Evidence map›Paper›PMID 28078560›Full record

ArticleMedical oncology (Northwood, London, England)2017

Knockdown of PYCR1 inhibits cell proliferation and colony formation via cell cycle arrest and apoptosis in prostate cancer.

Tengyue Zeng, Libing Zhu, Min Liao, Wenli Zhuo, Shunliang Yang, Weizhen Wu, Dong Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

56 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Cellular Signaling of Amino Acid Metabolism in Prostate Cancer.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. Article
  10. Novel Fragment Inhibitors of PYCR1 from Docking-Guided X-ray Crystallography.Journal of chemical information and modeling · 2024
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  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

7 authors at 2 institutions in 1 country.

Tengyue ZengDepartment of Urology, Fuzhou General Hospital, Fujian Medical University, No.156, Xi'erhuan North Road, Fuzhou, 350025, China.
Libing ZhuDepartment of Urology, Lushan Sanatorium of the PLA, Lushan, 332000, China.
Min LiaoDepartment of Urology, Fuzhou General Hospital, Fujian Medical University, No.156, Xi'erhuan North Road, Fuzhou, 350025, China.
Wenli ZhuoDepartment of Urology, Fuzhou General Hospital, Fujian Medical University, No.156, Xi'erhuan North Road, Fuzhou, 350025, China.
Shunliang YangDepartment of Urology, Fuzhou General Hospital, Fujian Medical University, No.156, Xi'erhuan North Road, Fuzhou, 350025, China.
Weizhen WuDepartment of Urology, Fuzhou General Hospital, Fujian Medical University, No.156, Xi'erhuan North Road, Fuzhou, 350025, China.
Dong WangDepartment of Urology, Fuzhou General Hospital, Fujian Medical University, No.156, Xi'erhuan North Road, Fuzhou, 350025, China. wangdongdr@sina.com.
Fujian Medical University · CNLushan Botanical Garden · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pyrroline-5-carboxylate reductase 1 (PYCR1) is an enzyme involved in cell metabolism, which has been shown to be up-regulated in cancers. However, the functions of PYCR1 in prostate cancers (PCa) are still largely unknown. In the present study, we found that PYCR1 was highly expressed in prostate cancer tissues and then knocked down PYCR1 in PCa cell lines (DU145, PC-3 and LNCap) via lentivirus-mediated gene delivery and analyzed its biological function. Both qRT-PCR and western blotting indicated that PYCR1 was suppressed efficiently after sh-PYCR1 infection. Further analysis indicated knockdown of PYCR1 significantly inhibited PCa cell growth and colony formation ability. The inhibition effects on growth were likely due to G2/M-phase arrest and enhanced cell apoptosis, as determined by flow cytometer analysis. At last, we verified the expression levels of cell cycle regulatory proteins, including CDK1, CDK2, CDK4 and Cyclin B1 were all downregulated and cell apoptotic-related proteins, including cleaved caspase 3 and cleaved PARP were increased in PCa cells after PYCR1 knockdown. Furthermore, PYCR1 has been shown not to be directly regulated by androgen receptor (AR) levels. These results show the functions of PYCR1 in PCa tumorigenesis for the first time and suggest that PYCR1 might be a good potential therapy approach for treating PCa.

Indexed as

ApoptosisCell Line, TumorCell Proliferationdelta-1-Pyrroline-5-Carboxylate ReductaseG2 Phase Cell Cycle CheckpointsGene Knockdown TechniquesHEK293 CellsHumansMaleMiddle AgedM Phase Cell Cycle CheckpointsProstatic NeoplasmsPyrroline Carboxylate ReductasesReceptors, AndrogenRNA, Small InterferingSignal TransductionAR protein, humandelta-1-Pyrroline-5-Carboxylate ReductasePyrroline Carboxylate ReductasesReceptors, AndrogenRNA, Small InterferingApoptosisAR signalingCell cycleCell proliferationProstate cancerPYCR1

Identifiers

PMID28078560
OpenAlexW2576116195

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.