Evidence map›Paper›PMID 25945613›Full record

ArticleAutophagy2015

Critical role of CAV1/caveolin-1 in cell stress responses in human breast cancer cells via modulation of lysosomal function and autophagy.

Yin Shi, Shi-Hao Tan, Shukie Ng, Jing Zhou, Na-Di Yang, Gi-Bang Koo, Kerrie-Ann McMahon, Robert G Parton, Michelle M Hill, Miguel A Del Pozo and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Autophagy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

84 citing papers in PubMed, 119 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Cav-1 deficiency induces cardiac dysfunction via the AdipoR1-AMPK-mTOR autophagy pathway.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. Article

24 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

12 authors at 6 institutions in 8 countries.

Yin Shia Department of Physiology; Yong Loo Lin School of Medicine; National University of Singapore ; Singapore.
Shi-Hao Tan
Shukie Ng
Jing Zhou
Na-Di Yang
Gi-Bang Koo
Kerrie-Ann McMahon
Robert G Parton
Michelle M Hill
Miguel A Del Pozo
You-Sun Kim
Han-Ming Shen
Yong In University · KRNational University of Singapore · SGSuwon Research Institute · KRUniversity of Queensland · AUCenter for Vascular Biology Research · USRetina Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CAV1 (caveolin 1, caveolae protein, 22kDa) is well known as a principal scaffolding protein of caveolae, a specialized plasma membrane structure. Relatively, the caveolae-independent function of CAV1 is less studied. Autophagy is a process known to involve various membrane structures, including autophagosomes, lysosomes, and autolysosomes for degradation of intracellular proteins and organelles. Currently, the function of CAV1 in autophagy remains largely elusive. In this study, we demonstrate for the first time that CAV1 deficiency promotes both basal and inducible autophagy. Interestingly, the promoting effect was found mainly in the late stage of autophagy via enhancing lysosomal function and autophagosome-lysosome fusion. Notably, the regulatory function of CAV1 in lysosome and autophagy was found to be caveolae-independent, and acts through lipid rafts. Furthermore, the elevated autophagy level induced by CAV1 deficiency serves as a cell survival mechanism under starvation. Importantly, downregulation of CAV1 and enhanced autophagy level were observed in human breast cancer cells and tissues. Taken together, our data reveal a novel function of CAV1 and lipid rafts in breast cancer development via modulation of lysosomal function and autophagy.

Indexed as

AutophagyStress, PhysiologicalAnimalsBreast NeoplasmsCaveolin 1Cell SurvivalDown-RegulationFemaleHumansLysosomesMCF-7 CellsMembrane FusionMembrane MicrodomainsMiceModels, BiologicalPhagosomesCaveolin 1Vacuolar Proton-Translocating ATPasesATP6V0D1, ATPase H+ transporting lysosomal 38kDa, V0 subunit d1autophagyBaf, bafilomycin A1breast cancerCAV1, caveolin 1caveolin 1CHO, water-soluble cholesterolCQ, choloroquineCTSL, cathepsin LCTxB, cholera toxin subunit BDRF, detergent-resistant fractionDSF, detergent-soluble fractionEGF, epidermal growth factorKO, knockoutLAMP1, lysosomal-associated membrane protein 1lipid raftslysosomeMAP1LC3/LC3, microtubule-associated protein 1 light chain 3MBCD, methyl-β-cyclodextrinMEF, mouse embryonic fibroblastsMTOR, mechanistic target of rapamycinPBS, phosphate-buffered salinePI, propidium iodidePLA, proximity ligation assayPTRF, polymerase I and transcript release factortfLC3B, mRFP-GFP tandem fluorescent-tagged LC3BTFRC, transferrin receptorTSC, tuberous sclerosis complexWT, wild type.

Identifiers

PMID25945613
PMCPMC4509445
OpenAlexW1667584926

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.