ArticleAmerican journal of cancer research2023
The transcription factor TBP promotes hepatocellular carcinoma progression by activating AKT3.
Article in American journal of cancer research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 1 citations in OpenAlex.
- Androgen receptor drives lenvatinib resistance in hepatocellular carcinoma through transcriptional activation of EIF3I and a downstream ceRNA axis.Oncology letters · 2026Article
- SP1 activates AKT3 to facilitate the development of diabetic nephropathy.Journal of endocrinological investigation · 2025Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present work was performed to clarify the role of TATA-binding protein (TBP) in hepatocellular carcinoma (HCC). TBP expression in adjacent liver tissues and HCC tissue sample was detected by immunohistochemistry and qRT-PCR. With CCK-8, BrdU, flow cytometry, and transwell assays, the malignancy of cancer cell lines were evaluated. The binding sites of TBP and AKT serine/threonine kinase 3 (Akt3) promoter region were predicted by PROMO database, and the binding relationship between TBP and AKT3 promoter was verified with dual luciferase reporter gene assay and ChIP-qPCR assay. The effect of TBP on AKT3 expression was examined by immunoblotting. The signaling pathways associated with AKT3 were predicted by gene set enrichment analysis (GSEA) with LinkedOmics database. It was revealed that, TBP expression in HCC tissues and cell lines was up-regulated, which was associated with the short survival time of patients. Up-regulation of TBP promoted the viability and aggressiveness of HCC cells, while knockdown of TBP had opposite effects. TBP could bind with AKT3 promoter region, and TBP overexpression promoted the expression of AKT3, while its knockdown worked oppositely. Additionally, TBP/AKT3 axis modulated mTOR expression in HCC cells. In conclusion, TBP promotes the transcription of AKT3, thus accelerating the malignant progression of HCC.
Indexed as
Identifiers
38058816PMC10695801W4389452737What OpenQuestion holds
Registered trials
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