Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

TP53 mutations in triple-negative breast cancer cells confer sensitivity to ASCT2 inhibition via arginine uptake.

Cell death & disease - 21 May 2026

Lyu Xiaodan, Wei Yuancheng, Chen Ziyi, Zou Qianlin, Wang Jia, Han Yi, Xu Chenxi, Hu Haolin, Zhou Zizhang, Yuan Shengtao, Yang Mei, Sun Li

Abstract excerpt

Targeting dysregulated glutamine metabolism via ASCT2 inhibition has therapeutic potential in cancer, but its clinical translation is hindered by tumor metabolic heterogeneity and the lack of predictive biomarkers. This study aims to define genetic determinants of ASCT2 inhibitor sensitivity and uncover compensatory resistance mechanisms to enable precision therapeutic strategies. We systematically evaluated...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Arginine
Share to Cell Line, Tumor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to TP53 gene

Share to Minor Histocompatibility Antigens

Share to Mutation

Share to Triple Negative Breast Neoplasms

Share to Tumor Suppressor Protein p53

Source

Open in PubMed Open full text

Identifiers

PMID: 42168145
DOI: 10.1038/s41419-026-08814-x
PMCID: PMC13365229

Genes

TP53
SLC7A3
CASTOR1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

TP53 mutations in triple-negative breast cancer cells confer sensitivity to ASCT2 inhibition via arginine uptake.PMID 42168145Read ↗

AADAT-Driven Metabolic Control of Malate and CoQ <sub>10</sub> Shapes Immune Evasion in Triple-Negative Breast CancerSemantic proximity Read ↗

Anaplastic Thyroid Cancer Cells Upregulate Mitochondrial One-Carbon Metabolism To Meet Purine Demand, Eliciting A Critical Targetable VulnerabilitySemantic proximity Read ↗

Metabolic stress induces GD2+ cancer stem cell-like phenotype in triple-negative breast cancer.Semantic proximity Read ↗

Wild-type IDH2 is a therapeutic target for triple-negative breast cancer.Semantic proximity Read ↗

CircPVT1 weakens miR-33a-5p unleashing the c-MYC/GLS1 metabolic axis in breast cancerSemantic proximity Read ↗

Invasive lobular carcinoma integrated multi-omics analysis reveals silencing of Arginosuccinate synthase and upregulation of nucleotide biosynthesis in tamoxifen resistanceSemantic proximity Read ↗

Hypoxia-induced switch in SNAT2/SLC38A2 regulation generates endocrine-resistance in breast cancerSemantic proximity Read ↗

Bioinformatics-based analysis of amino acid metabolism-related features to predict clinical prognosis and immunotherapy response in triple-negative breast cancerSemantic proximity Read ↗

TP53 mutation hits energy metabolism and increases glycolysis in breast cancer.Semantic proximity Read ↗

The amino acid transporter SLC7A11 expression in breast cancerSemantic proximity Read ↗

Stanniocalcin 2 governs cancer cell adaptation to nutrient insufficiency through alleviation of oxidative stressSemantic proximity Read ↗

GLUT1 inhibition blocks growth of RB1-positive Triple Negative Breast CancerSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.