Evidence map›Paper›PMID 27753527›Full record

ArticleCell cycle (Georgetown, Tex.)2017

Doxycycline inhibits the cancer stem cell phenotype and epithelial-to-mesenchymal transition in breast cancer.

Le Zhang, Liang Xu, Fengchun Zhang, Erina Vlashi

Registry-linked trialOpen access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell cycle (Georgetown, Tex.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05521048 (Doxycycline Injection of Cutaneous Schwannoma in Neurofibromatosis Type 2), which is not on this map. Cited by 66 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 1 pooled it
5.2field-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.

NCT05521048 phase1 / phase2active not recruitingnot on this mapstarted 2022, after this paper: background citation

Doxycycline Injection of Cutaneous Schwannoma in Neurofibromatosis Type 2

TypeinterventionalSponsorMassachusetts Eye and Ear InfirmaryRan2022 to 2026Enrolled19ConditionsNeurofibromatosis Type 2ArmsDoxycycline Injection [Doxy]
3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Role of Sam68 in different types of cancer (Review).International journal of molecular medicine · 2025
    Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review

6 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 2 countries.

Le Zhanga Department of Oncology , Ruijin Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , P.R. China.
Liang Xua Department of Oncology , Ruijin Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , P.R. China.
Fengchun Zhanga Department of Oncology , Ruijin Hospital, Shanghai Jiao Tong University School of Medicine , Shanghai , P.R. China.
Erina Vlashib Department of Radiation Oncology , David Geffen School of Medicine at UCLA , Los Angeles , CA , USA.
Shanghai Jiao Tong University · CNUniversity of California, Los Angeles · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Experimental evidence suggest that breast tumors originate from breast cancer stem cells (BCSCs), and that mitochondrial biogenesis is essential for the anchorage-independent clonal expansion and survival of CSCs, thus rendering mitochondria a significant target for novel treatment approaches. One of the recognized side effects of the FDA-approved drug, doxycycline is the inhibition of mitochondrial biogenesis. Here we investigate the mechanism by which doxycycline exerts its inhibitory effects on the properties of breast cancer cells and BCSCs, such as mammosphere forming efficiency, invasion, migration, apoptosis, the expression of stem cell markers and epithelial-to-mesenchymal transition (EMT) related markers of breast cancer cells. In addition, we explored whether autophagy plays a role in the inhibitory effect of doxycycline on breast cancer cells. We find that doxycyline can inhibit the viability and proliferation of breast cancer cells and BCSCs, decrease mammosphere forming efficiency, migration and invasion, and EMT of breast cancer cells. Expression of stem cell factors Oct4, Sox2, Nanog and CD44 were also significantly downregulated after doxycycline treatment. Moreover, doxycycline could down-regulate the expression of the autophagy marker LC-3BI and LC-3BII, suggesting that inhibiting autophagy may be responsible in part for the observed effects on proliferation, EMT and stem cell markers. The potent inhibition of EMT and cancer stem-like characteristics in breast cancer cells by doxycycline treatment suggests that this drug can be repurposed as an anti-cancer drug in the treatment of breast cancer patients in the clinic.

Indexed as

AutophagyBiomarkers, TumorBreast NeoplasmsCell MovementCell Self RenewalCell SurvivalDoxycyclineEpithelial-Mesenchymal TransitionFemaleHumansInhibitory Concentration 50MCF-7 CellsNeoplasm InvasivenessNeoplastic Stem CellsPhenotypeSpheroids, CellularBiomarkers, TumorDoxycyclineautophagybreast cancercancer stem cellsdoxycyclineepithelial-to-mesenchymal transitionmitochondria

Identifiers

PMID27753527
PMCPMC5405729
OpenAlexW2538151572

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.