Open AccessThe long non‐coding RNA HLNC1 potentiates hepatocellular carcinoma progression via interaction with USP49
Author(s) -
Qian Xinye,
Li Shitong,
Yang Zhoujing,
Zhang Jun
Publication year - 2020
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.23462
Subject(s) - rna , long non coding rna , cancer research , hepatocellular carcinoma , transcriptome , in vivo , biology , microbiology and biotechnology , chemistry , gene expression , gene , genetics
Background The hepatocellular carcinoma (HCC) represents a serious malignancy worldwide especially in China. Our transcriptome analysis identifies a novel long non‐coding RNA (lncRNA) termed HLNC1. However, the function of HLNC1 in HCC remains to be determined. Methods Novel lncRNAs were screened using lncRNA profiling. Relative expression was quantified by qRT‐PCR. In vitro experiments such as migration and viability assays were performed. In vivo implantation experiments were conducted to investigate tumorigenic functions. RNA‐RNA interaction assay was performed to determine USP49 as HLNC1 binding partner. Results We found that HLNC1 was markedly upregulated in HCC samples and cell lines. HLNC1 could promote viability and migration of HCC cells. Meanwhile, we could also observe an oncogenic effect of HLNC1 in vivo. By RNA‐RNA interaction assay, we unraveled USP49 transcript as the HLNC1 binding partner. HLNC1‐ USP49 interaction dramatically destabilized USP49 . Heat‐shock factor 1 (HSF1) was shown to directly induce HLNC1 expression. The therapeutic potential of targeting HLNC1 was investigated using antisense oligonucleotides (ASOs). The ASO construct which significantly depleted HLNC1 expression could strongly attenuate xenograft tumor growth. Conclusions Our data suggested that HLNC1 may advance HCC progression and act as a potential target for intervention.