Evidence map›Paper›PMID 20652449›Full record

ArticleMedical oncology (Northwood, London, England)2011

Knockdown of eIF4E suppresses cell growth and migration, enhances chemosensitivity and correlates with increase in Bax/Bcl-2 ratio in triple-negative breast cancer cells.

Fei-fei Zhou, Min Yan, Gui-fang Guo, Fang Wang, Hui-juan Qiu, Fei-meng Zheng, Yan Zhang, Qiang Liu, Xiao-feng Zhu, Liang-ping Xia

Abstract read
PubMed Publisher
In one paragraph

Article in Medical oncology (Northwood, London, England), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Targeting mTOR and eIF4E: a feasible scenario in ovarian cancer therapy.Cancer drug resistance (Alhambra, Calif.) · 2021
    Review
  5. Article
  6. Therapeutic Opportunities in Eukaryotic Translation.Cold Spring Harbor perspectives in biology · 2018
    Review
  7. Article
  8. Developing anti-neoplastic biotherapeutics against eIF4F.Cellular and molecular life sciences : CMLS · 2017
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
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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

10 authors at 2 institutions in 1 country.

Fei-fei ZhouState Key Laboratory of Oncology in South China, Cancer Center, Sun Yat-Sen University, and Department of Cancer Center, The First People's Hospital of Foshan, 651 Dongfeng Road East, 510060, Guangzhou, China.
Min Yan
Gui-fang Guo
Fang Wang
Hui-juan Qiu
Fei-meng Zheng
Yan Zhang
Qiang Liu
Xiao-feng Zhu
Liang-ping Xia
Sun Yat-sen University Cancer Center · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Elevated activity of the eukaryotic translation initiation factor 4E (eIF4E) plays crucial roles in tumorigenesis and disease progression by disproportionately increasing translation of mRNAs coding proteins that play significant roles in all aspects of malignancy, providing that eIF4E as an attractive target for therapeutic intervention. In this study, we showed that inhibition of eIF4E by small interfering RNAs (siRNA) resulted in cell cycle arrest and suppression of colony formation in MDA-MB-231 triple-negative (TN) breast cancer cells. Migration transwell assay revealed that repression of eIF4E effectively inhibited motility of MDA-MB-231 cancer cells. Importantly, we showed that silencing of eIF4E sensitized MDA-MB-231 cells to chemotherapeutic drugs of cisplatin, adriamycin, paclitaxel and docetaxel as assessed by MTT assay. Moreover, Western blot assay showed that eIF4E siRNA increased Bax/Bcl-2 ratio in MDA-MB-231 cells. Taken together, we showed that knockdown of eIF4E suppressed cell growth and migration, enhanced chemosensitivity, suggesting a potential therapeutic target in TN breast carcinoma.

Indexed as

Antineoplastic Agentsbcl-2-Associated X ProteinBlotting, WesternBreast NeoplasmsCell Cycle CheckpointsCell Line, TumorCell MovementCell ProliferationCell SeparationDrug Resistance, NeoplasmErb-b2 Receptor Tyrosine KinasesEukaryotic Initiation Factor-4EFemaleFlow CytometryGene Knockdown TechniquesHumansAntineoplastic Agentsbcl-2-Associated X ProteinERBB2 protein, humanErb-b2 Receptor Tyrosine KinasesEukaryotic Initiation Factor-4EProto-Oncogene Proteins c-bcl-2Receptors, EstrogenReceptors, ProgesteroneRNA, Small Interfering

Identifiers

PMID20652449
OpenAlexW2049053321

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.