ArticleFrontiers in oncology2022
POLD2 is activated by E2F1 to promote triple-negative breast cancer proliferation.
Article in Frontiers in oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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9 citing papers in PubMed, 14 citations in OpenAlex.
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- Multi-omics Analysis Implicates Mitochondrial Complex Assembly Protein COX18 in Mitochondrial Signaling and Tumorigenesis across Cancers.Cell biochemistry and biophysics · 2025Article
- Noncanonical association of EZH2 with E2F1 promotes tumor proliferation through chromatin remodeling.Experimental & molecular medicine · 2025Article
- DNA Polymerase Delta 2 Activates Cell Cycle in Lung Adenocarcinoma, Leading to High Malignancy and Poor Prognosis.Annals of surgical oncology · 2025Article
- LncRNA16 inhibits pyroptosis and promotes platinum resistance in non-small cell lung cancer by sponging miRNA1827 to regulate MBD3/GSDME expression.Cancer cell international · 2025Article
- The identification and prediction of lung adenocarcinoma prognosis using a novel gene signature associated with DNA replication.Translational cancer research · 2025Article
- PFKP deubiquitination and stabilization by USP5 activate aerobic glycolysis to promote triple-negative breast cancer progression.Breast cancer research : BCR · 2024Article
- SP1 transcriptionally regulates UBE2N expression to promote lung adenocarcinoma progression.Molecular biomedicine · 2023Article
- HLA-B*57:01/Carbamazepine-10,11-Epoxide Association Triggers Upregulation of the NFκB and JAK/STAT Pathways.Cells · 2023Article
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1 author at 1 institution in 1 country.
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Abstract
Triple-negative breast cancer (TNBC) is a highly malignant breast cancer subtype with a poor prognosis. Improved insight into the molecular biology basis of TNBC progression is urgently needed. Herein, we reported that POLD2 was highly expressed in TNBC and patients with high POLD2 expression in their tumors had poor clinical outcomes. In functional studies, knockdown of POLD2 inhibited the proliferation of TNBC. Mechanistically, we revealed that transcription factor E2F1 directly bound to the promoter of POLD2 and regulated its expression in TNBC cells, which in turn contributed to the proliferation of TNBC. Additionally, rescue experiments validated that E2F1-mediated cell proliferation in TNBC was dependent on POLD2. Taken together, our results elucidated a novel mechanism of the E2F1-POLD2 axis in TNBC proliferation, and POLD2 may be a potential therapeutic target for TNBC treatment.
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