Evidence map›Paper›PMID 39322688›Full record

ArticleBritish journal of cancer2024

Nuclear receptor TLX functions to promote cancer stemness and EMT in prostate cancer via its direct transactivation of CD44 and stem cell-regulatory transcription factors.

Sin Ting Chow, Jiaqi Fan, Xingxing Zhang, Yuliang Wang, Youjia Li, Chi-Fai Ng, Xiaojuan Pei, Qingyou Zheng, Fei Wang, Dinglan Wu and 1 more

Abstract read
In one paragraph

Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Deciphering precursor cell dynamics in esophageal preneoplasia via genetic barcoding and single-cell transcriptomics.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. 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.

Sin Ting Chow *School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong, China.
Jiaqi Fan *School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong, China.
Xingxing ZhangSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong, China.
Yuliang WangSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong, China.
Youjia LiSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong, China.
Chi-Fai NgDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, Hong Kong, China.ORCID http://orcid.org/0000-0002-1723-9646
Xiaojuan PeiDepartment of Pathology, Shenzhen Hospital, Southern Medical University, Shenzhen, Guandong, China.
Qingyou ZhengDepartment of Urology, Shenzhen Hospital, Southern Medical University, Shenzhen, Guangdong Province, China.
Fei WangDepartment of Urology, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou, Hainan Province, China.
Dinglan WuDepartment of Surgery, Faculty of Medicine, The Chinese University of Hong Kong, Hong Kong, Hong Kong, China. wudinglan@163.com.ORCID http://orcid.org/0000-0002-5057-9626
Franky Leung ChanSchool of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, Hong Kong, China. franky-chan@cuhk.edu.hk.ORCID http://orcid.org/0000-0003-0567-2052

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81872283 and 82273341Research Grants Council, University Grants Committee (RGC, UGC) 14110918
6 · The paper itself

Abstract

backgroundProstate cancer stem cells (PCSCs) play crucial roles in therapy-resistance and metastasis in castration-resistant prostate cancer (CRPC). Certain functional link between cancer stemness and epithelial-mesenchymal transition (EMT) is involved in CRPC. However, up-stream regulators controlling these two processes in PCSCs are still poorly understood. Recently, we have shown that orphan nuclear receptor TLX can promote tumour initiation and progression in CRPC by repressing androgen receptor and oncogene-induced senescence.

methodsPCSCs were isolated from various prostate cancer cell lines and clinical tumour tissues using multiple methods for various in vitro and in vivo oncogenic growth analyses. Direct targets of TLX involved in stemness and EMT regulation were determined by specific reporter gene assays and ligand-driven modulation of TLX activity.

resultsPCSCs isolated from various sources exhibited increased expression of TLX. Functional and molecular characterisation showed that TLX could function to promote cancer stemness and EMT in prostate cancer cells via its direct transactivation of CD44, SOX2, POU5F1 and NANOG, which share certain functional crosstalk in these two cellular processes.

conclusionsTLX could act as a key up-stream regulator in transcriptional control of stemness and EMT in PCSCs, which contribute to their tumorigenicity, castration-resistance and metastasis potentials in advanced prostate cancer.

Indexed as

Epithelial-Mesenchymal TransitionHyaluronan ReceptorsNeoplastic Stem CellsTranscriptional ActivationAnimalsCell Line, TumorGene Expression Regulation, NeoplasticHumansMaleMiceNanog Homeobox ProteinOctamer Transcription Factor-3Orphan Nuclear ReceptorsProstatic NeoplasmsProstatic Neoplasms, Castration-ResistantReceptors, Cytoplasmic and NuclearCD44 protein, humanHyaluronan ReceptorsNanog Homeobox ProteinNANOG protein, humanNR2E1 protein, humanOctamer Transcription Factor-3Orphan Nuclear ReceptorsPOU5F1 protein, humanReceptors, Cytoplasmic and NuclearSOX2 protein, humanSOXB1 Transcription Factors

Identifiers

PMID39322688
PMCPMC11519473

What OpenQuestion holds

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Registered trials

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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.