Evidence map›Paper›PMID 12808053›Full record

ArticleMolecular biology of the cell2003

Biphasic estradiol-induced AKT phosphorylation is modulated by PTEN via MAP kinase in HepG2 cells.

Maria Marino, Filippo Acconcia, Anna Trentalance

Open access · greenAbstract read
In one paragraph

Article in Molecular biology of the cell, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.5field-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

33 citing papers in PubMed, 117 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Tamoxifen Suppresses the Immune Response toPathogens (Basel, Switzerland) · 2021
    Article
  7. Review
  8. Review
  9. Review
  10. Estrogen receptor signaling mechanisms.Advances in protein chemistry and structural biology · 2019
    Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Xenoestrogens challenge 17β-estradiol protective effects in colon cancer.World journal of gastrointestinal oncology · 2014
    Review
  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

3 authors at 1 institution in 1 country.

Maria MarinoDipartimento di Biologia, Università Roma Tre, V. le G. Marconi, 446, Italy. m.marino@uniroma3.it
Filippo Acconcia
Anna Trentalance
Roma Tre University · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We reported previously in HepG2 cells that estradiol induces cell cycle progression throughout the G1-S transition by the parallel stimulation of both PKC-alpha and ERK signaling molecules. The analysis of the cyclin D1 gene expression showed that only the MAP kinase pathway was involved. Here, the presence of rapid/nongenomic, estradiol-regulated, PI3K/AKT signal transduction pathway, its modulation by the levels of the tumor suppressor PTEN, its cross-talk with the ERK pathway, and its involvement in DNA synthesis and cyclin D1 gene promoter activity have all been studied in HepG2 cells. 17beta-Estradiol induced the rapid and biphasic phosphorylation of AKT. These phosphorylations were independent of each other, being the first wave of activation independent of the estrogen receptor (ER), whereas the second was dependent on ER. Both activations were dependent on PI3K activity; furthermore, the ERK pathway modulated AKT phosphorylation by acting on the PTEN levels. The results showed that the PI3K pathway, as well as ER, were strongly involved in both G1-S progression and cyclin D1 promoter activity by acting on its proximal region (-254 base pairs). These data indicate that in HepG2 cells, different rapid/nongenomic estradiol-induced signal transduction pathways modulate the multiple steps of G1-S phase transition.

Indexed as

Protein Serine-Threonine KinasesCyclin D1DNAEstradiolMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesPhosphorylationPromoter Regions, GeneticProto-Oncogene ProteinsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseTumor Suppressor ProteinsCyclin D1DNAEstradiolMitogen-Activated Protein KinasesPhosphatidylinositol 3-KinasesPhosphoric Monoester HydrolasesProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseTumor Suppressor Proteins

Identifiers

PMID12808053
PMCPMC194905
OpenAlexW2141082176

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.