Evidence map›Paper›PMID 25607248›Full record

ArticleAutophagy2015

Poly-ADP-ribosylation of HMGB1 regulates TNFSF10/TRAIL resistance through autophagy.

Minghua Yang, Liying Liu, Min Xie, Xiaofang Sun, Yan Yu, Rui Kang, Liangchun Yang, Shan Zhu, Lizhi Cao, Daolin Tang

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 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 65 citations in OpenAlex.

  1. HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025
    Review
  2. Article
  3. Article
  4. Article
  5. The PRMT6/PARP1/CRL4B Complex Regulates the Circadian Clock and Promotes Breast Tumorigenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  6. Article
  7. Article
  8. The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022
    Review
  9. Review
  10. PARP-1-Associated Pathological Processes: Inhibition by Natural Polyphenols.International journal of molecular sciences · 2021
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Accelerated degradation of cFLIPScientific reports · 2019
    Article
  19. Article
  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

10 authors at 5 institutions in 2 countries.

Minghua Yanga Department of Pediatrics; Xiangya Hospital ; Central South University ; Changsha , Hunan China.
Liying Liu
Min Xie
Xiaofang Sun
Yan Yu
Rui Kang
Liangchun Yang
Shan Zhu
Lizhi Cao
Daolin Tang
Xiangya Hospital Central South University · CNCentral South University · CNKey Laboratory of Guangdong Province · CNUniversity of Pittsburgh · USUPMC Hillman Cancer Center · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
Targeting HMGB1-mediated Autophagy in Cancer TherapyR01CA160417 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI TANG, DAOLIN · 2012 to 2023
$3.0M
NCI NIH HHS P30CA047904NCI NIH HHS R01CA160417
6 · The paper itself

Abstract

Both apoptosis ("self-killing") and autophagy ("self-eating") are evolutionarily conserved processes, and their crosstalk influences anticancer drug sensitivity and cell death. However, the underlying mechanism remains unclear. Here, we demonstrated that HMGB1 (high mobility group box 1), normally a nuclear protein, is a crucial regulator of TNFSF10/TRAIL (tumor necrosis factor [ligand] superfamily, member 10)-induced cancer cell death. Activation of PARP1 (poly [ADP-ribose] polymerase 1) was required for TNFSF10-induced ADP-ribosylation of HMGB1 in cancer cells. Moreover, pharmacological inhibition of PARP1 activity or knockdown of PARP1 gene expression significantly inhibited TNFSF10-induced HMGB1 cytoplasmic translocation and subsequent HMGB1-BECN1 complex formation. Furthermore, suppression of the PARP1-HMGB1 pathway diminished autophagy, increased apoptosis, and enhanced the anticancer activity of TNFSF10 in vitro and in a subcutaneous tumor model. These results indicate that PARP1 acts as a prominent upstream regulator of HMGB1-mediated autophagy and maintains a homeostatic balance between apoptosis and autophagy, which provides new insight into the mechanism of TNFSF10 resistance.

Indexed as

AnimalsApoptosisApoptosis Regulatory ProteinsAutophagyCell Line, TumorHMGB1 ProteinHumansMicePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesSignal TransductionTNF-Related Apoptosis-Inducing LigandApoptosis Regulatory ProteinsHMGB1 ProteinPARP1 protein, humanParp1 protein, mousePoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) PolymerasesTNF-Related Apoptosis-Inducing LigandTNFSF10 protein, humanTnfsf10 protein, mouseapoptosisATG, autophagy-relatedautophagyDISC, death-inducing signaling complexHMGB1HMGB1, high mobility group box 1MAP1LC3A/LC3, microtubule-associated protein 1 light chain 3 αPARP-1PARP1, poly (ADP-ribose) polymerase 1PARylation, poly-ADP-ribosylationRIPK1/RIP, receptor (TNFRSF)-interacting serine-threonine kinase 1shRNA, short hairpin RNATNFSF10/TRAIL, tumor necrosis factor (ligand) superfamily, member 10TNF, tumor necrosis factorTRAILTUNEL, TdT-mediated dUTP-X nick end labeling

Identifiers

PMID25607248
PMCPMC4502776
OpenAlexW2062886301

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.