ArticleCurrent cancer drug targets2025
TCF19 Enhances Glioma Cell Proliferation via Modulating the Β-Catenin Signaling Pathway through Accelerating DHX32 Transcription.
Article in Current cancer drug targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Emerging Role of Transcription Factor 19 (TCF19) in Inflammatory Disease and Cancer.Biomolecules · 2026Review
- A bioinformatics screen identifies TCF19 as an aggressiveness-sustaining gene in prostate cancer.Molecular oncology · 2025Article
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Authors and funding
5 authors.
Funding
Abstract
backgroundTranscription factor 19 (TCF19) is considered a crucial transcription factor and acts as an oncogene in a few cancers. Nevertheless, the effect and mechanism of TCF19 on glioma remain unknown.
objectiveThis research aimed to explore the function of TCF19 on glioma progression and clarify the potential mechanism.
methodsTCF19 and DHX32 expressions in glioma were determined using bioinformatics, Quantitative real-time PCR, and immunohistochemistry. MTT assay was carried out to detect the biological function of TCF19 and DHX32 in glioma cell multiplication. Cell-cycle distri-bution and apoptosis were measured by using FACS. The function of TCF19 on glioma growth was examined using tumor xenografts assay. Bioinformatics analysis, ChIP-qRT-PCR, and reporter gene assay were employed to illustrate the TCF19 target regulating DHX32 tran-scription.
resultsTCF19 was observably upregulated in glioma and has important clinical significance. Overexpressing TCF19 expedited glioma cell multiplication and cell-cycle transition, meanwhile preventing apoptosis. TCF19 knockdown inhibited cell proliferation, cell-cycle transition, and tumour growth, simultaneously accelerating apoptosis. TCF19 expressions had a positive correlation with DHX32 expressions in glioma. It was demonstrated that TCF19 activated DHX32 transcriptional activity in glioma by combining it with the promoter of DHX32. DHX32 promoted glioma cell growth and cell-cycle transition while restraining apoptosis. Overexpressing DHX32 eliminated the function of TCF19 knockdown on cell multiplication, cell-cycle transition, and apoptosis. Moreover, TCF19 activated the β-catenin pathway by enhancing DHX32 transcriptional activity.
conclusionTCF19 promotes glioma cell multiplication and cell-cycle transition while suppressing apoptosis by modulating the β-catenin signaling pathway via accelerating DHX32 transcription. These findings provide a promising therapeutic target for glioma.
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