Evidence map›Paper›PMID 26124933›Full record

ArticleIranian journal of basic medical sciences2015

PI3K/Akt inhibition and down-regulation of BCRP re-sensitize MCF7 breast cancer cell line to mitoxantrone chemotherapy.

Tahereh Komeili-Movahhed, Shamileh Fouladdel, Elmira Barzegar, Shekoufeh Atashpour, Mohammad Hossein Ghahremani, Seyed Nasser Ostad, Zahra Madjd, Ebrahim Azizi

Open access · greenAbstract read
In one paragraph

Article in Iranian journal of basic medical sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
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

8 authors at 2 institutions in 1 country.

Tahereh Komeili-MovahhedMolecular Research Laboratory, Department of Pharmacology and Toxicology, Tehran University of Medical Sciences, Tehran, Iran ; Cellular and Molecular Research Center, Qom University of Medical Sciences, Qom, Iran.
Shamileh FouladdelMolecular Research Laboratory, Department of Pharmacology and Toxicology, Tehran University of Medical Sciences, Tehran, Iran.
Elmira BarzegarMolecular Research Laboratory, Department of Pharmacology and Toxicology, Tehran University of Medical Sciences, Tehran, Iran.
Shekoufeh AtashpourMolecular Research Laboratory, Department of Pharmacology and Toxicology, Tehran University of Medical Sciences, Tehran, Iran.
Mohammad Hossein GhahremaniDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran ; Department of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Seyed Nasser OstadDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Zahra MadjdOncopathology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Ebrahim AziziMolecular Research Laboratory, Department of Pharmacology and Toxicology, Tehran University of Medical Sciences, Tehran, Iran.
Tehran University of Medical Sciences · IRIran University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesMultidrug resistance (MDR) of cancer cells is a major obstacle to successful chemotherapy. Overexpression of breast cancer resistance protein (BCRP) is one of the major causes of MDR. In addition, it has been shown that PI3K/Akt signaling pathway involves in drug resistance. Therefore, we evaluated the effects of novel approaches including siRNA directed against BCRP and targeted therapy against PI3K/Akt signaling pathway using LY294002 (LY) to re-sensitize breast cancer MCF7 cell line to mitoxantrone (MTX) chemotherapy. MATERIALS AND

methodsAnticancer effects of MTX, siRNA, and LY alone and in combination were evaluated in MCF7 cells using MTT cytotoxicity assay and flow cytometry analysis of cell cycle distribution and apoptosis induction.

resultsMTT and apoptosis assays showed that both MTX and LY inhibited cell proliferation and induced apoptosis in MCF7 cells. Results indicated that inhibition of BCRP by siRNA or PI3K/Akt signaling pathway by LY significantly increased sensitivity of MCF7 cells to antiproliferation and apoptosis induction of MTX. Furthermore, MTX showed G2/M arrest, whereas LY induced G0/G1 arrest in cell cycle distribution of MCF7 cells. Combination of siRNA or LY with MTX chemotherapy significantly increased accumulation of MCF7 cells in the G2/M phase of cell cycle.

conclusionCombination of MTX chemotherapy with BCRP siRNA and PI3K/Akt inhibition can overcome MDR in breast cancer cells. This study furthermore suggests that novel therapeutic approaches are needed to enhance anticancer effects of available drugs in breast cancer.

Indexed as

BCRPBreast cancerCombination therapyMitoxantronePI3K/AktsiRNA

Identifiers

PMID26124933
PMCPMC4475655
OpenAlexW1550217583

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.