Evidence map›Paper›PMID 33436723›Full record

ArticleScientific reports2021

Autophagy is deregulated in cancer-associated fibroblasts from oral cancer and is stimulated during the induction of fibroblast senescence by TGF-β1.

May Leng Tan, E Kenneth Parkinson, Lee Fah Yap, Ian C Paterson

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.9field-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

24 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Autophagy in oral cancer: Promises and challenges (Review).International journal of molecular medicine · 2024
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

May Leng TanDepartment of Oral and Craniofacial Sciences, Level 9, Postgraduate and Research Tower, Faculty of Dentistry, University of Malaya, 50603, Kuala Lumpur, Malaysia.
E Kenneth ParkinsonCentre for Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and the London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
Lee Fah YapDepartment of Oral and Craniofacial Sciences, Level 9, Postgraduate and Research Tower, Faculty of Dentistry, University of Malaya, 50603, Kuala Lumpur, Malaysia.
Ian C PatersonDepartment of Oral and Craniofacial Sciences, Level 9, Postgraduate and Research Tower, Faculty of Dentistry, University of Malaya, 50603, Kuala Lumpur, Malaysia. ipaterson@um.edu.my.
University of Malaya · MYQueen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many of the characteristics ascribed to cancer-associated fibroblasts (CAFs) are shared by activated, autophagic and senescent fibroblasts. Whilst most oral squamous cell carcinomas (OSCCs) are genetically unstable (GU-OSCC), genetically stable variants (GS-OSCC) have been described and, notably, CAF activation (myofibroblast differentiation) and senescence are characteristics particularly associated with GU-OSCCs. However, it is not known whether autophagy is disrupted in these cells or whether autophagy regulates the development of the myofibroblast and senescent phenotypes. In this study, we show that senescent CAFs from GU-OSCCs contained more autophagosomes than normal human oral fibroblasts (NHOFs) and CAFs from GS-OSCCs possibly due to autophagic impairment. Further, we show that deregulation of autophagy in normal fibroblasts, either by inhibition with autophagy inhibitor, SAR405, or activation with TGF-β1, induced fibroblast activation and senescence: In response to TGF-β1, autophagy was induced prior to the development of the activated and senescent phenotypes. Lastly, we show that both SAR405- and TGF-β1-treated NHOFs enhance OSCC cell migration but only TGF-β1-treated cells increase OSCC invasion through Matrigel, indicating that TGF-β1 has additional effects that are independent of fibroblast activation/senescence. These results suggest a functional role for autophagy in the development of myofibroblast and CAF phenotypes.

Indexed as

AutophagyCarcinoma, Squamous CellCell DifferentiationCell MovementCellular SenescenceFibroblastsHumansMouth NeoplasmsMyofibroblastsNeoplasm InvasivenessPyridinesPyrimidinonesTransforming Growth Factor beta1PyridinesPyrimidinonesSAR405Transforming Growth Factor beta1

Identifiers

PMID33436723
PMCPMC7804411
OpenAlexW3118851201

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.