Evidence map›Paper›PMID 26506233›Full record

ArticleOncotarget2015

Loss of COX5B inhibits proliferation and promotes senescence via mitochondrial dysfunction in breast cancer.

Shui-Ping Gao, He-Fen Sun, Hong-Lin Jiang, Liang-Dong Li, Xin Hu, Xiao-En Xu, Wei Jin

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
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 2 institutions in 1 country.

Shui-Ping GaoDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Collaborative Innovation Center for Cancer Medicine, Fudan University Shanghai Cancer Center, Shanghai, China.
He-Fen SunDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Collaborative Innovation Center for Cancer Medicine, Fudan University Shanghai Cancer Center, Shanghai, China.
Hong-Lin JiangDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Collaborative Innovation Center for Cancer Medicine, Fudan University Shanghai Cancer Center, Shanghai, China.
Liang-Dong LiDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Collaborative Innovation Center for Cancer Medicine, Fudan University Shanghai Cancer Center, Shanghai, China.
Xin HuDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Collaborative Innovation Center for Cancer Medicine, Fudan University Shanghai Cancer Center, Shanghai, China.
Xiao-En XuDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Collaborative Innovation Center for Cancer Medicine, Fudan University Shanghai Cancer Center, Shanghai, China.
Wei JinDepartment of Breast Surgery, Key Laboratory of Breast Cancer in Shanghai, Collaborative Innovation Center for Cancer Medicine, Fudan University Shanghai Cancer Center, Shanghai, China.
Fudan University Shanghai Cancer Center · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COX5B, a peripheral subunit of the cytochrome c oxidase complex, has previously been reported to maintain the stability of this complex. However, its functions and mechanisms involved in breast cancer progression remain unclear. Here, by performing SILAC assays in breast cancer cell models and detecting COX5B expression in tissues, we found that COX5B expression was elevated in breast cancer. Down-regulation of COX5B in breast cancer cell lines can suppress cell proliferation and induced cell senescence which was accompanied by elevating production of IL-8 and other cytokines. Interestingly, conditioned medium from COX5B knockdown cells could promote breast cancer cell migration. Mechanistic studies reveal that COX5B silence induces an increase in production of ROS, depolarization of MMP and a decrease in ATP. What's more, silence of COX5B leads to metabolic disorders, such as increased glucose uptake and decreased lactate secretion. Collectively, our study shows that loss of COX5B induces mitochondrial dysfunction and subsequently leads to cell growth suppression and cell senescence. Cytokines such as IL-8 secreted by senescent cells may in turn alter the microenvironment which could enhance cell migration. These findings may provide a novel paradigm for the treatment which combined anti-cancer drugs with particular cytokine inhibitors such as IL-8 blockers.

Indexed as

Cell ProliferationAnimalsBlotting, WesternBreast NeoplasmsCell Line, TumorCell MovementCellular SenescenceElectron Transport Complex IVEnzyme-Linked Immunosorbent AssayFemaleGene Knockdown TechniquesHeterograftsHumansImmunohistochemistryKaplan-Meier EstimateMiceCOX5B protein, humanElectron Transport Complex IVReactive Oxygen SpeciesRNA, Small InterferingCOX5Bcytokinemitochondrial dysfunctionproliferationsenescence

Identifiers

PMID26506233
PMCPMC4791237
OpenAlexW1859313465

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.