Evidence map›Paper›PMID 26011939›Full record

ArticleOncotarget2015

PC-1/PrLZ confers resistance to rapamycin in prostate cancer cells through increased 4E-BP1 stability.

Lan Yu, Zeng-Fu Shang, Jian Wang, Hongtao Wang, Fang Huang, Zhe Zhang, Ying Wang, Jianguang Zhou, Shanhu Li

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Isoform 1 of TPD52 (PC-1) promotes neuroendocrine transdifferentiation in prostate cancer cells.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  10. 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

9 authors at 2 institutions in 1 country.

Lan YuLaboratory of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing 100850, PR China.
Zeng-Fu ShangSchool of Radiation Medicine and Protection, Medical College of Soochow University, Collaborative Innovation Center of Radiation Medicine of Jiangsu Higher Education Institutions, Suzhou, Jiangsu 215123, PR China.
Jian WangLaboratory of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing 100850, PR China.
Hongtao WangState Key Laboratory of Experimental Hematology Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin 300200, PR China.
Fang HuangLaboratory of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing 100850, PR China.
Zhe ZhangLaboratory of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing 100850, PR China.
Ying WangLaboratory of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing 100850, PR China.
Jianguang ZhouLaboratory of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing 100850, PR China.
Shanhu LiLaboratory of Medical Molecular Biology, Beijing Institute of Biotechnology, Beijing 100850, PR China.
Institute of Hematology & Blood Diseases Hospital · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An important strategy for improving advanced PCa treatment is targeted therapies combined with chemotherapy. PC-1, a prostate Leucine Zipper gene (PrLZ), is specifically expressed in prostate tissue as an androgen-induced gene and is up-regulated in advanced PCa. Recent work confirmed that PC-1 expression promotes PCa growth and androgen-independent progression. However, how this occurs and whether this can be used as a biomarker is uncertain. Here, we report that PC-1 overexpression confers PCa cells resistance to rapamycin treatment by antagonizing rapamycin-induced cytostasis and autophagy (rapamycin-sensitivity was observed in PC-1-deficient (shPC-1) C4-2 cells). Analysis of the mTOR pathway in PCa cells with PC-1 overexpressed and depressed revealed that eukaryotic initiation factor 4E-binding protein 1(4E-BP1) was highly regulated by PC-1. Immunohistochemistry assays indicated that 4E-BP1 up-regulation correlates with increased PC-1 expression in human prostate tumors and in PCa cells. Furthermore, PC-1 interacts directly with 4E-BP1 and stabilizes 4E-BP1 protein via inhibition of its ubiquitination and proteasomal degradation. Thus, PC-1 is a novel regulator of 4E-BP1 and our work suggests a potential mechanism through which PC-1 enhances PCa cell survival and malignant progression and increases chemoresistance. Thus, the PC-1-4E-BP1 interaction may represent a therapeutic target for treating advanced PCa.

Indexed as

Adaptor Proteins, Signal TransducingBiomarkers, TumorCell Cycle ProteinsCell Line, TumorDisease ProgressionHumansMalePhosphoproteinsPhosphoric Diester HydrolasesPhosphorylationProstatic NeoplasmsPyrophosphatasesSignal TransductionSirolimusAdaptor Proteins, Signal TransducingBiomarkers, TumorCell Cycle Proteinsectonucleotide pyrophosphatase phosphodiesterase 1EIF4EBP1 protein, humanPhosphoproteinsPhosphoric Diester HydrolasesPyrophosphatasesSirolimus4E-BP1mTOR pathwayPC-1/PrLZPCarapamycin-resistance

Identifiers

PMID26011939
PMCPMC4653010
OpenAlexW2116694731

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.