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

EPIC-0307-mediated selective disruption of PRADX–EZH2 interaction and enhancement of temozolomide sensitivity to glioblastoma via inhibiting DNA repair and MGMT

3 Jun 2023

Abstract excerpt

BACKGROUND: Temozolomide (TMZ) treatment efficacy in glioblastoma (GBM) has been limited by resistance. The level of O-6-methylguanine-DNA methyltransferase (MGMT) and intrinsic DNA damage repair factors are important for the TMZ response in patients. Here, we reported a novel compound, called EPIC-0307, that increased TMZ sensitivity by inhibiting specific DNA damage repair proteins and MGMT expression. METHODS:...

Read the complete abstract on PubMed

Topics

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

Share to DNA Repair Mechanisms
Share to Epigenetics and DNA Methylation
Share to Glioma Diagnosis and Treatment

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 37279651
DOI: 10.1093/neuonc/noad102

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

EPIC-0307-mediated selective disruption of PRADX–EZH2 interaction and enhancement of temozolomide sensitivity to glioblastoma via inhibiting DNA repair and MGMTPMID 37279651Read ↗

A novel compound EPIC-0412 reverses temozolomide resistance via inhibiting DNA repair/MGMT in glioblastomaSemantic proximity Read ↗

Histone deacetylase 6 acts upstream of DNA damage response activation to support the survival of glioblastoma cellsSemantic proximity Read ↗

Induction Of XLF And 53BP1 Expression Is Associated With Temozolomide Resistance In Glioblastoma CellsSemantic proximity Read ↗

Chemical screens identify HDAC6 as an epigenetic vulnerability in acquired Temozolomide-resistant models of glioblastomaSemantic proximity Read ↗

Differential gene expression-based connectivity mapping identified novel drug candidate and improved Temozolomide efficacy for GlioblastomaSemantic proximity Read ↗

RBBP4-p300 axis modulates expression of genes essential for cell survival and is a potential target for therapy in glioblastomaSemantic proximity Read ↗

PRMT5 inhibition sensitizes glioblastoma tumor models to temozolomideSemantic proximity Read ↗

EPIC-1042 as a potent PTRF/Cavin1–caveolin-1 interaction inhibitor to induce PARP1 autophagic degradation and suppress temozolomide efflux for glioblastomaSemantic proximity Read ↗

PDIA3P1 promotes Temozolomide resistance in glioblastoma by inhibiting C/EBPβ degradation to facilitate proneural-to-mesenchymal transitionSemantic proximity Read ↗

Genome‐Wide CRISPR‐Cas9 Screening Identifies NF‐κB/E2F6 Responsible for EGFRvIII‐Associated Temozolomide Resistance in GlioblastomaSemantic proximity Read ↗

E3 ligase MAEA-mediated ubiquitination and degradation of PHD3 promotes glioblastoma progressionSemantic proximity Read ↗

DNA-methylation-mediated activating of lncRNA SNHG12 promotes temozolomide resistance in glioblastomaSemantic proximity Read ↗

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