Early Growth Response 1 Strengthens Pol-III-Directed Transcription and Transformed Cell Proliferation by Controlling PTEN/AKT Signalling Activity

Wu, Zhenpeng; Huang, Liyun; Zhao, Shasha; Wang, Juan; Zhang, Cheng; Song, Xiaoye; Chen, Qi‐Yue; Du, Jiannan; Yu, Deen; Sun, Xiaofeng; Zhang, Yue; Deng, Wensheng; Zhang, Shihua; Deng, Huan

doi:10.3390/ijms23094930

Cited by 4 publications

(4 citation statements)

References 43 publications

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“…Cell counting was performed every 24 hr, and the resulting data were subjected to statistical analysis. For CCK-8 assays, cells were seeded in 96-well plates, and cell proliferation was monitored based on the protocol as described previously ( Wu et al, 2022 ). For EdU assays, cell proliferation was assessed using the protocol as described previously ( Wu et al, 2022 ).…”

Section: Methodsmentioning

confidence: 99%

“…For CCK-8 assays, cells were seeded in 96-well plates, and cell proliferation was monitored based on the protocol as described previously ( Wu et al, 2022 ). For EdU assays, cell proliferation was assessed using the protocol as described previously ( Wu et al, 2022 ). The rate of EdU-positive cells was obtained by comparing the number of the EdU-positive cells to that of the total cells.…”

Section: Methodsmentioning

confidence: 99%

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STAT3 promotes RNA polymerase III-directed transcription by controlling the miR-106a-5p/TP73 axis

Zhang

Zhao

Deng

et al. 2023

eLife

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Deregulation of Pol III products causes a range of diseases, including neural diseases and cancers. However, the factors and mechanisms that modulate Pol III-directed transcription remain to be found, although massive advances have been achieved. Here, we show that STAT3 positively regulates the activities of Pol III-dependent transcription and cancer cell growth. RNA-seq analysis revealed that STAT3 inhibits the expression of TP73, a member of the p53 family. We found that TP73 is not only required for the regulation of Pol III-directed transcription mediated by STAT3 but also independently suppresses the synthesis of Pol III products. Mechanistically, TP73 can disrupt the assembly of TFIIIB subunits and inhibit their occupancies at Pol III target loci by interacting with TFIIIB subunit TBP. MiR-106a-5p can activate Pol III-directed transcription by targeting the TP73 mRNA 3’ UTR to reduce TP 73 expression. We show that STAT3 activates the expression of miR-106a-5p by binding to the miRNA promoter, indicating that the miR-106a-5p links STAT3 with TP73 to regulate Pol III-directed transcription. Collectively, these findings indicate that STAT3 functions as a positive regulator in Pol III-directed transcription by controlling the miR-106a-5p/TP73 axis.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

STAT3 promotes RNA polymerase III-directed transcription by controlling the miR-106a-5p/TP73 axis

Zhang

Zhao

Deng

et al. 2023

eLife

Self Cite

View full text Add to dashboard Cite

show abstract

“…Cell counting was performed every 24 hours and the resulting data were subjected to statistical analysis. For CCK8 assays, cells were seeded in 96-well plates, cell proliferation was monitored based on the protocol as described previously ( Wu et al, 2022 ). For EdU assays, cell proliferation was assessed using the protocol as described previously ( Wu et al, 2022 ).…”

Section: Methodsmentioning

confidence: 99%

“…For CCK8 assays, cells were seeded in 96-well plates, cell proliferation was monitored based on the protocol as described previously ( Wu et al, 2022 ). For EdU assays, cell proliferation was assessed using the protocol as described previously ( Wu et al, 2022 ). The rate of EdU-positive cells was obtained by comparing the number of the EdU-positive cells to that of the total cells.…”

Section: Methodsmentioning

confidence: 99%

STAT3 promotes RNA polymerase III-directed transcription by controlling the miR-106a-5p/TP73 axis

Zhang

Zhao

Deng

et al. 2022

Preprint

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Deregulation of Pol III products causes a range of diseases, including neural diseases and cancers. However, the pathways and factors that control Pol III-directed transcription have yet to be elucidated. Here, we show that STAT3 positively regulates the activities of Pol III-dependent transcription and cancer cell growth. RNA-seq analysis revealed that STAT3 inhibits the expression of TP73, a member of the p53 family. We found that TP73 is not only required for the regulation of Pol III-directed transcription mediated by STAT3 but also independently suppresses the synthesis of Pol III products. Mechanistically, TP73 can disrupt the assembly of TFIIIB subunits and inhibit their occupancies at Pol III target loci by interacting with TFIIB subunit TBP. MiR-106a-5p can activate Pol III-directed transcription by targeting the TP73 mRNA 3′ UTR to reduce TP 73 expression. We show that STAT3 activates the expression of miR-106a-5p by binding to the microRNA promoter, indicating that miR-106a-5p links STAT3 to TP73 and Pol III transcription. Collectively, these findings indicate that STAT3 functions as a positive regulator in Pol III-directed transcription by controlling the miR-106a-5p/TP73 axis.

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Decoding PTEN: from biological functions to signaling pathways in tumors

Huang,

Zhang,

Zhang

et al. 2024

Mol Biol Rep

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Early Growth Response 1 Strengthens Pol-III-Directed Transcription and Transformed Cell Proliferation by Controlling PTEN/AKT Signalling Activity

Cited by 4 publications

References 43 publications

STAT3 promotes RNA polymerase III-directed transcription by controlling the miR-106a-5p/TP73 axis

STAT3 promotes RNA polymerase III-directed transcription by controlling the miR-106a-5p/TP73 axis

STAT3 promotes RNA polymerase III-directed transcription by controlling the miR-106a-5p/TP73 axis

Decoding PTEN: from biological functions to signaling pathways in tumors

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