Evidence map›Paper›PMID 36526675›Full record

ArticleBritish journal of cancer2023

STAT3 potentiates RNA polymerase I-directed transcription and tumor growth by activating RPA34 expression.

Cheng Zhang, Juan Wang, Xiaoye Song, Deen Yu, Baoqiang Guo, Yaoyu Pang, Xiaomei Yin, Shasha Zhao, Huan Deng, Shihua Zhang and 1 more

Open access · greenAbstract read
In one paragraph

Article in British journal of cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.4field-weighted citation impact, top 35% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

Cheng ZhangSchool of Life Science and Health, Wuhan University of Science and Technology, Wuhan, 430065, China.
Juan WangSchool of Life Science and Health, Wuhan University of Science and Technology, Wuhan, 430065, China.
Xiaoye SongSchool of Life Science and Health, Wuhan University of Science and Technology, Wuhan, 430065, China.
Deen YuSchool of Life Science and Health, Wuhan University of Science and Technology, Wuhan, 430065, China.
Baoqiang GuoDepartment of Life Sciences, Manchester Metropolitan University, Manchester, M15 6BH, UK.
Yaoyu PangInstitute of Systems, Molecular and Integrative Biology, University of Liverpool, Liverpool, L69 3GE, UK.
Xiaomei YinSchool of Life Science and Health, Wuhan University of Science and Technology, Wuhan, 430065, China.
Shasha ZhaoSchool of Life Science and Health, Wuhan University of Science and Technology, Wuhan, 430065, China. zhaoshasha@wust.edu.cn.ORCID 0000-0001-6973-9063
Huan DengSchool of Life Science and Health, Wuhan University of Science and Technology, Wuhan, 430065, China. denghuan@wust.edu.cn.ORCID 0000-0001-7160-861X
Shihua ZhangSchool of Life Science and Health, Wuhan University of Science and Technology, Wuhan, 430065, China. zhangshihua@wust.edu.cn.ORCID 0000-0002-0111-7679
Wensheng DengSchool of Life Science and Health, Wuhan University of Science and Technology, Wuhan, 430065, China. dengwensheng@wust.edu.cn.ORCID 0000-0003-2454-2288
Wuhan University of Technology · CNWuhan University of Science and Technology · CNManchester Metropolitan University · GBUniversity of Liverpool · GBWuchang University of Technology · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31671357National Natural Science Foundation of China (National Science Foundation of China) 62172312
6 · The paper itself

Abstract

backgroundDeregulation of either RNA polymerase I (Pol I)-directed transcription or expression of signal transducer and activator of transcription 3 (STAT3) correlates closely with tumorigenesis. However, the connection between STAT3 and Pol I-directed transcription hasn't been investigated.

methodsThe role of STAT3 in Pol I-directed transcription was determined using combined techniques. The regulation of tumor cell growth mediated by STAT3 and Pol I products was analyzed in vitro and in vivo. RNAseq, ChIP assays and rescue assays were used to uncover the mechanism of Pol I transcription mediated by STAT3.

resultsSTAT3 expression positively correlates with Pol I product levels and cancer cell growth. The inhibition of STAT3 or Pol I products suppresses cell growth. Mechanistically, STAT3 activates Pol I-directed transcription by enhancing the recruitment of the Pol I transcription machinery to the rDNA promoter. STAT3 directly activates Rpa34 gene transcription by binding to the RPA34 promoter, which enhances the occupancies of the Pol II transcription machinery factors at this promoter. Cancer patients with RPA34 high expression lead to poor survival probability and short survival time.

conclusionSTAT3 potentiates Pol I-dependent transcription and tumor cell growth by activating RPA34 in vitro and in vivo.

Indexed as

RNA Polymerase ISTAT3 Transcription FactorTranscription, GeneticHumansPromoter Regions, GeneticRNA Polymerase IIRNA Polymerase IRNA Polymerase IISTAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID36526675
PMCPMC9977892
OpenAlexW4311821014

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.