Evidence map›Paper›PMID 30643434›Full record

ReviewOncoTargets and therapy2019

The progression of HMGB1-induced autophagy in cancer biology.

Tianwei Xu, Lihua Jiang, Zhaoxia Wang

Open access · goldAbstract readReview
In one paragraph

Review in OncoTargets and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

54 citing papers in PubMed, 96 citations in OpenAlex.

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

3 authors at 1 institution in 1 country.

Tianwei XuDepartment of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China, wangzhaoxia@njmu.edu.cn.
Lihua JiangDepartment of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China, wangzhaoxia@njmu.edu.cn.
Zhaoxia WangDepartment of Oncology, The Second Affiliated Hospital of Nanjing Medical University, Nanjing, China, wangzhaoxia@njmu.edu.cn.
Second Affiliated Hospital of Nanjing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an important process of cellular degradation and has been proven to contribute to tumorigenesis. High-mobility group box 1 (HMGB1) is an abundant nonhistone protein that has been widely reported to play a central role in the induction of autophagy. In nucleus, HMGB1 upregulates the expression of HSP27 to induce autophagy. In cytoplasm, the Beclin-1/PI3K-III complex can be activated by HMGB1 to promote autophagy. Extracellular HMGB1 binds to the receptor for advanced glycation end products to induce autophagy. Recent studies have shown that HMGB1-induced autophagy exerts multiple functions in various cancers like proliferation. Moreover, inhibition of HMGB1-induced autophagy can reverse chemoresistance, which is regulated by noncoding RNAs such as microRNAs and lncRNAs. Here, we provide a brief introduction to HMGB1 and HMGB1-induced autophagy in cancer. We also discuss the challenges associated with performing further investigations on this issue. HMGB1-induced autophagy exerts significant functions in cancer and has potential utility for new strategy to reverse drug resistance.

Indexed as

autophagycancerdrug resistanceHMGB1noncoding RNA

Identifiers

PMID30643434
PMCPMC6317470
OpenAlexW2907306792

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.