Evidence map›Paper›PMID 28802057›Full record

ArticleThe Journal of pathology2017

High-mobility group box 1 released by autophagic cancer-associated fibroblasts maintains the stemness of luminal breast cancer cells.

Xi-Long Zhao, Yong Lin, Jun Jiang, Zhuo Tang, Shuai Yang, Lu Lu, Yan Liang, Xue Liu, Jiao Tan, Xu-Gang Hu and 10 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 124 citations in OpenAlex.

  1. Review
  2. Article
  3. HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Multiple functions of HMGB1 in cancer.Frontiers in oncology · 2024
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

9 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

20 authors at 2 institutions in 2 countries.

Xi-Long ZhaoInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Yong LinInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Jun JiangBreast Disease Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Zhuo TangInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Shuai YangInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Lu LuInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Yan LiangInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Xue LiuInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Jiao TanInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Xu-Gang HuInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Qin NiuInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Wen-Juan FuInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Ze-Xuan YanInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
De-Yu GuoInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Yi-Fang PingInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Ji Ming WangCancer and Inflammation Program, Center for Cancer Research, National Cancer Institute at Frederick, Frederick, MD, USA.
Xia ZhangInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Hsiang-Fu KungInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Xiu-Wu BianInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.ORCID 0000-0003-4383-0197
Xiao-Hong YaoInstitute of Pathology and Southwest Cancer Centre, Southwest Hospital, Third Military Medical University, Chongqing, PR China.
Army Medical University · CNFrederick National Laboratory for Cancer Research · US

Funding

The Role of Cellular Receptors Involved in Inflammation and Tumor ProgressionZ01BC010015 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI WANG, JI MING · 1996 to 2008
$944k
Intramural NIH HHS Z01 BC010015
6 · The paper itself

Abstract

Cancer stem cells/cancer-initiating cells (CICs) and their microenvironmental niche play a vital role in malignant tumour recurrence and metastasis. Cancer-associated fibroblasts (CAFs) are major components of the niche of breast cancer-initiating cells (BCICs), and their interactions may profoundly affect breast cancer progression. Autophagy has been considered to be a critical process for CIC maintenance, but whether it is involved in the cross-talk between CAFs and CICs to affect tumourigenesis and pathological significance has not been determined. In this study, we found that the presence of CAFs containing high levels of microtubule-associated protein 1 light chain 3 (LC3II), a marker of autophagosomes, was associated with more aggressive luminal human breast cancer. CAFs in human luminal breast cancer tissues with high autophagy activity enriched BCICs with increased tumourigenicity. Mechanistically, autophagic CAFs released high-mobility group box 1 (HMGB1), which activated its receptor, Toll-like receptor (TLR) 4, expressed by luminal breast cancer cells, to enhance their stemness and tumourigenicity. Furthermore, immunohistochemistry of 180 luminal breast cancers revealed that high LC3II/TLR4 levels predicted an increased relapse rate and a poorer prognosis. Our findings demonstrate that autophagic CAFs play a critical role in promoting the progression of luminal breast cancer through an HMGB1-TLR4 axis, and that both autophagy in CAFs and TLR4 on breast cancer cells constitute potential therapeutic targets. Copyright © 2017 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Indexed as

AgedAged, 80 and overAutophagyBreast NeoplasmsCancer-Associated FibroblastsCell Line, TumorCell Transformation, NeoplasticFemaleHMGB1 ProteinHumansMicrotubule-Associated ProteinsMiddle AgedNeoplasm Recurrence, LocalNeoplastic Stem CellsToll-Like Receptor 4Tumor MicroenvironmentHMGB1 ProteinHMGB1 protein, humanMicrotubule-Associated ProteinsTLR4 protein, humanToll-Like Receptor 4autophagybreast cancer-initiating cell (BCIC)cancer-associated fibroblast (CAF)high-mobility group box 1 (HMGB1)Toll-like receptor 4 (TLR4)

Identifiers

PMID28802057
PMCPMC8171497
OpenAlexW2766376966

What OpenQuestion holds

Textmetadata
LicenceTDM
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.