Evidence map›Paper›PMID 31061066›Full record

ArticleCancer research2019

Targeting the High-Mobility Group Box 3 Protein Sensitizes Chemoresistant Ovarian Cancer Cells to Cisplatin.

Anirban Mukherjee, Van Huynh, Kailee Gaines, Wade Alan Reh, Karen M Vasquez

Open access · bronzeAbstract read
In one paragraph

Article in Cancer research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.9field-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

42 citing papers in PubMed, 64 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
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  7. Article
  8. Article
  9. Article
  10. HMGB3 and SUB1 Bind to and Facilitate the Repair ofJournal of the American Chemical Society · 2024
    Article
  11. Structure and Functions of HMGB3 Protein.International journal of molecular sciences · 2024
    Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
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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

5 authors at 1 institution in 1 country.

Anirban MukherjeeDivision of Pharmacology and Toxicology, College of Pharmacy, Dell Pediatric Research Institute, The University of Texas at Austin, Austin, Texas.
Van HuynhDivision of Pharmacology and Toxicology, College of Pharmacy, Dell Pediatric Research Institute, The University of Texas at Austin, Austin, Texas.
Kailee GainesDivision of Pharmacology and Toxicology, College of Pharmacy, Dell Pediatric Research Institute, The University of Texas at Austin, Austin, Texas.
Wade Alan RehDivision of Pharmacology and Toxicology, College of Pharmacy, Dell Pediatric Research Institute, The University of Texas at Austin, Austin, Texas.
Karen M VasquezDivision of Pharmacology and Toxicology, College of Pharmacy, Dell Pediatric Research Institute, The University of Texas at Austin, Austin, Texas. karen.vasquez@austin.utexas.edu.ORCID 0000-0002-6958-5073
Austin College · US

Funding

Project 4: Coordinating Nucleolytic Pathways During Crosslink RepairP01CA193124 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI WOOD, RICHARD D · 2017 to 2022
$9.6M
REPAIR OF GENOME DESTABILIZING DNA STRUCTURESR01CA093729 · NCI · UNIVERSITY OF TX MD ANDERSON CAN CTR · PI Karen M Vasquez · 2002 to 2026
$8.2M
NCI NIH HHS P01 CA193124NCI NIH HHS R01 CA093729
6 · The paper itself

Abstract

Chemotherapeutic regimens for ovarian cancer often include the use of DNA interstrand crosslink-inducing agents (e.g., platinum drugs) or DNA double-strand break-inducing agents. Unfortunately, the majority of patients fail to maintain a durable response to treatment, in part, due to drug resistance, contributing to a poor survival rate. In this study, we report that cisplatin sensitivity can be restored in cisplatin-resistant ovarian cancer cells by targeting the chromatin-associated high-mobility group box 3 (HMGB3) protein. HMGB proteins have been implicated in the pathogenesis and prognosis of ovarian cancer, and HMGB3 is often upregulated in cancer cells, making it a potential selective target for therapeutic intervention. Depletion of HMGB3 in cisplatin-sensitive and cisplatin-resistant cells resulted in transcriptional downregulation of the kinases ATR and CHK1, which attenuated the ATR/CHK1/p-CHK1 DNA damage signaling pathway. HMGB3 was associated with the promoter regions of

Indexed as

Drug Resistance, NeoplasmAntineoplastic AgentsApoptosisCell ProliferationCisplatinFemaleHMGB3 ProteinHumansOvarian NeoplasmsRNA, Small InterferingTumor Cells, CulturedAntineoplastic AgentsCisplatinHMGB3 ProteinRNA, Small Interfering

Identifiers

PMID31061066
PMCPMC6606364
OpenAlexW2943268764

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.