Evidence map›Paper›PMID 38012382›Full record

ArticleBritish journal of cancer2024

EEF1A2 promotes HIF1A mediated breast cancer angiogenesis in normoxia and participates in a positive feedback loop with HIF1A in hypoxia.

Saket Awadhesbhai Patel, Md Khurshidul Hassan, Monali Naik, Nachiketa Mohapatra, Poornima Balan, Purna Sai Korrapati, Manjusha Dixit

Open access · greenAbstract read
In one paragraph

Article in British journal of cancer, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. European journal of nuclear medicine and molecular imaging · 2026
    Article
  5. Review
  6. Article
  7. Interplay of Interleukin-1Oncology research · 2026
    Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. 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

7 authors at 3 institutions in 1 country.

Saket Awadhesbhai PatelNational Institute of Science Education and Research, School of Biological Sciences, Bhubaneswar, 752050, Odisha, India.
Md Khurshidul HassanNational Institute of Science Education and Research, School of Biological Sciences, Bhubaneswar, 752050, Odisha, India.
Monali NaikNational Institute of Science Education and Research, School of Biological Sciences, Bhubaneswar, 752050, Odisha, India.
Nachiketa MohapatraApollo Hospitals, Plot No. 251,Old Sainik School Road, Bhubaneswar, 750015, Odisha, India.
Poornima BalanCSIR-Central Leather Research Institute, Sardar Patel Road, Adyar, Chennai, 600020, India.
Purna Sai KorrapatiCSIR-Central Leather Research Institute, Sardar Patel Road, Adyar, Chennai, 600020, India.
Manjusha DixitNational Institute of Science Education and Research, School of Biological Sciences, Bhubaneswar, 752050, Odisha, India. manjusha@niser.ac.in.ORCID 0000-0002-6997-1054
National Institute of Science Education and Research · INCentral Leather Research Institute · INApollo Hospitals · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe eukaryotic elongation factor, EEF1A2, has been identified as an oncogene in various solid tumors. Here, we have identified a novel function of EEF1A2 in angiogenesis.

methodsChick chorioallantoic membrane, tubulogenesis, aortic ring, Matrigel plug, and skin wound healing assays established EEF1A2's role in angiogenesis.

resultHigher EEF1A2 levels in breast cancer cells enhanced cell growth, movement, blood vessel function, and tubule formation in HUVECs, as confirmed by ex-ovo and in-vivo tests. The overexpression of EEF1A2 could be counteracted by Plitidepsin. Under normoxic conditions, EEF1A2 triggered HIF1A expression via ERK-Myc and mTOR signaling in TNBC and ER/PR positive cells. Hypoxia induced the expression of EEF1A2, leading to a positive feedback loop between EEF1A2 and HIF1A. Luciferase assay and EMSA confirmed HIF1A binding on the EEF1A2 promoter, which induced its transcription. RT-PCR and polysome profiling validated that EEF1A2 affected VEGF transcription and translation positively. This led to increased VEGF release from breast cancer cells, activating ERK and PI3K-AKT signaling in endothelial cells. Breast cancer tissues with elevated EEF1A2 showed higher microvessel density.

conclusionEEF1A2 exhibits angiogenic potential in both normoxic and hypoxic conditions, underscoring its dual role in promoting EMT and angiogenesis, rendering it a promising target for cancer therapy.

Indexed as

Breast NeoplasmsAngiogenesisEndothelial CellsFeedbackFemaleHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitPeptide Elongation Factor 1Phosphatidylinositol 3-KinasesVascular Endothelial Growth Factor AEEF1A2 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitPeptide Elongation Factor 1Phosphatidylinositol 3-KinasesVascular Endothelial Growth Factor A

Identifiers

PMID38012382
PMCPMC10803557
OpenAlexW4389043874

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.