ArticleAnnals of translational medicine2021
Long noncoding TMPO antisense RNA 1 promotes hepatocellular carcinoma proliferation and epithelial-mesenchymal transition by targeting the microRNA-126-3p/LRP6/β-catenin axis.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 11 citations in OpenAlex.
- The regulation of LRPs by miRNAs in cancer: influencing cancer characteristics and responses to treatment.Cancer cell international · 2025Review
- Article
- Making Sense of Antisense lncRNAs in Hepatocellular Carcinoma.International journal of molecular sciences · 2023Review
- circSMARCA5 Is an Upstream Regulator of the Expression of miR-126-3p, miR-515-5p, and Their mRNA Targets,International journal of molecular sciences · 2022Article
- A long non-coding RNA with important roles in the carcinogenesis.Frontiers in cell and developmental biology · 2022Review
- Long noncoding RNA LINC01124 activates hepatocellular carcinoma cell proliferation, migration, and invasion by absorbing microRNA-1247-5p and overexpressing FOXO3.Oncology research · 2021Article
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Authors and funding
6 authors at 4 institutions in 1 country.
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Abstract
backgroundLong noncoding RNAs (lncRNAs) play a central role in the pathogenesis of various tumors, including hepatocellular carcinoma (HCC). TMPO antisense RNA 1 (TMPO-AS1) has been reported in many tumors. Nevertheless, the underlying mechanism whereby TMPO-AS1 influences HCC remains unclear. Our research aimed to reveal the molecular mechanism governing the function of TMPO-AS1 in HCC.
methodsTMPO-AS1 expression levels in HCC tissues/cells were evaluated using reverse transcriptase-polymerase chain reaction. The effect of TMPO-AS1 on the progression of HCC was observed by Cell Counting Kit-8 (CCK8), clone formation, wound healing, and transwell. The direct interaction between TMPO-AS1 and microRNA (miR)-126-3p was observed using a dual-luciferase reporter.
resultsWe found TMPO-AS1 expression to be remarkably higher in HCC specimens and associated with poor prognosis. Silencing of TMPO-AS1 not only inhibited HCC cell proliferation but also significantly reduced epithelial-to-mesenchymal transition-induced invasion and migration to a remarkable degree. According to the results from the online database analysis tools implemented to identify if TMPO-AS1 could target miR-126-3p, we found that miR-126-3p had a negative relationship with TMPO-AS1 in HCC specimens. Meanwhile, the luciferase reporter assay confirmed that TMPO-AS1 could directly act on miR-126-3p. Moreover, the silencing of miR-126-3p dramatically abolish the inhibitive influence of sh-TMPO-AS1 on HCC development.
conclusionsOur research demonstrated that TMPO-AS1 acts as a sponge for the tumor suppressor miR-126-3p in HCC and promotes the expression of LRP6 indirectly. Taken together, our results show that TMPO-AS1 may be regarded as a novel therapeutic target in the treatment of liver cancer.
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