The role of sleep deprivation in prostate cancer and a preliminary exploration of its mechanisms

IF 3.2 4区医学 Q2 PATHOLOGY

Pathology, research and practice Pub Date : 2026-04-01 Epub Date: 2026-01-27 DOI:10.1016/j.prp.2026.156379

Jialong Zhang , Lexing Yang , Jun He , Weiyi Li, Hongzhi Wang, Chaozhao Liang

{"title":"The role of sleep deprivation in prostate cancer and a preliminary exploration of its mechanisms","authors":"Jialong Zhang , Lexing Yang , Jun He , Weiyi Li, Hongzhi Wang, Chaozhao Liang","doi":"10.1016/j.prp.2026.156379","DOIUrl":null,"url":null,"abstract":"<div><div>Previous studies suggested the link between sleep deprivation and prostate cancer, but its impact on disease progression is unclear. Moreover, clarifying this relationship could offer insights into prostate cancer mechanisms and potential treatments. In the present study, questionnaire and sleep monitoring of prostate cancer patients indicate that worse sleep quality correlates with higher Gleason scores. Subsequently, to study the effects of sleep deprivation in vivo, a sleep deprivation mouse model was established. Our findings show that sleep deprivation could accelerate tumor growth. Then, we performed transcriptome sequencing to infer the underlying mechanism. RNA sequencing found inflammation related pathways were activated in the sleep deprivation model. Moreover, we identified CXCL13 as a key mediator of sleep deprivation induced prostate progression. And inhibition of CXCR5, the receptor of CXCL13, reduced its tumor promoting effects. Molecular mechanism studies showed that CXCL13 enhanced cancer cell proliferation via activating JNK signaling pathway. In summary, our findings suggest that sleep deprivation may accelerate prostate cancer progression by activating the CXCL13/CXCR5/JNK signaling axis. These results provide preliminary insights into a potential therapeutic direction.</div></div>","PeriodicalId":19916,"journal":{"name":"Pathology, research and practice","volume":"280 ","pages":"Article 156379"},"PeriodicalIF":3.2000,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pathology, research and practice","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0344033826000300","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/1/27 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"PATHOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Previous studies suggested the link between sleep deprivation and prostate cancer, but its impact on disease progression is unclear. Moreover, clarifying this relationship could offer insights into prostate cancer mechanisms and potential treatments. In the present study, questionnaire and sleep monitoring of prostate cancer patients indicate that worse sleep quality correlates with higher Gleason scores. Subsequently, to study the effects of sleep deprivation in vivo, a sleep deprivation mouse model was established. Our findings show that sleep deprivation could accelerate tumor growth. Then, we performed transcriptome sequencing to infer the underlying mechanism. RNA sequencing found inflammation related pathways were activated in the sleep deprivation model. Moreover, we identified CXCL13 as a key mediator of sleep deprivation induced prostate progression. And inhibition of CXCR5, the receptor of CXCL13, reduced its tumor promoting effects. Molecular mechanism studies showed that CXCL13 enhanced cancer cell proliferation via activating JNK signaling pathway. In summary, our findings suggest that sleep deprivation may accelerate prostate cancer progression by activating the CXCL13/CXCR5/JNK signaling axis. These results provide preliminary insights into a potential therapeutic direction.

查看原文本刊更多论文

睡眠剥夺在前列腺癌中的作用及其机制的初步探讨

先前的研究表明睡眠不足与前列腺癌之间存在联系，但其对疾病进展的影响尚不清楚。此外，澄清这种关系可以为前列腺癌的机制和潜在的治疗提供见解。本研究通过对前列腺癌患者的问卷调查和睡眠监测发现，睡眠质量越差，Gleason评分越高。随后，为了在体内研究睡眠剥夺的影响，我们建立了睡眠剥夺小鼠模型。我们的研究结果表明，睡眠不足会加速肿瘤的生长。然后，我们进行转录组测序来推断潜在的机制。RNA测序发现，在睡眠剥夺模型中，炎症相关通路被激活。此外，我们确定了CXCL13是睡眠剥夺诱导前列腺进展的关键介质。抑制CXCL13的受体CXCR5可降低其促肿瘤作用。分子机制研究表明，CXCL13通过激活JNK信号通路促进癌细胞增殖。总之，我们的研究结果表明，睡眠剥夺可能通过激活CXCL13/CXCR5/JNK信号轴来加速前列腺癌的进展。这些结果为潜在的治疗方向提供了初步的见解。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文求助全文

来源期刊

Pathology, research and practice 医学-病理学

CiteScore

5.00

自引率

3.60%

发文量

405

审稿时长

24 days

期刊介绍： Pathology, Research and Practice provides accessible coverage of the most recent developments across the entire field of pathology: Reviews focus on recent progress in pathology, while Comments look at interesting current problems and at hypotheses for future developments in pathology. Original Papers present novel findings on all aspects of general, anatomic and molecular pathology. Rapid Communications inform readers on preliminary findings that may be relevant for further studies and need to be communicated quickly. Teaching Cases look at new aspects or special diagnostic problems of diseases and at case reports relevant for the pathologist''s practice.