Evidence map›Paper›PMID 39369166›Full record

ArticleOncogene2024

Androgen-ablative therapies inducing CXCL8 regulates mTORC1/SREBP2-dependent cholesterol biosynthesis to support progression of androgen receptor negative prostate cancer cells.

Xingyu Xiong, Shiyu Zhang, Weizhen Zhu, Jiajia Du, Xinyang Liao, Siping Hu, Jie Yang, Weitao Zheng, Shi Qiu, Hang Xu and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Oncogene, 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. Review
  2. Phytochemical Analysis and Anticancer Activity ofPharmaceuticals (Basel, Switzerland) · 2026
    Article
  3. Review
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

12 authors.

Xingyu Xiong *Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China.
Shiyu Zhang *Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China.
Weizhen Zhu *Department of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China.
Jiajia DuState Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, SC, China.
Xinyang LiaoDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China.
Siping HuDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China.
Jie YangDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China.
Weitao ZhengDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China.
Shi QiuDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China.
Hang XuDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China. hangxu@wchscu.cn.ORCID 0000-0002-1665-7870
Qiang WeiDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China. weiqiang933@126.com.ORCID 0000-0003-3750-3042
Lu YangDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu, SC, China. wycleflue@163.com.ORCID 0000-0002-3955-150X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Treatment with androgen-ablative therapies effectively inhibited androgen receptor (AR)-positive (AR+) prostate cancer (PCa) cell subtypes, but it resulted in an increase in AR-negative (AR-) PCa cell subtypes. The present study aimed to investigate the debated mechanisms responsible for the changing proportion of cell types, identifying CXCL8 as a synthetic essential effector of AR- PCa cells. AR- PCa cells were found to be susceptible to CXCL8 depletion or inhibition, which impaired their survival. Mechanistically, androgen-ablative therapies resulted in the suppression of AR signaling, leading to the upregulation of CXCL8 gene transcription. CXCL8, in turn, activated the mTORC1 pathway, which increased de novo cholesterol synthesis by activating sterol regulatory element-binding protein-2 (SREBP2). Together, these results suggested that the CXCL8-mTORC1-SREBP2 axis contributed to the exacerbation of tumorigenicity in AR- PCa cells under androgen-ablative therapies.

Indexed as

CholesterolInterleukin-8Mechanistic Target of Rapamycin Complex 1Prostatic NeoplasmsReceptors, AndrogenSterol Regulatory Element Binding Protein 2Androgen AntagonistsAndrogensAnimalsCell Line, TumorDisease ProgressionGene Expression Regulation, NeoplasticHumansMaleMiceSignal TransductionAndrogen AntagonistsAndrogensAR protein, humanCholesterolCXCL8 protein, humanInterleukin-8Mechanistic Target of Rapamycin Complex 1Receptors, AndrogenSREBF2 protein, humanSterol Regulatory Element Binding Protein 2

Identifiers

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.