Evidence map›Paper›PMID 40274762›Full record

ArticleCell death & disease2025

BCAT2 binding to PCBP1 regulates the PI3K/AKT signaling pathway to inhibit autophagy-related apoptosis and ferroptosis in prostate cancer.

Wangli Mei, Mengyu Wei, Chaozhi Tang, Weiyi Li, Bowen Ye, Shiyong Xin, Weiguo Ma, Lin Ye

Abstract read
In one paragraph

Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. 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

8 authors.

Wangli Mei *Department of Urology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Mengyu Wei *Department of Urology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Chaozhi Tang *Department of Urology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Weiyi LiDepartment of Urology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Bowen YeDepartment of Urology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China.
Shiyong XinDepartment of Urology, First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China. xinshiyong66@163.com.ORCID http://orcid.org/0000-0002-6015-8665
Weiguo MaDepartment of Urology, Tongxin People's Hospital, Ningxia, 751300, China. maweiguo_87@126.com.
Lin YeDepartment of Urology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, 200120, China. ericyelin@tongji.edu.cn.ORCID http://orcid.org/0000-0002-3304-4558

Funding

National Natural Science Foundation of China (National Science Foundation of China) 81972409 & 81672549Natural Science Foundation of Ningxia Province (Ningxia Provincial Natural Science Foundation) 2024AAC03844
6 · The paper itself

Abstract

Prostate cancer (PCa) has emerged as a predominant cause of cancer-related mortality among men globally. The mechanisms of branched-chain amino acids (BCAAs) contributing to the development of PCa remain inadequately elucidated. The objective of this study was to examine the involvement of BCAAs and BCAT2 in tumorigenesis. BCAAs exhibited elevated expression levels in PCa tissues and cells. Among the critical enzymes involved in the BCAA metabolic pathway, only BCAT2 demonstrated significant expression in PCa and was closely associated with tumor progression and patient prognosis. RNA sequencing along with related functional experiments indicated that BCAT2 can inhibit autophagy, autophagy-related apoptosis, and ferroptosis in PCa. Furthermore, the results of co-immunoprecipitation, mass spectrometry, and other methodologies established that PCBP1, as a downstream protein interacting with BCAT2, co-regulates the PI3K/AKT pathway, thereby influencing progression of PCa. Moreover, BCAT2 interacted with PCBP1 at Leucine 239 to collaboratively regulate the PI3K/AKT signaling pathway, which is crucial for the initiation and progression of PCa. Targeting BCAT2 may represent a promising therapeutic strategy to prevent proliferation of PCa.

Indexed as

ApoptosisAutophagyFerroptosisHeterogeneous-Nuclear RibonucleoproteinsPhosphatidylinositol 3-KinasesProstatic NeoplasmsProto-Oncogene Proteins c-aktRNA-Binding ProteinsAnimalsCell Line, TumorDNA-Binding ProteinsGene Expression Regulation, NeoplasticHumansMaleMiceProtein BindingDNA-Binding ProteinsHeterogeneous-Nuclear RibonucleoproteinsPCBP1 protein, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA-Binding Proteins

Identifiers

PMID40274762
PMCPMC12022009

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.