LncRNA HCG11 accelerates the progression of hepatocellular carcinoma via miR-26a-5p/ATG12 axis.

Abstract:

OBJECTIVE:Hepatocellular carcinoma (HCC) is one of the most commonly diagnosed cancers globally. LncRNA HLA complex group 11 (HCG11) has been reported to play an oncogenic role in multiple cancers. Nevertheless, the role and regulatory mechanism of HCG11 in HCC are not fully addressed. PATIENTS AND METHODS:The abundance of HCG11 and miR-26a-5p was measured by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) in HCC tissues and cells. Cell proliferation, apoptosis, metastasis, and autophagy were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, transwell migration, invasion assays, and Western blot assay, respectively. The binding sites between miR-26a-5p and HCG11 or autophagy-related 12 (ATG12) were predicted by starBase bioinformatic software, and the combination was confirmed by Dual-Luciferase reporter assay. The abundance of ATG12 was examined by Western blot assay. Murine xenograft model was established to validate the function of HCG11 in vivo. RESULTS:The enrichment of HCG11 was enhanced in HCC tissues and cells and was negatively related to the prognosis of HCC patients. The abundance of miR-26a-5p was inversely correlated with the level of HCG11 in HCC tissues. HCG11 interference suppressed the proliferation, metastasis, and autophagy while promoted the apoptosis of HCC cells. MiR-26a-5p bound to lncRNA HCG11 and ATG12. The depletion of miR-26a-5p or the accumulation of ATG12 could alleviate the suppressive effects induced by HCG11 intervention on the proliferation, metastasis, autophagy, and the promoting impact on the apoptosis of HCC cells. HCG11 promoted the growth of murine xenograft tumor and autophagy through miR-26a-5p/ATG12 axis in vivo. CONCLUSIONS:LncRNA HCG11 accelerated the proliferation, metastasis, and autophagy while impeded the apoptosis of HCC cells via HCG11/miR-26a-5p/ATG12 axis. HCG11 might be a potential therapeutic target for the treatment of HCC.

authors

Li ML,Zhang Y,Ma LT

doi

10.26355/eurrev_201912_19771

subject

Has Abstract

pub_date

2019-12-01 00:00:00

pages

10708-10720

issue

24

eissn

1128-3602

issn

2284-0729

journal_volume

23

pub_type

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