Evidence map›Paper›PMID 27624978›Full record

ArticleScientific reports2016

Integrin α6/Akt/Erk signaling is essential for human breast cancer resistance to radiotherapy.

Ting Hu, Rui Zhou, Yanxia Zhao, Gang Wu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 93 citations in OpenAlex.

  1. Structure, function and usage of integrin alpha 6 (CD49f): A comprehensive review.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2026
    Review
  2. Beyond DNA damage: 3D tumor models and the integrin mechanobiology of radioresistance.Journal of experimental & clinical cancer research : CR · 2026
    Review
  3. Article
  4. Article
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  7. Integrin α6 Targeted Tumor Theranostics.Phenomics (Cham, Switzerland) · 2025
    Review
  8. Review
  9. Article
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  13. Article
  14. Exploiting Matrix Stiffness to Overcome Drug Resistance.ACS biomaterials science & engineering · 2024
    Review
  15. Article
  16. Review
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  18. Article
  19. Application of nano-radiosensitizers in combination cancer therapy.Bioengineering & translational medicine · 2023
    Review
  20. Article

1 more citing papers are in PubMed but not listed here.

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

4 authors at 2 institutions in 1 country.

Ting HuCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 JieFang Avenue, Wuhan 430022, China.
Rui ZhouCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 JieFang Avenue, Wuhan 430022, China.
Yanxia ZhaoCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 JieFang Avenue, Wuhan 430022, China.
Gang WuCancer Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 1277 JieFang Avenue, Wuhan 430022, China.
Huazhong University of Science and Technology · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Integrin α6 (ITGA6), a transmembrane glycoprotein adhesion receptor protein, is widely upregulated in many types of tumors and promotes migration and invasion in cancer cells. However, the role that the ITGA6-associated signaling network plays in radiosensitivity in breast cancer has not been described. The expression of ITGA6 was examined in human breast cancer and normal breast cell lines using western blot analysis. We also explored the role of ITGA6 in the regulation of radiation sensitivity in breast cancer using the colony formation assays, cell cycle analyses, apoptosis assays and immunofluorescence analyses. The results showed that the protein and mRNA expression levels of ITGA6 was higher in breast cancer cells than in normal cells. ITGA6 protectived responses to radiotherapy in breast cancer cells by altering cell apoptosis, DNA damage repair and cell-cycle regulation. Furthermore, ITGA6 enhanced radiation resistance via PI3K/Akt and MEK/Erk signaling. In addition, overexpressing ITGA6 promoted radiation resistance in cells, and this effect was neutralized by the PI3K inhibitor LY294002 and MEK inhibitor U0126. Taken together, these findings indicate that ITGA6 might be involved in a mechanism that underlies radiation resistance and that ITGA6 could be a potential target for therapies aimed at overcoming radiation resistance in breast cancer.

Indexed as

Signal TransductionApoptosisBreast NeoplasmsCell Cycle CheckpointsCell Line, TumorDNA DamageDNA RepairExtracellular Signal-Regulated MAP KinasesFemaleG2 PhaseGene Expression Regulation, NeoplasticHumansIntegrin alpha6Mitogen-Activated Protein Kinase KinasesMitosisPhosphatidylinositol 3-KinasesExtracellular Signal-Regulated MAP KinasesIntegrin alpha6Mitogen-Activated Protein Kinase KinasesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Messenger

Identifiers

PMID27624978
PMCPMC5022055
OpenAlexW2519598273

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.