Evidence map›Paper›PMID 35332131›Full record

ArticleCell death & disease2022

HMGB3 promotes PARP inhibitor resistance through interacting with PARP1 in ovarian cancer.

Hanlin Ma, Gonghua Qi, Fang Han, Wei Lu, Jiali Peng, Rongrong Li, Shi Yan, Cunzhong Yuan, Beihua Kong

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2022. 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
4.9field-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

30 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Overview of high mobility group box 3 (HMGB3] protein.Molecular genetics and genomics : MGG · 2025
    Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Structure and Functions of HMGB3 Protein.International journal of molecular sciences · 2024
    Review
  20. Article
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

9 authors at 2 institutions in 1 country.

Hanlin MaDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Gonghua QiDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Fang HanDepartment of Ophthalmology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Wei LuDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Jiali PengDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Rongrong LiDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Shi YanDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Cunzhong YuanDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Beihua KongDepartment of Obstetrics and Gynecology, Qilu Hospital of Shandong University, Jinan, 250012, China. kongbeihua@sdu.edu.cn.ORCID 0000-0002-5911-0242
Qilu Hospital of Shandong University · CNShandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Poly (ADP-ribose) polymerase (PARP) inhibitor (PARPi) resistance remains a therapeutic challenge in ovarian cancer. High-mobility group box 3 (HMGB3) plays significant roles in the development of drug resistance of many cancers. However, the function of HMGB3 in PARPi resistance is poorly understood. In the current study, we clarified that HMGB3 was aberrantly overexpressed in high-grade serous ovarian carcinoma (HGSOC) tissues, and high HMGB3 levels indicated shorter overall survival and drug resistance in HGSOC. The overexpression of HMGB3 increased the insensitivity of ovarian cancer to PARPi, whereas HMGB3 knockdown reduced PARPi resistance. Mechanistically, PARP1 was identified as a novel interaction partner of HMGB3, which could be blocked using olaparib and was enhanced upon DNA damage conditions. We further showed that loss of HMGB3 induced PARP1 trapping at DNA lesions and inhibited the PARylation activity of PARP1, resulting in an increased DNA damage response and cell apoptosis. The PARPi-resistant role of HMGB3 was also verified in a xenograft mouse model. In conclusion, HMGB3 promoted PARPi resistance via interacting with PARP1, and the targeted inhibition of HMGB3 might overcome PARPi resistance in ovarian cancer therapy.

Indexed as

Antineoplastic AgentsOvarian NeoplasmsAnimalsCarcinoma, Ovarian EpithelialCell Line, TumorDrug Resistance, NeoplasmFemaleHumansMicePhthalazinesPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) PolymerasesAntineoplastic AgentsPARP1 protein, humanPhthalazinesPoly (ADP-Ribose) Polymerase-1Poly(ADP-ribose) Polymerase InhibitorsPoly(ADP-ribose) Polymerases

Identifiers

PMID35332131
PMCPMC8948190
OpenAlexW4220854416

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.