TCF19 Enhances Glioma Cell Proliferation via Modulating the Β-Catenin Signaling Pathway through Accelerating DHX32 Transcription.

Background: Transcription 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.

Objective: This research aimed to explore the function of TCF19 on glioma progression and clarify the potential mechanism.

Methods: TCF19 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.

Results: TCF19 was observably upregulated in glioma and has important clinical significance. Overexpressing TCF19 expedited glioma cell multiplication and cell-cycle transition, mean-while preventing apoptosis. TCF19 knockdown inhibited cell proliferation, cell-cycle transi-tion, and tumour growth, simultaneously accelerating apoptosis. TCF19 expressions had a positive correlation with DHX32 expressions in glioma. It was demonstrated that TCF19 acti-vated 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 en-hancing DHX32 transcriptional activity.

Conclusion: TCF19 promotes glioma cell multiplication and cell-cycle transition while sup-pressing apoptosis by modulating the β-catenin signaling pathway via accelerating DHX32 transcription. These findings provide a promising therapeutic target for glioma.