Evidence map›Paper›PMID 29080043›Full record

ArticleEndocrine2018

PI3K/Akt/mTOR pathway involvement in regulating growth hormone secretion in a rat pituitary adenoma cell line.

Carmelina Di Pasquale, Erica Gentilin, Simona Falletta, Mariaenrica Bellio, Mattia Buratto, Ettore Degli Uberti, Maria Chiara Zatelli

Abstract read
PubMed Publisher
In one paragraph

Article in Endocrine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 11% 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

16 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  7. Review
  8. The p300 Inhibitor A-485 Exerts Antitumor Activity in Growth Hormone Pituitary Adenoma.The Journal of clinical endocrinology and metabolism · 2022
    Article
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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 1 institution in 1 country.

Carmelina Di PasqualeDepartment of Medical Sciences, Section of Endocrinology & Internal Medicine, University of Ferrara, Ferrara, Italy.
Erica GentilinDepartment of Medical Sciences, Section of Endocrinology & Internal Medicine, University of Ferrara, Ferrara, Italy.
Simona FallettaDepartment of Medical Sciences, Section of Endocrinology & Internal Medicine, University of Ferrara, Ferrara, Italy.
Mariaenrica BellioDepartment of Medical Sciences, Section of Endocrinology & Internal Medicine, University of Ferrara, Ferrara, Italy.
Mattia BurattoDepartment of Medical Sciences, Section of Endocrinology & Internal Medicine, University of Ferrara, Ferrara, Italy.
Ettore Degli UbertiDepartment of Medical Sciences, Section of Endocrinology & Internal Medicine, University of Ferrara, Ferrara, Italy.
Maria Chiara ZatelliDepartment of Medical Sciences, Section of Endocrinology & Internal Medicine, University of Ferrara, Ferrara, Italy. ztlmch@unife.it.ORCID 0000-0001-8408-7796
University of Ferrara · IT

Funding

Italian Ministry of Education, Research and University RBAP1153LSItalian Ministry of Education, Research and University RBAP11884M
6 · The paper itself

Abstract

purposeInsulin-like growth factor 1 (IGF1) controls growth hormone (GH) secretion via a negative feed-back loop that may disclose novel mechanisms possibly useful to control GH hyper-secretion. Our aim was to understand whether PI3K/Akt/mTOR pathway is involved in IGF1 negative feedback on GH secretion.

methodsCell viability, GH secretion, Akt, and Erk 1/2 phosphorylation levels in the rat GH3 cell line were assessed under treatment with IGF1 and/or everolimus, an mTOR inhitior.

resultsWe found that IGF1 improves rat GH3 somatotroph cell viability via the PI3K/Akt/mTOR pathway and confirmed that IGF1 exerts a negative feedback on GH secretion by a transcriptional mechanism. We demonstrated that the negative IGF1 loop on GH secretion requires Akt activation that seems to play a pivotal role in the control of GH secretion. Furthermore, Akt activation is independent of PI3K and probably mediated by mTORC2. In addition, we found that Erk 1/2 is not involved in GH3 cell viability regulation, but may have a role in controlling GH secretion, independently of IGF1.

conclusionOur data confirm that mTOR inhibitors may be useful to reduce pituitary adenoma cell viability, while Erk 1/2 pathway may be considered as a useful therapeutic target to control GH secretion. Our results open the field for further studies searching for effective drugs to control GH hyper-secretion.

Indexed as

AdenomaAnimalsCell Line, TumorEverolimusFeedback, PhysiologicalGrowth HormoneImidazolesIndazolesInsulin-Like Growth Factor IPhosphatidylinositol 3-KinasesPhosphorylationPiperazinesPituitary NeoplasmsProto-Oncogene Proteins c-aktQuinolinesRatsdactolisibEverolimusGrowth HormoneImidazolesIndazolesinsulin-like growth factor-1, ratInsulin-Like Growth Factor ImTOR protein, ratPhosphatidylinositol 3-KinasesPiperazinesProto-Oncogene Proteins c-aktQuinolinesSCH772984TOR Serine-Threonine KinasesGrowth hormoneInsulin-like growth factor 1MAPK pathwayPI3K/Akt/mTOR pathway

Identifiers

PMID29080043
OpenAlexW2765935892

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.