Evidence map›Paper›PMID 29455665›Full record

ReviewMolecular cancer2018

PTEN/PTENP1: 'Regulating the regulator of RTK-dependent PI3K/Akt signalling', new targets for cancer therapy.

Nahal Haddadi, Yiguang Lin, Glena Travis, Ann M Simpson, Najah T Nassif, Eileen M McGowan

Open access · goldAbstract readReview
In one paragraph

Review in Molecular cancer, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 192 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
192citing papers in PubMed, 1 pooled it
9.9field-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

192 citing papers in PubMed, 1 synthesis or guideline pooled it, 296 citations in OpenAlex.

  1. Pooled it
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  16. The cross-talk between GSK-3β, RKIP, and PTEN as potential targets for therapeutic implications in cancer: a comprehensive insight.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2026
    Review
  17. The Role of miRNA-21 in the Metastasis of Hepatocellular Carcinoma as a Therapeutic Target.International journal of hematology-oncology and stem cell research · 2026
    Review
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132 more citing papers are in PubMed but not listed here.

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.

Nahal HaddadiSchool of Life Sciences, Faculty of Science, University of Technology Sydney, 15 Broadway, Ultimo, Sydney, NSW, 2007, Australia.
Yiguang LinSchool of Life Sciences, Faculty of Science, University of Technology Sydney, 15 Broadway, Ultimo, Sydney, NSW, 2007, Australia.
Glena TravisSchool of Life Sciences, Faculty of Science, University of Technology Sydney, 15 Broadway, Ultimo, Sydney, NSW, 2007, Australia.
Ann M SimpsonSchool of Life Sciences, Faculty of Science, University of Technology Sydney, 15 Broadway, Ultimo, Sydney, NSW, 2007, Australia.
Najah T NassifSchool of Life Sciences, Faculty of Science, University of Technology Sydney, 15 Broadway, Ultimo, Sydney, NSW, 2007, Australia. Najah.Nassif@uts.edu.au.
Eileen M McGowanCentral Laboratory, The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, 510080, China. Eileen.McGowan@uts.edu.au.
University of Technology Sydney · AUFirst Affiliated Hospital of Guangdong Pharmaceutical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulation of the PI-3 kinase (PI3K)/Akt signalling pathway is essential for maintaining the integrity of fundamental cellular processes, cell growth, survival, death and metabolism, and dysregulation of this pathway is implicated in the development and progression of cancers. Receptor tyrosine kinases (RTKs) are major upstream regulators of PI3K/Akt signalling. The phosphatase and tensin homologue (PTEN), a well characterised tumour suppressor, is a prime antagonist of PI3K and therefore a negative regulator of this pathway. Loss or inactivation of PTEN, which occurs in many tumour types, leads to overactivation of RTK/PI3K/Akt signalling driving tumourigenesis. Cellular PTEN levels are tightly regulated by a number of transcriptional, post-transcriptional and post-translational regulatory mechanisms. Of particular interest, transcription of the PTEN pseudogene, PTENP1, produces sense and antisense transcripts that exhibit post-transcriptional and transcriptional modulation of PTEN expression respectively. These additional levels of regulatory complexity governing PTEN expression add to the overall intricacies of the regulation of RTK/PI-3 K/Akt signalling. This review will discuss the regulation of oncogenic PI3K signalling by PTEN (the regulator) with a focus on the modulatory effects of the sense and antisense transcripts of PTENP1 on PTEN expression, and will further explore the potential for new therapeutic opportunities in cancer treatment.

Indexed as

AnimalsAntineoplastic AgentsHumansMicroRNAsNeoplasmsPhosphatidylinositol 3-KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSignal TransductionAntineoplastic AgentsMicroRNAsPhosphatidylinositol 3-KinasesProtein-Tyrosine KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseCancermicroRNA (miRNA)Phosphatase and tensin homologue (PTEN)PI-3 kinase (PI3K)PseudogenePTENP1Tyrosine kinase

Identifiers

PMID29455665
PMCPMC5817727
OpenAlexW2795174081

What OpenQuestion holds

Textmetadata
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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.