Jing Tan, Haiping Lian, Qi Zheng, Tingting Yang, Tuo Wang
{"title":"TCF19通过加速DHX32转录调控Β-Catenin信号通路促进胶质瘤细胞增殖","authors":"Jing Tan, Haiping Lian, Qi Zheng, Tingting Yang, Tuo Wang","doi":"10.2174/0115680096360071241215171342","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Objective: </strong>This research aimed to explore the function of TCF19 on glioma progression and clarify the potential mechanism.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>","PeriodicalId":10816,"journal":{"name":"Current cancer drug targets","volume":" ","pages":""},"PeriodicalIF":2.3000,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"TCF19 Enhances Glioma Cell Proliferation via Modulating the Β-Catenin Signaling Pathway through Accelerating DHX32 Transcription.\",\"authors\":\"Jing Tan, Haiping Lian, Qi Zheng, Tingting Yang, Tuo Wang\",\"doi\":\"10.2174/0115680096360071241215171342\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Objective: </strong>This research aimed to explore the function of TCF19 on glioma progression and clarify the potential mechanism.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p>\",\"PeriodicalId\":10816,\"journal\":{\"name\":\"Current cancer drug targets\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":2.3000,\"publicationDate\":\"2025-01-20\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current cancer drug targets\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.2174/0115680096360071241215171342\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ONCOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current cancer drug targets","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.2174/0115680096360071241215171342","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ONCOLOGY","Score":null,"Total":0}
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.
期刊介绍：
Current Cancer Drug Targets aims to cover all the latest and outstanding developments on the medicinal chemistry, pharmacology, molecular biology, genomics and biochemistry of contemporary molecular drug targets involved in cancer, e.g. disease specific proteins, receptors, enzymes and genes.
Current Cancer Drug Targets publishes original research articles, letters, reviews / mini-reviews, drug clinical trial studies and guest edited thematic issues written by leaders in the field covering a range of current topics on drug targets involved in cancer.
As the discovery, identification, characterization and validation of novel human drug targets for anti-cancer drug discovery continues to grow; this journal has become essential reading for all pharmaceutical scientists involved in drug discovery and development.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
