ArticleNPJ systems biology and applications2021
Integrated genetic and metabolic landscapes predict vulnerabilities of temozolomide resistant glioblastoma cells.
Article in NPJ systems biology and applications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- tLyP-1 peptide-modified MnO₂ co-delivering si-SLC16A1 and temozolomide synergistically suppresses glioblastoma via hypoxia modulation and metabolic stress.Journal of nanobiotechnology · 2026Article
- Rotenone Inhibited Osteosarcoma Cell Growth Through USP47-Induced Decreases in FEN1 Stability and DNA Integrity.Drug design, development and therapy · 2026Article
- Impacts of competition and phenotypic plasticity on the viability of adaptive therapy.Mathematical biosciences · 2025Article
- Deuterium metabolic imaging phenotypes mouse glioblastoma heterogeneity through glucose turnover kinetics.eLife · 2025Article
- Gene expression profiling and the isocitrate dehydrogenase mutational landscape of temozolomide‑resistant glioblastoma.Oncology letters · 2024Article
- Unlocking Glioblastoma Vulnerabilities with CRISPR-Based Genetic Screening.International journal of molecular sciences · 2024Review
- Ribonucleotide reductase regulatory subunit M2 drives glioblastoma TMZ resistance through modulation of dNTP production.Science advances · 2023Article
- Metabolomic and Lipidomic Profiling of Gliomas-A New Direction in Personalized Therapies.Cancers · 2022Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic reprogramming and its molecular underpinnings are critical to unravel the duality of cancer cell function and chemo-resistance. Here, we use a constraints-based integrated approach to delineate the interplay between metabolism and epigenetics, hardwired in the genome, to shape temozolomide (TMZ) resistance. Differential metabolism was identified in response to TMZ at varying concentrations in both the resistant neurospheroidal (NSP) and the susceptible (U87MG) glioblastoma cell-lines. The genetic basis of this metabolic adaptation was characterized by whole exome sequencing that identified mutations in signaling pathway regulators of growth and energy metabolism. Remarkably, our integrated approach identified rewiring in glycolysis, TCA cycle, malate aspartate shunt, and oxidative phosphorylation pathways. The differential killing of TMZ resistant NSP by Rotenone at low concentrations with an IC
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