Evidence map›Paper›PMID 24745346›Full record

ArticleBMC cancer2014

Inhibition of autophagy enhances the cytotoxic effect of PA-MSHA in breast cancer.

Wen-Huan Xu, Zhe-Bin Liu, Yi-Feng Hou, Qi Hong, Da-Li Hu, Zhi-Ming Shao

Abstract read
In one paragraph

Article in BMC cancer, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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. Review
  2. Frontiers in oncology · 2022
    Review
  3. Frontiers in oncology · 2020
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Role of autophagy in chronic kidney diseases.International journal of clinical and experimental medicine · 2015
    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

6 authors.

Wen-Huan Xu
Zhe-Bin Liu
Yi-Feng Hou
Qi Hong
Da-Li Hu
Zhi-Ming ShaoDepartment of Breast Surgery, Fudan University Shanghai Cancer Center, Shanghai 200032, P,R, China. zhimingshao@yahoo.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPA-MSHA, a genetically engineered Pseudomonas aeruginosa (PA) strain, is currently under investigation as a new anti-cancer drug. It can induce cell cycle arrest and apoptosis in different human cancer cells, including hormone receptor negative breast cancer cells. However, the underlying mechanism of tumor lethality mediated by PA-MSHA remains to be fully investigated.

methodsThe effect of PA-MSHA on human hormone receptor negative breast cancer cells was analyzed by morphological measurement, western blot, cell proliferation assay and mouse xenograft model.

resultsPA-MSHA was found to induce endoplasmic reticulum (ER) stress in breast cancer cell lines through the IRE1 signaling pathway. Inhibiting autophagy potentiated the cytotoxic effect of PA-MSHA while treating breast cancer cell lines. In mouse xenograft model, PA-MSHA produced more pronounced tumor suppression in mice inoculated with IRE1 gene knockdown. MDA-MB-231HM cells.

conclusionsThese findings demonstrated inhibiting autophagy together with PA-MSHA might be a promising therapeutic strategy in treating hormone receptor negative breast cancer cells.

Indexed as

AnimalsApoptosisAutophagyBreast NeoplasmsCell Line, TumorCell ProliferationEndoplasmic Reticulum StressEndoribonucleasesFemaleGene Knockdown TechniquesHemagglutininsHumansMiceProtein Serine-Threonine KinasesPseudomonas aeruginosaSignal TransductionEndoribonucleasesERN1 protein, humanHemagglutininsProtein Serine-Threonine Kinases

Identifiers

PMID24745346
PMCPMC4000616

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Registered trials

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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.