达抑制裸鼠 HCCLM3 细胞的皮下和肺转移。机制上,整合素-β1(ITGB1)被鉴定为 HCC 中 miR-3653 的下游靶标。ITGB1 过表达逆转了 miR-3653 对 HCCLM3 细胞生长、转移和 EMT 的抑制作用。