Evidence map›Paper›PMID 25823028›Full record

ArticleOncogene2016

CD133 and DNA-PK regulate MDR1 via the PI3K- or Akt-NF-κB pathway in multidrug-resistant glioblastoma cells in vitro.

G Xi, E Hayes, R Lewis, S Ichi, B Mania-Farnell, K Shim, T Takao, E Allender, C S Mayanil, T Tomita

RetractedOpen access · greenAbstract readRetracted Publication
PubMed Publisher
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.

  1. Pooled it
  2. Review
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  17. Unraveling the journey of cancer stem cells from origin to metastasis.Biochimica et biophysica acta. Reviews on cancer · 2019
    Review
  18. The emerging role of miR-19 in glioma.Journal of cellular and molecular medicine · 2018
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

G XiDivision of Pediatric Neurosurgery, Stanley Manne Children's Research Institute, Ann & Robert H Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
E HayesDivision of Pediatric Neurosurgery, Stanley Manne Children's Research Institute, Ann & Robert H Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
R LewisDivision of Pediatric Neurosurgery, Stanley Manne Children's Research Institute, Ann & Robert H Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
S IchiDivision of Pediatric Neurosurgery, Stanley Manne Children's Research Institute, Ann & Robert H Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
B Mania-FarnellDepartment of Biological Sciences, Purdue University Calumet, Hammond, IN, USA.
K ShimDivision of Pediatric Neurosurgery, Stanley Manne Children's Research Institute, Ann & Robert H Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
T TakaoDivision of Pediatric Neurosurgery, Stanley Manne Children's Research Institute, Ann & Robert H Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
E AllenderDivision of Pediatric Neurosurgery, Stanley Manne Children's Research Institute, Ann & Robert H Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
C S MayanilDivision of Pediatric Neurosurgery, Stanley Manne Children's Research Institute, Ann & Robert H Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
T TomitaDivision of Pediatric Neurosurgery, Stanley Manne Children's Research Institute, Ann & Robert H Lurie Children's Hospital of Chicago, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.
Northwestern University · USLurie Children's Hospital · USPurdue University Northwest · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chemotherapy is an adjuvant treatment for glioblastomas, however, chemotherapy remains palliative because of the development of multidrug resistance (MDR). Following prolonged chemotherapy, MDR protein 1 (MDR1) and CD133 increase in recurrent glioblastomas. CD133 positive (CD133+) glioma cancer stem-like cells (GCSCs) markedly promote drug resistance and exhibit increased DNA damage repair capability; thus they have a key role in determining tumor chemosensitivity. Although CD133, DNA-dependent protein kinase (DNA-PK), and MDR1 are elevated in CD133+ GCSCs, the relationship among these molecules has not been elucidated. In this study, MDR glioblastoma cell lines were created in response to prolonged doxorubicin chemotherapy. CD133, DNA-PK and MDR1 were markedly elevated in these cells. CD133 and DNA-PK may increase MDR1 via the phosphatidylinositol-3-kinase (PI3K)-Akt signal pathway. PI3K downstream targets Akt and nuclear factor (NF)-κB, which interacts with the MDR1 promoter, were also elevated in these cells. Downregulation of CD133 and DNA-PK by small interfering RNA, or inhibition of PI3K or Akt, decreased Akt, NF-κB and MDR1 expression. The results indicate that CD133 and DNA-PK regulate MDR1 through the PI3K- or Akt-NF-κB signal pathway. Consequently, a novel chemotherapeutic regimen targeting CD133 and DNA-PK in combination with traditional protocols may increase chemotherapeutic efficacy and improve prognosis for individuals who present with glioblastoma.

Indexed as

AC133 AntigenAntigens, CDAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily BCell Line, TumorDNA-Activated Protein KinaseDoxorubicinDrug Resistance, NeoplasmEnzyme InhibitorsGlioblastomaGlycoproteinsHumansNF-kappa BNuclear ProteinsPeptidesPhosphatidylinositol 3-KinasesABCB1 protein, humanAC133 AntigenAntigens, CDAntineoplastic AgentsATP Binding Cassette Transporter, Subfamily BDNA-Activated Protein KinaseDoxorubicinEnzyme InhibitorsGlycoproteinsNF-kappa BNuclear ProteinsPeptidesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPRKDC protein, humanPROM1 protein, humanProto-Oncogene Proteins c-akt

Identifiers

PMID25823028
OpenAlexW2061521956

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.