Evidence map›Paper›PMID 22562171›Full record

ArticleEndocrinology2012

Reprimo (RPRM) is a novel tumor suppressor in pituitary tumors and regulates survival, proliferation, and tumorigenicity.

Mei Xu, Aaron J Knox, Katherine A Michaelis, Katja Kiseljak-Vassiliades, Bette K Kleinschmidt-DeMasters, Kevin O Lillehei, Margaret E Wierman

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 47 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Sex-specific thermoregulatory effects of estrogen signaling inbioRxiv : the preprint server for biology · 2025
    Article
  5. Review
  6. Extrinsic induction of apoptosis and tumor suppression via the p53-Reprimo-Hippo-YAP/TAZ-p73 pathway.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  7. The expression ofFrontiers in endocrinology · 2024
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Expression ofFrontiers in neuroanatomy · 2018
    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 3 institutions in 1 country.

Mei XuDepartment of Medicine, Physiology, and Biophysics, University of Colorado Denver, Aurora, Colorado 80045, USA.
Aaron J Knox
Katherine A Michaelis
Katja Kiseljak-Vassiliades
Bette K Kleinschmidt-DeMasters
Kevin O Lillehei
Margaret E Wierman
Veterans Health Administration · USThe Medical Center of Aurora · USUniversity of Colorado Denver · US

Funding

Role of the Sterile20 (Ste20)-like kinase MST4 in Pituitary TumorigenesisI01BX001876 · VA · VA EASTERN COLORADO HEALTH CARE SYSTEM · PI WIERMAN, MARGARET E · 2014 to 2017
–
BLRD VA I01 BX001876
6 · The paper itself

Abstract

Reprimo (RPRM), initially identified as a downstream effector of p53-induced cell cycle arrest at G(2)/M, is a putative tumor suppressor silenced in some types of cancer. In microarrays, the RPRM transcript was repressed 26-fold in gonadotrope (null cell) human pituitary tumors compared with normal pituitary but in the absence of changes in p53. Inhibition of RPRM mRNA was confirmed by RT-PCR in all gonadotrope tumors, most GH samples, and variably in other tumor types. Human pituitary tumors showed no evidence of abnormal promoter hypermethylation as a mechanism of RPRM repression. RPRM stable expression in gonadotrope (LβT2) and GH (GH3) pituitary cells resulted in decreased rates of cell proliferation by 55 and 30%, respectively; however, RPRM reexpression did not alter G(2)/M transition. In addition, RPRM increased rates of apoptosis in response to growth factor deprivation as assessed by caspase-3 cleavage and nuclear condensation. Clonagenic assays showed a 5.3- and 3.7-fold suppression of colony growth in RPRM-overexpressing LβT2 and GH3 cells, respectively, supporting its role as a tumor suppressor. In cells stably expressing RPRM mRNA, protein levels were actively suppressed due to rapid degradation through ubiquitination and proteasomal targeting. Growth factor withdrawal, as a model of cellular stress, stabilized RPRM protein levels. Together these data suggest that RPRM is transiently up-regulated at a posttranscriptional level in times of cellular stress to restrict cell survival, proliferation, and tumor formation. When RPRM is silenced as in human pituitary tumors, unrestrained growth and tumor progression may occur.

Indexed as

Gene Expression Regulation, NeoplasticActive Transport, Cell NucleusAnimalsCell Cycle ProteinsCell DivisionCell LineCell Line, TumorCell ProliferationCell SurvivalCpG IslandsCytoplasmG2 PhaseGenes, Tumor SuppressorGlycoproteinsHumansMiceCell Cycle ProteinsGlycoproteinsREPRIMO protein, mouseRPRM protein, human

Identifiers

PMID22562171
PMCPMC4714648
OpenAlexW2054294818

What OpenQuestion holds

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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.