Evidence mapPaperPMID 40170077Full record

ReviewMolecular cancer2025

Regulation of cellular senescence in tumor progression and therapeutic targeting: mechanisms and pathways.

Bowei Liu, Zhigang Peng, Hao Zhang, Nan Zhang, Zaoqu Liu, Zhiwei Xia, Shaorong Huang, Peng Luo, Quan Cheng

Abstract readReview
In one paragraph

Review in Molecular cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing 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

59 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. CSPG4 Mediates Inflammatory, Cell Death, and Senescence Responses in Enteric Glia Exposed to Clostridioides difficile Toxins.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Cellular Senescence Triggered by Food and Environmental Genotoxins.International journal of molecular sciences · 2026
    Review
  15. Article
  16. Multiomics analysis reveals that senescent CXCL16Journal of translational medicine · 2026
    Article
  17. Article
  18. Article
  19. ALYREF-mediated mInternational journal of biological sciences · 2026
    Article
  20. 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

9 authors.

Bowei Liu *Department of Neurosurgery, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan, China.
Zhigang Peng *Department of Neurosurgery, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan, China.
Hao ZhangDepartment of Neurosurgery, The Second Affiliated Hospital, Chongqing Medical University, Chongqing, China.
Nan ZhangCollege of Life Science and Technology, Huazhong University of Science and Technology, Wuhan, China.
Zaoqu LiuInstitute of Basic Medical Sciences, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
Zhiwei XiaDepartment of Neurology, Hunan Aerospace Hospital, Hunan Normal University, Changsha, Hunan, China. xiazhiwei2011@gmail.com.
Shaorong HuangInstitute of Geriatrics, Jiangxi Provincial People's Hospital, The First Affiliated Hospital of Nanchang Medical College, Nanchang, Jiangxi, China. huangshaorong@ncmc.edu.cn.
Peng LuoDepartment of Oncology, Zhujiang Hospital, Southern Medical University, Guangzhou, China. luopeng@smu.edu.cn.
Quan ChengDepartment of Neurosurgery, Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan, China. chengquan@csu.edu.cn.

Funding

Hunan Youth Science and Technology Talent Project NO.2023RC3074Key R&D Program of Jiangxi Province, China NO.20243BBI91007National Natural Science Foundation of China NO.82372943Science Foundation of the AMHT Group NO.2022YK04
6 · The paper itself

Abstract

Cellular senescence, a stable state of cell cycle arrest induced by various stressors or genomic damage, is recognized as a hallmark of cancer. It exerts a context-dependent dual role in cancer initiation and progression, functioning as a tumor suppressor and promoter. The complexity of senescence in cancer arises from its mechanistic diversity, potential reversibility, and heterogeneity. A key mediator of these effects is the senescence-associated secretory phenotype (SASP), a repertoire of bioactive molecules that influence tumor microenvironment (TME) remodeling, modulate cancer cell behavior, and contribute to therapeutic resistance. Given its intricate role in cancer biology, senescence presents both challenges and opportunities for therapeutic intervention. Strategies targeting senescence pathways, including senescence-inducing therapies and senolytic approaches, offer promising avenues for cancer treatment. This review provides a comprehensive analysis of the regulatory mechanisms governing cellular senescence in tumors. We also discuss emerging strategies to modulate senescence, highlighting novel therapeutic opportunities. A deeper understanding of these processes is essential for developing precision therapies and improving clinical outcomes.

Indexed as

Cellular SenescenceNeoplasmsSignal TransductionAnimalsDisease ProgressionHumansMolecular Targeted TherapySenescence-Associated Secretory PhenotypeTumor MicroenvironmentCellular senescenceDNA damageSASPTherapyTumor

Identifiers

PMID40170077
PMCPMC11963325

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

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 Socratic graph.