ArticleOncology letters2023
USF1 modulates transcription and cellular functions by regulating multiple transcription factors in Huh7 cells.
Article in Oncology letters, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Targeted Interference with USF2 Binding to the SERPINE1 Proximal Promoter E-Box in Dual Mutant p53Biomedicines · 2026Review
- Knockdown of USF1 and USF2 drives prolonged changes in the gene expression response of M12-5B3 cells to DNA damage.PloS one · 2025Article
- Identification of ETV5 as a prognostic marker related to epigenetic modification in pan-cancer and facilitates tumor progression in hepatocellular carcinoma.Scientific reports · 2024Article
- Hepatitis B Virus Increases SphK1-S1P Synthesis by Promoting the Availability of the Transcription Factor USF1.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver cancer, including hepatocellular carcinoma (HCC), is a malignant tumor that has high rates of metastasis and mortality worldwide. Upstream transcription factor 1 (USF1) is a canonical transcription factor (TF) and is associated with the pathogenesis of several cancers, but its biological functions and molecular targets in HCC remain unclear. Huh7 cells that overexpress USF1 were used with whole transcriptome profiling through RNA sequencing and chromatin immunoprecipitation (ChIP) sequencing methods to investigate the downstream targets of USF1. Reverse transcription-quantitative PCR was then used to validate the downstream targets. The results showed that USF1 significantly regulates 350 differentially expressed genes (DEGs). The upregulated DEGs were primarily protein-coding genes enriched in immune and inflammation response pathways, while the downregulated DEGs were mainly coding long non-coding (lnc)RNAs, indicating the regulatory function of USF1. It was also demonstrated that USF1 directly binds to the promoter region of 2,492 genes, which may be involved in the viral progression and cell proliferation pathways. By integrating these two datasets, 16 overlapped genes were detected, including downregulated lncRNA-NEAT1 and upregulated TF-ETV5. The downregulated lncRNA-NEAT1 showed reverse expression pattern and prognosis result compared with that of USF1 in patients with liver cancer, while upregulated TF-ETV5 showed consistent results with USF1. Promoter region motif analysis indicated that ETV5 has more binding motifs and genes than USF1 itself for USF1-regulated DEGs, indicating that USF1 may indirectly modulate gene expression by regulating ETV5 expression in Huh7 cells. The study also validated the direct interaction between USF1 and the promoter of ETV5 using ChIP-qPCR. In summary, the results demonstrated that USF1 binds to the promoter region of thousands of genes and affects a large part of DEGs indirectly. Downstream genes, including lncRNA-NEAT1 and TF-ETV5, may also have potential functions in the regulated network by USF1 and have potential functions in the progression of HCC. The present findings suggested that USF1 and its downstream targets could be potential targets for HCC therapy in the future.
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