LncRNA RP11-307C12.11 promotes the growth of hepatocellular carcinoma by acting as a molecular sponge of miR-138
10.1016/j.livres.2019.11.003
- Author:
Deng YINAN
1
;
Cheng YUSHENG
;
Zeng KAINING
;
Li HAIBO
;
Huang YIMING
;
Jiang YIQUAN
;
Xia TINGTING
;
Zhang TONG
;
Yang YANG
Author Information
1. Department of Hepatic Surgery and Liver Transplantation Center
- Keywords:
Long non-coding RNAs(lncRNAs);
LncRNA RP11-307C12.11;
Hepatocellular carcinoma(HCC);
Growth;
MicroRNA(MiR)-138
- From:
Liver Research
2019;3(3):240-249
- CountryChina
- Language:Chinese
-
Abstract:
Background:Abnormal expression of long non-coding RNAs(lncRNAs)has been found in almost all tumors in humans,providing numerous potential diagnostic and prognostic biomarkers,and therapeutic targets. Materials and methods:The Cancer Genome Atlas(TCGA)database was used to screen potential LncRNAs,and 30 paired hepatocellular carcinoma(HCC)tissues were used to investigate RP11-307C12.11 expression levels by qRT-PCR and another 105 HCC tissues by in situ hybridizsation(ISH).RP11-307C12.11 overexpression and knockdown experiments were performed to investigate the effects of RP11-307C12.11 on HCC growth through in vitro and in vivo assays(MTT assay,colony formation assay,EdU assay,and xenograft model).The molecular mechanism underlying these effects was confirmed by MS2-RIP-assay,RIP assay,luciferase assay,and rescue experiments. Results:RP11-307C12.11 expression level was significantly higher in tumor tissues than in the adjacent normal tissues.Elevated RP11-307C12.11 expression level was associated with poor prognosis of HCC patients,and it may be represented as an independent prognostic biomarker in patients with HCC.Functionally,RP11-307C12.11 overexpression promoted HCC growth both in vitro and in vivo;however,its knockdown reversed these effects.Mechanistically,we found that RP11-307C12.11 expressed pre-dominantly in the cytoplasm and sponged microRNA(miR)-138 to regulate its common target CCND1 and PDK1. Conclusions:Thus,we found that RP11-307C12.11 acts as an oncogene in HCC by binding to miR-138,which might provide a novel target for HCC therapy.
