Evidence map›Paper›PMID 36841806›Full record

ArticleCell death & disease2023

NRP1 promotes prostate cancer progression via modulating EGFR-dependent AKT pathway activation.

Peng Zhang, Liang Chen, Fenfang Zhou, Zhiwen He, Gang Wang, Yongwen Luo

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
16.0field-weighted citation impact, top 1% of its field
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

34 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Targeting the ANGPTL4/NRP1/ABL1/RAD51 axis reverses cisplatin resistance by impairing DNA damage repair in head and neck cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Neuropilin-1: A Multifaceted Target for Cancer Therapy.Current oncology (Toronto, Ont.) · 2025
    Review
  17. Article
  18. Review
  19. 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

6 authors at 2 institutions in 2 countries.

Peng Zhang *Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.ORCID 0000-0002-9967-1597
Liang Chen *Department of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Fenfang ZhouDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Zhiwen HeDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China.
Gang WangDepartment of Biological Repositories, Zhongnan Hospital of Wuhan University, Wuhan, China. gangwang.uro@whu.edu.cn.
Yongwen LuoDepartment of Urology, Zhongnan Hospital of Wuhan University, Wuhan, China. luoywen@whu.edu.cn.ORCID 0000-0002-8724-6550
Wuhan University · CNHeritage Preservation · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Prostate cancer (PCa) is the most common malignant tumor with a high global incidence in males. The mechanism underlying PCa progression is still not clear. This study observed that NRP1 was highly expressed in PCa and associated with poor prognosis in PCa patients. Functionally, NRP1 depletion attenuated the proliferation and migration ability of PCa cells in vitro and in vivo, while NRP1 overexpression promoted PCa cell proliferation and migration. Moreover, it was observed that NRP1 depletion induced G1 phase arrest in PCa cells. Mechanistically, HIF1α is bound to the specific promoter region of NRP1, thereby regulating its transcriptional activation. Subsequently, NRP1 interacted with EGFR, leading to EGFR phosphorylation. This study also provided evidence that the b1/b2 domain of NRP1 was responsible for the interaction with the extracellular domain of EGFR. Moreover, EGFR mediated NRP1-induced activation of the AKT signaling pathway, which promoted the malignant progression of PCa. In addition, the administration of NRP1 inhibitor EG01377 significantly inactivated the EGFR/AKT signaling axis, thereby suppressing PCa progression. In conclusion, the findings from this study highlighted the molecular mechanism underlying NRP1 expression in PCa and provide a potential predictor and therapeutic target for clinical prognosis and treatment of PCa.

Indexed as

Neuropilin-1Prostatic NeoplasmsProto-Oncogene Proteins c-aktCell Line, TumorCell ProliferationErbB ReceptorsHumansMaleSignal TransductionEGFR protein, humanErbB ReceptorsNeuropilin-1NRP1 protein, humanProto-Oncogene Proteins c-akt

Identifiers

PMID36841806
PMCPMC9958327
OpenAlexW4322009567

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.