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Role of lncRNA LINC01194 in hepatocellular carcinoma via the miR-655-3p/SMAD family member 5 axis.
- Source :
-
Bioengineered [Bioengineered] 2022 Jan; Vol. 13 (1), pp. 1115-1125. - Publication Year :
- 2022
-
Abstract
- Long non-coding RNAs (lncRNAs) are involved in developing hepatocellular carcinoma (HCC). The present study explored the role of lncRNA LINC01194, which is upregulated in HCC tissues and might be a vital regulator in HCC progression. Levels of LINC01194, microRNA (miR)-655-3p, and SMAD family member 5 (SMAD5) were assessed using reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR). The bioactivity of Huh-7 cells was assessed using cell counting kit-8 and transwell assays and flow cytometry. Western blotting was conducted to measure the expression of invasion- and apoptosis-related proteins. The relationships between lncRNA LINC01194 and miR-655-3p, and miR-655-3p and SMAD5 were predicted using StarBase and TargetScan, and further verified using a dual-luciferase reporter assay. LINC01194 was overexpressed in HCC cells and in clinical samples. ILINC01194 silencing suppressed proliferation and migration; however, it promoted apoptosis in HCC cell lines. We also confirmed that miR-655-3p could bind to LINC01194, and miR-655-3p was downregulated in HCC. The upregulation of miR-655-3p suppressed HCC cell invasion and migration, and enhanced the number of apoptotic cells. SMAD5, which was overexpressed in HCC cell lines, was directly targeted by miR-655-3p. Therefore, LINC01194 promoted HCC development by decreasing miR-655-3p expression and may serve as a promising therapeutic target for HCC patients.
- Subjects :
- Apoptosis
Carcinoma, Hepatocellular genetics
Cell Line, Tumor
Cell Movement
Cell Proliferation
Female
Gene Expression Regulation, Neoplastic
Gene Knockdown Techniques
Humans
Liver Neoplasms genetics
Male
Neoplasm Staging
Up-Regulation
Carcinoma, Hepatocellular pathology
Liver Neoplasms pathology
MicroRNAs genetics
RNA, Long Noncoding genetics
Smad5 Protein genetics
Subjects
Details
- Language :
- English
- ISSN :
- 2165-5987
- Volume :
- 13
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Bioengineered
- Publication Type :
- Academic Journal
- Accession number :
- 34978464
- Full Text :
- https://doi.org/10.1080/21655979.2021.2017678