Evidence map›Paper›PMID 38951428›Full record

ArticleScience China. Life sciences2024

The p38/MAPK pathway as a therapeutic target to prevent therapeutic escape of breast cancer stem cells.

Weixiao Yan, Xiaotong Wang, Wenjing Wang, Qi Guo, Na Huang, Hao Chen, Xing-Jie Liang, Yu Han, Dandan Liu, Jinchao Zhang

Abstract read
PubMed Publisher
In one paragraph

Article in Science China. Life sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing 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

12 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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

10 authors.

Weixiao YanState Key Laboratory of New Pharmaceutical Preparations and Excipients; Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education; College of Chemistry and Materials Science, Chemical Biology Key Laboratory of Hebei Province, Hebei University, Baoding, 071002, China.
Xiaotong WangState Key Laboratory of New Pharmaceutical Preparations and Excipients; Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education; College of Chemistry and Materials Science, Chemical Biology Key Laboratory of Hebei Province, Hebei University, Baoding, 071002, China.
Wenjing WangState Key Laboratory of New Pharmaceutical Preparations and Excipients; Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education; College of Chemistry and Materials Science, Chemical Biology Key Laboratory of Hebei Province, Hebei University, Baoding, 071002, China.
Qi GuoState Key Laboratory of New Pharmaceutical Preparations and Excipients; Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education; College of Chemistry and Materials Science, Chemical Biology Key Laboratory of Hebei Province, Hebei University, Baoding, 071002, China.
Na HuangState Key Laboratory of New Pharmaceutical Preparations and Excipients; Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education; College of Chemistry and Materials Science, Chemical Biology Key Laboratory of Hebei Province, Hebei University, Baoding, 071002, China.
Hao ChenState Key Laboratory of New Pharmaceutical Preparations and Excipients; Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education; College of Chemistry and Materials Science, Chemical Biology Key Laboratory of Hebei Province, Hebei University, Baoding, 071002, China.
Xing-Jie LiangCAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, National Center for Nanoscience and Technology, Beijing, 100190, China.
Yu HanState Key Laboratory of New Pharmaceutical Preparations and Excipients; Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education; College of Chemistry and Materials Science, Chemical Biology Key Laboratory of Hebei Province, Hebei University, Baoding, 071002, China.
Dandan LiuState Key Laboratory of New Pharmaceutical Preparations and Excipients; Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education; College of Chemistry and Materials Science, Chemical Biology Key Laboratory of Hebei Province, Hebei University, Baoding, 071002, China. leo-liudan@163.com.
Jinchao ZhangState Key Laboratory of New Pharmaceutical Preparations and Excipients; Key Laboratory of Medicinal Chemistry and Molecular Diagnosis of the Ministry of Education; College of Chemistry and Materials Science, Chemical Biology Key Laboratory of Hebei Province, Hebei University, Baoding, 071002, China. jczhang6970@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer stem cells (CSCs) play an important role in metastasis development, tumor recurrence, and treatment resistance, and are essential for the eradication of cancer. Currently, therapies fail to eradicate CSCs due to their therapeutic stress-induced cellular escape, which leads to enhanced aggressive behaviors compared with CSCs that have never been treated. However, the underlying mechanisms regulating the therapeutic escape remain unknown. To this end, we established a model to isolate the therapeutic escaped CSCs (TSCSCs) from breast CSCs and performed the transcription profile to reveal the mechanism. Mechanistically, we demonstrated that the behavior of therapeutic escape was regulated through the p38/MAPK signaling pathway, resulting in TSCSCs exhibiting enhanced motility and metastasis. Notably, blocking the p38/MAPK signaling pathway effectively reduced motility and metastasis ability both in vitro and in vivo, which were further supported by downregulated motility-related genes and epithelial-mesenchymal transition (EMT)-related proteins vimentin and N-cadherin. The obtained findings reveal the p38/MAPK pathway as a potential therapeutic target for TSCSCs and would provide profound implications for cancer therapy.

Indexed as

Breast NeoplasmsCell MovementEpithelial-Mesenchymal TransitionMAP Kinase Signaling SystemNeoplastic Stem Cellsp38 Mitogen-Activated Protein KinasesAnimalsCell Line, TumorFemaleGene Expression Regulation, NeoplasticHumansMiceMice, Inbred BALB Cp38 Mitogen-Activated Protein Kinasesbreast cancer stem cellsmolecular mechanismmotilityp38/MAPK signaling pathwaytherapeutic escape

Identifiers

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.