Evidence map›Paper›PMID 26207671›Full record

ArticleCell adhesion & migration2015

Snail promotes cell migration through PI3K/AKT-dependent Rac1 activation as well as PI3K/AKT-independent pathways during prostate cancer progression.

Veronica Henderson, Basil Smith, Liza J Burton, Diandra Randle, Marisha Morris, Valerie A Odero-Marah

Open access · goldAbstract read
In one paragraph

Article in Cell adhesion & migration, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
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  8. Role of ELMO1 in inflammation and cancer-clinical implications.Cellular oncology (Dordrecht, Netherlands) · 2022
    Review
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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

6 authors at 2 institutions in 1 country.

Veronica Hendersona Center for Cancer Research and Therapeutic Development; Department of Biological Sciences ; Clark Atlanta University ; Atlanta , GA USA.
Basil Smith
Liza J Burton
Diandra Randle
Marisha Morris
Valerie A Odero-Marah
AID Atlanta · USCenter for Cancer Research · US

Funding

TRAINNING COREP20MD002285 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2007 to 2016
$10.9M
Technologies/Resources for Core LaboratoriesG12MD007590 · NIMHD · CLARK ATLANTA UNIVERSITY · PI KHAN, SHAFIQ A · 2012 to 2018
$7.6M
NIMHD NIH HHS 1P20MD002285NIMHD NIH HHS G12 MD007590NIMHD NIH HHS G12MD007590NIMHD NIH HHS P20 MD002285
6 · The paper itself

Abstract

Snail, a zinc-finger transcription factor, induces epithelial-mesenchymal transition (EMT), which is associated with increased cell migration and metastasis in cancer cells. Rac1 is a small G-protein which upon activation results in formation of lamellipodia, the first protrusions formed by migrating cells. We have previously shown that Snail promotes cell migration through down-regulation of maspin tumor suppressor. We hypothesized that Snail's regulation of cell migration may also involve Rac1 signaling regulated by PI3K/AKT and/or MAPK pathways. We found that Snail overexpression in LNCaP and 22Rv1 prostate cancer cells increased Rac1 activity associated with increased cell migration, and the Rac1 inhibitor, NSC23766, could inhibit Snail-mediated cell migration. Conversely, Snail downregulation using shRNA in the aggressive C4-2 prostate cancer cells decreased Rac1 activity and cell migration. Moreover, Snail overexpression increased ERK and PI3K/AKT activity in 22Rv1 prostate cancer cells. Treatment of Snail-overexpressing 22Rv1 cells with LY294002, PI3K/AKT inhibitor or U0126, MEK inhibitor, decreased cell migration significantly, but only LY294002 significantly reduced Rac1 activity, suggesting that Snail promotes Rac1 activation via the PI3K/AKT pathway. Furthermore, 22Rv1 cells overexpressing Snail displayed decreased maspin levels, while inhibition of maspin expression in 22Rv1 cells with siRNA, led to increased PI3K/AKT, Rac1 activity and cell migration, without affecting ERK activity, suggesting that maspin is upstream of PI3K/AKT. Overall, we have dissected signaling pathways by which Snail may promote cell migration through MAPK signaling or alternatively through PI3K/AKT-Rac1 signaling that involves Snail inhibition of maspin tumor suppressor. This may contribute to prostate cancer progression.

Indexed as

Cell Line, TumorCell MovementDisease ProgressionEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMalePhosphatidylinositol 3-KinasesProstatic NeoplasmsProto-Oncogene Proteins c-aktSignal TransductionSnail Family Transcription FactorsTranscription FactorsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSnail Family Transcription FactorsTranscription FactorsCaP, prostate cancercell migrationEMT, epithelial to mesenchymal transitionERK, Extracellular signal-regulated kinasesMAPK pathwayP-AKT, Phospho-AKTP-ERK, Phospho-ERKPI3K/AKT pathwayPI3K/AKT pathway, Phosphoinositide 3-kinases/Protein Kinase BRac1Rac1, Ras-related C3 botulinum toxin substrate 1snail

Identifiers

PMID26207671
PMCPMC4594564
OpenAlexW1852191371

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.