Evidence map›Paper›PMID 31928132›Full record

ArticleCancer biology & therapy2020

SIRT6-PARP1 is involved in HMGB1 polyADP-ribosylation and acetylation and promotes chemotherapy-induced autophagy in leukemia.

Qian Kong, Yunyao Li, Qixiang Liang, Jianwei Xie, Xinyu Li, Jianpei Fang

Open access · bronzeAbstract read
In one paragraph

Article in Cancer biology & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
4.8field-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.

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

19 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. HMGB1: A Central Node in Cancer Therapy Resistance.International journal of molecular sciences · 2025
    Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. The mechanism of HMGB1 secretion and release.Experimental & molecular medicine · 2022
    Review
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

6 authors at 1 institution in 1 country.

Qian KongDepartment of Pediatrics, TheThird Affiliated Hospital of Sun Yat-Sen University, Guangzhou, P.R. China.
Yunyao LiGuangdong Provincial Key Laboratory of Malignant Tumour Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, P.R. China.
Qixiang LiangDepartment of Stomatology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, P.R. China.
Jianwei XieGuangdong Provincial Key Laboratory of Malignant Tumour Epigenetics and Gene Regulation, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou, P.R. China.
Xinyu LiDepartment of Pediatrics, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangdong, P.R. China.ORCID 0000-0001-9893-8598
Jianpei FangDepartment of Pediatrics, Sun Yat-Sen Memorial Hospital of Sun Yat-Sen University, Guangdong, P.R. China.
Sun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High mobility group box protein 1 (HMGB1) is an evolutionarily conserved non-histone chromatin-binding protein. In a previous study, we showed that treating leukemic cells with chemotherapeutic drugs leads to the translocation of HMGB1, which is involved in autophagy and ultimately promotes chemoresistance in leukemia. However, the underlying translocation mechanism of HMGB1 in chemotherapy-induced autophagy remains unclear. In this study, we showed that knockdown of SIRT6 or PARP1 gene expression significantly inhibited HMGB1 cytoplasmic translocation and autophagy. Meanwhile, we found that SIRT6, an important upstream protein of PARP1, associated with PARP1, leading to the stimulation of polyADP-ribose polymerase activity. We further demonstrated that SIRT6 and PARP1 activation were required for chemotherapy-induced ADP-ribosylation of HMGB1 in leukemic cells and then influenced the acetylation of HMGB1, finally promoting the autophagy of leukemic cells mediated by HMGB1 translocation. These findings provide new insights into the mechanism of chemotherapeutic drug resistance. Targeting the HMGB1 translocation may overcome autophagy-related chemoresistance in leukemia.

Indexed as

AutophagyPoly ADP RibosylationAcetylationAntibiotics, AntineoplasticApoptosisBiomarkers, TumorCell ProliferationDaunorubicinGene Expression Regulation, NeoplasticHMGB1 ProteinHumansLeukemiaPoly (ADP-Ribose) Polymerase-1SirtuinsTumor Cells, CulturedAntibiotics, AntineoplasticBiomarkers, TumorDaunorubicinHMGB1 ProteinHMGB1 protein, humanPARP1 protein, humanPoly (ADP-Ribose) Polymerase-1SIRT6 protein, humanSirtuinsAutophagychemoresistanceHMGB1leukemiaPARP1SIRT6

Identifiers

PMID31928132
PMCPMC7515491
OpenAlexW3000334603

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.