ArticleMolecular therapy oncolytics2022
PBX3-activated DLG1-AS1 can promote the proliferation, invasion, and migration of TNBC cells by sponging miR-16-5p.
Article in Molecular therapy oncolytics, 2022. 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, 11 citations in OpenAlex.
- Comprehensive analysis of cuproptosis-related lncRNAs in immunotherapy response and prognosis in papillary thyroid cancer.Gland surgery · 2026Article
- Association of lncRNA AGAP11 with prognosis and malignant progression in triple-negative breast cancer.Discover oncology · 2026Article
- DNA methylation patterns in breast cancer, paired benign tissue from ipsilateral and contralateral breast, and healthy controls.Breast cancer research : BCR · 2025Article
- PBX3-HMGCR Axis Promotes Hepatocellular Carcinoma Progression Through Enhancing De Novo Cholesterol Biosynthesis.International journal of molecular sciences · 2025Article
- Targeting PRDX2 to inhibit tumor growth and metastasis in triple-negative breast cancer: the role of FN1 and the PI3K/AKT/SP1 pathway.Journal of translational medicine · 2025Article
- Identification of shared gene signatures in major depressive disorder and triple-negative breast cancer.BMC psychiatry · 2024Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
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Abstract
DLG1-AS1 and PBX3 have been identified as acting as an oncogene in cervical cancer. However, they have not been well explored in triple-negative breast cancer (TNBC). As TNBC is one of the malignancies causing increasing death throughout the world, this study aimed to probe into the regulatory relationship between DLG1-AS1 and PBX3 in TNBC cells. In this study, real-time quantitative PCR (qRT-PCR) and western blot experiments were conducted to investigate the RNA and protein levels of genes of interest in TNBC cells. Functional experiments were implemented, such as 5-ethynyl-2'-deoxyuridine (EdU), transwell, and wound healing assays, to assess the changes in TNBC cell phenotype. Chromatin immunoprecipitation, luciferase reporter, RNA binding protein immunoprecipitation, and RNA pull-down assays were conducted to investigate the binding relationships among subject genes. The results show that DLG1-AS1 and PBX3 displayed high expression in TNBC cells, and PBX3 worked as the transcriptional activator of DLG1-AS1. Also, DLG1-AS1 served as an oncogene in TNBC cells and as a sponge for miR-16-5p to up-regulate JARID2. Meanwhile, JARID2 and PBX3 exerted oncogenic effects on TNBC cell growth. In conclusion, PBX3-activated DLG1-AS1 can promote the proliferation, invasion, and migration of TNBC cells by sponging miR-16-5p and elevating JARID2 expression.
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