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Record W4409628844 · doi:10.1158/1538-7445.am2025-1625

Abstract 1625: Redox homeostasis is a therapeutic vulnerability in lethal neuroendocrine prostate cancer

2025· article· en· W4409628844 on OpenAlexaff
Mu‐En Wang, Wei-Ling Tu, Ji-Hoon Kim, Yi Lu, Alyssa Bawcom, Andrew J. Armstrong, Qianben Wang, Yuzhuo Wang, Jiaoti Huang, Ming Chen

Bibliographic record

VenueCancer Research · 2025
Typearticle
Languageen
FieldBiochemistry, Genetics and Molecular Biology
TopicCancer, Hypoxia, and Metabolism
Canadian institutionsUniversity of British Columbia
Fundersnot available
KeywordsProstate cancerMedicineVulnerability (computing)CancerHomeostasisOncologyCancer researchInternal medicineComputer science

Abstract

fetched live from OpenAlex

Abstract Background: Neuroendocrine prostate cancer (NEPC) is an aggressive and lethal subtype of prostate cancer that often develops after second-generation anti-androgen therapies. The current treatment options for NEPC are limited and only produce disappointing results, highlighting the urgent need for novel therapies. Previously, we have found that NEPC cells are vulnerable to BCL2 and GPX4 inhibitors compared to their counterparts, prostate adenocarcinoma (PADC). Here, we aim to determine whether and how combining BCL2 and GPX4 inhibitors would enable optimal therapeutic effects in NEPC. Methods: We conducted drug synergism analyses of BCL2 and GPX4 inhibitors using NEPC cell lines and determined their impacts on the major cell death pathways by performing rescuing experiments. To further determine the molecular mechanisms of BCL2 and GPX4 inhibitors-induced cell death in NEPC, we measured the intracellular reactive oxygen species (ROS) levels and tested the rescuing effects of various antioxidants and reducing agents on cell death. Finally, we determined the in vivo therapeutic efficacy of BCL2 and GPX4 inhibitors in an NCI-H660 cell line-derived xenograft (CDX) tumor model. Results: Our results demonstrate that the BCL2 inhibitor ABT-199 and GPX4 inhibitor C18 synergistically induced apoptosis in NEPC cell lines in a ROS-independent manner. Although N-acetylcysteine (NAC) rescued ABT-199 and C18 cotreatment-induced apoptosis, the CellROX Green assay revealed no significant changes in ROS levels in ABT-199 and C18-cotreated cells. Surprisingly, reducing agents including tris(2-carboxyethyl)phosphine (TCEP) and Dithiothreitol (DTT) strongly rescued cell death induced by ABT-199 and C18 cotreatment. Our findings therefore suggested that the cell-killing effects of ABT-199 and C18 were due to ROS-independent disruption of redox homeostasis. Lastly, our preclinical tumor study showed that the ABT-199 and C18 combinatorial therapy significantly suppressed the tumor growth of NEPC. Conclusions: Our study validated the combination of BCL2 and GPX4 inhibitors as a feasible approach for the treatment of NEPC and suggested that redox homeostasis is a therapeutic vulnerability in NEPC. Citation Format: Mu-En Wang, Wei-Ling Tu, Ji-Hoon Kim, Yi Lu, Alyssa Bawcom, Andrew J. Armstrong, Qianben Wang, Yuzhuo Wang, Jiaoti Huang, Ming Chen. Redox homeostasis is a therapeutic vulnerability in lethal neuroendocrine prostate cancer [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2025; Part 1 (Regular Abstracts); 2025 Apr 25-30; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2025;85(8_Suppl_1):Abstract nr 1625.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

How this classification was reachedexpand

Full frame machine prediction

Teacher imitation

Not calibrated prevalence, not ground truth. Human validation pending. The Gemma side is a direct model label for every work in the frame, read from the title-only record. The Codex side is a classifier learned from the 10,348 direct Codex labels and calibrated to design-weighted sample rates; fields without enough sample support carry no Codex call. Candidate is the union of the two sides; consensus is their intersection. These outputs are machine_predicted_unvalidated and are not human labels.

metaresearch head score (Codex)0.000
metaresearch head score (Gemma)0.000
Version: metacan-v3-hybrid-931329e0061cValidation status: machine_predicted_unvalidated
Candidate categoriesnone
Consensus categoriesnone
DomainCandidate signal: none · Consensus signal: none
Study designCandidate signal: Bench or experimental · Consensus signal: Bench or experimental
GenreCandidate signal: Empirical · Consensus signal: Empirical
Teacher disagreement score0.002
Threshold uncertainty score0.008

Distilled classifier scores by category (both heads)

CategoryCodexGemma
Metaresearch0.0000.000
Meta-epidemiology (narrow)0.0000.000
Meta-epidemiology (broad)0.0000.000
Bibliometrics0.0000.000
Science and technology studies0.0000.000
Scholarly communication0.0000.000
Open science0.0000.000
Research integrity0.0000.001
Insufficient payload (model declined to judge)0.0020.000

Machine scores (provisional)

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

Opus teacher head0.044
GPT teacher head0.404
Teacher spread0.359 · how far apart the two teachers sit on this one work
Validation statusscore_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Classification

machine, unvalidated

Machine predicted; a candidate call from one source (direct Gemma or distilled Codex), not a consensus.

The models applied no category: nothing in the taxonomy fit this work.
Study designBench or experimental
Domainnot available
GenreEmpirical

How this classification was reached, model by model and score by score, is at the end of the page under "How this classification was reached".

Quick stats

Citations1
Published2025
Admission routes1
Has abstractyes

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