ArticleAging2024
LncRNA SH3BP5-AS1 promotes hepatocellular carcinoma progression by sponging miR-6838-5p and activation of PTPN4.
Article in Aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Propofol attenuates cerebral ischemia-reperfusion-mediated neuronal apoptosis and oxidative damage by regulating the miR-6838-5p/AQP11 axis.Archives of medical science : AMS · 2026Article
- Long non-coding RNAs in cancer glycolysis and metabolism: mechanisms and translational opportunities.Cell death & disease · 2025Review
- Exosome-mediated metabolic reprogramming: effects on thyroid cancer progression and tumor microenvironment remodeling.Molecular cancer · 2025Review
- Long non-coding RNAs and autophagy: dual drivers of Hepatocellular carcinoma progression.Cell death discovery · 2025Review
- Prognostic value of LncRNA SH3BP5-AS1 in non-small cell lung cancer and its regulatory effect on tumor progression.Discover oncology · 2025Article
- Identification and validation of palmitoylation-related biomarkers in gestational diabetes mellitus.Scientific reports · 2025Article
- Glycolysis-associated lncRNAs in cancer energy metabolism and immune microenvironment: a magic key.Frontiers in immunology · 2024Review
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLong noncoding RNAs (LncRNAs) have been demonstrated to have significant roles in the carcinogenesis of hepatocellular carcinoma (HCC). In this work, we sought to determine LncRNA SH3BP5-AS1's function and mechanism in the emergence of HCC.
resultsFirst, we discovered that the advanced tumor stage was strongly correlated with high levels of LncRNA SH3BP5-AS1 expression in HCC. MiR-6838-5p expression was down-regulated and inversely correlated with SH3BP5-AS1 expression. Additionally, overexpression of SH3BP5-AS1 boosted cell invasion, migration, and proliferation. The oncogenic effects of the inhibitor of miR-6838-5p were eliminated when PTPN4 was suppressed, following the identification of PTPN4 as a direct target of miR-6838-5p. In addition, SH3BP5-AS1 promoted cellular glycolysis via miR-6838-5p sponging and PTPN4 activation. Lastly, by directly interacting to the promoter of SH3BP5-AS1, HIF-1α could control the transcription of the gene.
conclusionsOur research suggests that SH3BP5-AS1 controls miR-6838-5p/PTPN4 in order to act as a new carcinogenic LncRNA during the growth of HCC cells.
methodsThe expression levels of SH3BP5-AS1, miR-6838-5p and PTPN4 were detected by qRT-PCR and Western blot. The effects of LncRNA SH3BP5-AS1/miR-6838-5p/PTPN4 on the proliferation, metastasis and glycolysis of HCC cells were clarified by experimental cellular functionality assays, cell derived xenograft and Glycolysis assay.
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