Evidence map›Paper›PMID 39961401›Full record

ArticleMolecular metabolism2025

BIX01294 suppresses PDAC growth through inhibition of glutaminase-mediated glutathione dynamics.

Se Seul Im, Jihyeon Seo, Ji Eun You, Hye Won Bang, YongHwan Kim, Jiyeon Kweon, Yongsub Kim, Dong-Myung Shin, Jaekyoung Son

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular metabolism, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

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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

2 citing papers in PubMed.

  1. Article
  2. 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

9 authors.

Se Seul ImDepartment of Biochemistry and Molecular Biology, Brain Korea 21 project, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, South Korea.
Jihyeon SeoDepartment of Biochemistry and Molecular Biology, Brain Korea 21 project, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, South Korea.
Ji Eun YouDepartment of Biochemistry and Molecular Biology, Brain Korea 21 project, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, South Korea.
Hye Won BangDepartment of Biochemistry and Molecular Biology, Brain Korea 21 project, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, South Korea.
YongHwan KimDepartment of Cell and Genetic Engineering, Brain Korea 21 project, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, South Korea.
Jiyeon KweonDepartment of Cell and Genetic Engineering, Brain Korea 21 project, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, South Korea.
Yongsub KimDepartment of Cell and Genetic Engineering, Brain Korea 21 project, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, South Korea.
Dong-Myung ShinDepartment of Cell and Genetic Engineering, Brain Korea 21 project, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, South Korea.
Jaekyoung SonDepartment of Biochemistry and Molecular Biology, Brain Korea 21 project, Asan Medical Center, University of Ulsan College of Medicine, Seoul 05505, South Korea. Electronic address: jaekson@amc.seoul.kr.

Funding

NCIRD CDC HHS U01 IP000104
6 · The paper itself

Abstract

objectivesIncreased expression of glutaminase (GLS) has been found to correlate with more aggressive disease and poorer prognosis in patients with several types of cancer, including breast, lung, and pancreatic cancer. G9a histone methyltransferase inhibitors may have anticancer activity. The present study assessed whether BIX01294 (BIX), a G9a histone methyltransferase inhibitor, can inhibit glutaminase (GLS) in pancreatic ductal adenocarcinoma (PDAC) cells.

methodsThe effects of BIX on mitochondrial metabolism in PDAC cells were evaluated by targeted liquid chromatography-tandem mass spectrometry (LC-MS/MS) metabolomic analysis. To assess the impact of BIX on glutathione dynamics, real-time changes in glutathione levels were monitored by FreSHtracer-based GSH assays.

resultsBIX significantly inhibited the growth of PDAC cells, both in vitro and in vivo, and robustly induced apoptotic cell death. BIX significantly increased the cellular NADP

conclusionsCollectively, these findings suggest that BIX could be a potent therapeutic agent in patients with PDAC through its inhibition of GLS-mediated cellular redox balance.

Indexed as

Carcinoma, Pancreatic DuctalGlutaminaseGlutathionePancreatic NeoplasmsThiadiazolesAnimalsApoptosisCell Line, TumorCell ProliferationFemaleHistone-Lysine N-MethyltransferaseHumansMiceMice, NudeMitochondriaSulfidesbis-2-(5-phenylacetamido-1,2,4-thiadiazol-2-yl)ethyl sulfideGlutaminaseGlutathioneHistone-Lysine N-MethyltransferaseSulfidesThiadiazolesBIX01294GlutaminaseGlutathioneKDM6BPancreatic cancer

Identifiers

PMID39961401
PMCPMC11905835

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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.