ArticleCancer management and research2020
miR-143-3p Targets lncRNA PSMG3-AS1 to Inhibit the Proliferation of Hepatocellular Carcinoma Cells.
Article in Cancer management and research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 27 citations in OpenAlex.
- Comprehensive analysis of cuproptosis-related lncRNAs in immunotherapy response and prognosis in papillary thyroid cancer.Gland surgery · 2026Article
- Unveiling the oncogenic functions of lncRNA PSMG3-AS1: a review of its biological roles in cancer.Discover oncology · 2025Review
- Biological functions and potential mechanisms of miR‑143‑3p in cancers (Review).Oncology reports · 2024Review
- Milk fat miRNome changes in response to LPS challenge in Holstein cows.Veterinary research · 2023Article
- MicroRNA-143 acts as a tumor suppressor through Musashi-2/DLL1/Notch1 and Musashi-2/Snail1/MMPs axes in acute myeloid leukemia.Journal of translational medicine · 2023Article
- Prognostic and Immune Infiltration Value of Proteasome Assembly Chaperone (PSMG) Family Genes in Lung Adenocarcinoma.International journal of medical sciences · 2023Article
- Long non-coding RNA PSMG3 Antisense RNA 1 is correlated with oral squamous cell carcinoma and regulates cancer cell proliferation by targeting premature microRNA-141.American journal of cancer research · 2023Article
- Differential MicroRNA Expression in Porcine Endometrium Related to Spontaneous Embryo Loss during Early Pregnancy.International journal of molecular sciences · 2022Article
- PSMG3-AS1 enhances glioma resistance to temozolomide via stabilizing c-Myc in the nucleus.Brain and behavior · 2022Article
- KRAS-related long noncoding RNAs in human cancers.Cancer gene therapy · 2022Review
- KRAS-related long noncoding RNAs in human cancers.Cancer gene therapy · 2022Review
- IL-2 Modulates TAMs Derived Exosomal MiRNAs to Ameliorate Hepatocellular Carcinoma Development and Progression.Journal of oncology · 2022Article
- Identifying Autophagy-Related lncRNAs and Potential ceRNA Networks in NAFLD.Frontiers in genetics · 2022Article
- Exploration of the Effect on Genome-Wide DNA Methylation byInternational journal of molecular sciences · 2021Article
- Downregulation of SOX2-OT Prevents Hepatocellular Carcinoma Progression Through miR-143-3p/MSI2.Frontiers in oncology · 2021Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe molecular pathogenesis of liver cancer remains unclear; some ncRNAs have been considered as potential drug targets for cancer treatment. LncRNA PSMG3‑AS1 has been reported to promote breast cancer, while its role in hepatocellular carcinoma (HCC) is unknown.
methodsBioinformatics analysis was conducted to investigate the relationship between miR-143-3p and PSMG3-AS1. RT-qPCR was used to detect the expression levels of miR-143-3p and PSMG3-AS1 and the correlation between them in HCC. The survival curve was used to analyze the effect of PSMG3-AS1 on the prognosis of liver cancer. RT-qPCR was used to detect the effect of different concentration gradients of miR-143-3p on PSMG3-AS1. CCK8 and clone formation experiments were used to examine the role of miR-143-3p and PSMG3-AS1 in regulating the proliferation of SNU-182 and SNU-398 cells.
resultsOur preliminary bioinformatics analysis showed that miR-143-3p can target PSMG3-AS1. We, therefore, analyzed the interaction between PSMG3-AS1 and miR-143-3p in HCC. We found that PSMG3-AS1 was upregulated, while miR-143-3p was downregulated in HCC. The expression levels of PSMG3‑AS1 and miR-143-3p were closely and inversely correlated with each other. High expression levels of PSMG3‑AS1 predicted poor survival. In HCC cells, overexpression of PSMG3-AS1 led to increased proliferation rates. Overexpression of miR-143-3p played an opposite role and reversed the effect of overexpression of PSMG3‑AS1. DISCUSSIONS: miR-143-3p may target PSMG3‑AS1 to inhibit the proliferation of HCC cells.
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