ArticleMolecular medicine reports2017
Long non‑coding RNA AB019562 promotes cell proliferation and metastasis in human hepatocellular carcinoma.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The Impact of Long Non-Coding RNAs in the Pathogenesis of Hepatocellular Carcinoma.Frontiers in oncology · 2021Review
- Long Noncoding RNA MIR100HG Knockdown Attenuates Hepatocellular Carcinoma Progression by Regulating MicroRNA-146b-5p/Chromobox 6.Gastroenterology research and practice · 2021Article
- Silencing long intergenic non-coding RNA 00707 enhances cisplatin sensitivity in cisplatin-resistant non-small-cell lung cancer cells by sponging miR-145.Oncology letters · 2019Article
- H19 Facilitates Tongue Squamous Cell Carcinoma Migration and Invasion via Sponging miR-let-7.Oncology research · 2019Article
- Behind the curtain of non-coding RNAs; long non-coding RNAs regulating hepatocarcinogenesis.World journal of gastroenterology · 2018Review
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6 authors.
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Abstract
Increasing evidence has supported the prognostic and therapeutic values of long non-coding RNAs (LncRNAs) in human tumorigenesis. Hepatocellular carcinoma (HCC), as one of the most refractory diseases, continues to warrant investigation for novel clues to enable early diagnosis. In the present study, the role of LncRNA AB019562 in cell proliferation and metastasis was investigated in HCC. Reverse transcription‑quantitative polymerase chain reaction analysis was performed to determine the expression of AB019562 in clinical HCC samples and cultured HCC cells. In addition, a specific small interfering RNA against AB019562 was designed and transfected into HCC cells. A3‑(4,5‑ dimethylthiazol‑2‑yl)‑2,5‑diphenyltetrazolium bromide assay and a transwell assay were used to assess the effects of AB019562 knockdown on cell proliferation and metastasis, respectively. The results revealed that the expression of AB019562 was increased 4‑fold in the clinical HCC tissues, compared with adjacent non‑cancerous tissue counterparts. AB019562 was differentially expressed in the HCC cell lines. The knockdown of AB019562 reduced the rate of cell proliferation by 28.6% in HepG2 cells and by 24% in SMMC‑7721 cells. Cell cycle assays revealed that the proportion of cells in the G0/G1 phase was significantly increased, whereas those in the S and G2/M phases were decreased in the AB019562‑knockdowncells. The results of the transwell assay showed that the knockdown of AB019562 inhibited cell migration abilities by up to 67% in the HepG2 cells and 63% in the SMMC‑7721 cells, and significantly suppressed invasive abilities by up to 75% in the HepG2 cells and 60% in the SMMC‑7721 cells. Furthermore, AB019562 knockdown increased the apoptotic rates of the two cell lines and activated the expression of caspase‑3, but not caspase‑8. These data demonstrated the pro‑oncogenic properties of AB019562 and suggested that AB019562 may serve as a novel biomarker for the diagnosis and treatment of patients with HCC.
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