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Abstract
BackgroundHepatocellular carcinoma (HCC) is one of the cancers of highest incidence and mortality worldwide. The proliferation and invasion of tumor cells are the main reason for poor prognosis after HCC surgery. Long non-coding RNA (lncRNA) has been shown to play a key role in the progression of HCC. LncRNA-CR594175 is one of the highly expressed lncRNAs in HCC tumors and their metastatic tumors that we have obtained by the High-throughput screening method.MethodsTo elucidate the role of lncRNA-CR594175 in regulating the proliferation and invasion of human hepatoma cell line, HepG2, we operated through lncRNA-CR594175 silencing to inhibit the progression of HCC, either through in vitro or in vivo experiments.ResultsWe found that lncRNA-CR594175 was lower in adjacent non-cancerous tissues than in primary HCC, and was lower in primary HCC than in its metastasis. Silencing of lncRNA-CR594175 inhibited the proliferation and invasion of HepG2 cells and growth of subcutaneous tumors. The results revealed that lncRNA-CR594175, as a RNA sponge, broke the negative regulation of hsa-miR-142-3p on Catenin, beta-1 (CTNNB1), and once lncRNA-CR594175 was silenced, the hsa-miR142-3p regained its negative regulation on CTNNB1 which can promote HCC progression by activating the wnt pathway.ConclusionsOur present study demonstrated for the first time that lncRNA-CR594175 silencing suppressed proliferation and invasion of HCC cells in vivo and in vitro by restoring the negative regulation of hsa-miR-142-3p on CTNNB1, laying a solid theoretical base for using lncRNA-CR594175 as genetic target therapy for HCC and offering a reasonable explanation for inactivation of miRNA in different tumors or in the tumor at different stages.
Highlights
Hepatocellular carcinoma (HCC) is one of the cancers of highest incidence and mortality worldwide
Assessment of mRNA and protein levels of CTNNB1 and hsa-miR-142-3p and Long noncoding RNA (lncRNA)-CR594175 levels through RTqPCR and Western blotting in adjacent non-cancerous, primary HCC and metastatic tissues The data of CTNNB1 mRNA and protein levels demonstrated that in comparison with adjacent noncancerous tissues, CTNNB1 protein was increased in HCC and its metastasis (p < 0.01), and more in HCC metastasis than in primary HCC (p < 0.05); but there were no obvious differences between the mRNA levels in the three groups of tissues (p > 0.05)
The levels of lncRNA-CR594175 and hsa-miR142-3p in the adjacent tissues, HCC and its metastasis were positively correlated with CTNNB1 protein levels and was higher in the HCC and their metastasis than that in the adjacent tissues (p < 0.05) (Fig. 1a)
Summary
Hepatocellular carcinoma (HCC) is one of the cancers of highest incidence and mortality worldwide [1], featuring a low complete resection rate and a high postoperative recurrence rate [2, 3], which is mainly driven by high invasiveness and intrahepatic and/or extrahepatic metastasis [4]. In recent years, searching for new therapeutic targets for HCC treatment never stopped. Both microRNAs (miRNAs) and lncRNAs play important roles in regulating cellular processes [5,6,7]. The expression of lncRNA-CR594175 increases from adjacent non-cancerous, to primary HCC, to metastasis tissues, which suggests that lncRNA-CR594175 may be involved in proliferation and invasion of HCC. According to our screening data, CTNNB1 was highly correlated with the process of HCC development
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