c_Myc
- Known as:
- c_Myc
- Catalog number:
- 1X-433-C100
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Exbio
- Gene target:
- c_Myc
Related products to: c_Myc
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- MYC amplification is common and often extrachromosomal (ecDNA) in cancer. To define how MYC DNA copy gains arise from diploid genomes, we assessed whether epigenetic enzymes directly control focal MYC over-replication and amplification. We demonstrate that H3K4 methylation primes MYC for amplification by the H3K9/K36 tri-demethylase KDM4C, while the H3K36 tri-methyltransferase SETD2 restrains copy gains. These relationships are also observed in tumor datasets. SETD2 loss or inhibition promotes recruitment of catalytically active KDM4C, which initiates and drives stepwise MYC copy gains. Suppressing apoptosis or losing TP53 accelerates the emergence of higher-level MYC amplification events, including extrachromosomal circular ecDNAs (eccDNAs) and inherited copy gains. Non-transformed cells with these alterations are tumorigenic. Furthermore, KDM4C inhibition suppresses MYC amplification. These data define a chromatin-apoptotic axis directly controlling the initiation and progression of MYC amplification from diploid to hyper-amplification while also identifying potential biomarkers and therapeutic targets to constrain MYC-amplified tumors. - Source: PubMed
Publication date: 2026/10/02
Ferman Benjamin IAzadegan ChloeSantoro JohnUdara AnushkaLineberger Madison ALautert-Dutra WilliamSumner EthanMcCullough LoganO'Donnell ErinChetal KashishWilson JadeGray ZachAhmed MannaDeng ZhijieXiong YanUmit Kaniskan HChakraborty DamayantiClarke Thomas LMurphy Sedona EWalsh MartinBellacosa AlfonsoLee HayanJin JianVan Rechem CapucineLawrence Michael SSadreyev Ruslan IWhetstine Johnathan R - Fibroblast growth factor receptor (FGFR) signaling is a major oncogenic pathway in multiple cancer types and an important determinant of therapeutic response and resistance. However, its role in coordinating apoptotic susceptibility with tumor immune escape remains insufficiently integrated. This review summarizes how FGFR signaling regulates mitochondrial apoptosis through the RAS-RAF-MEK-ERK, PI3K-AKT-mTOR, PLCγ-PKC/Ca², and JAK-STAT pathways. These signaling networks converge on BCL-2 family proteins, BH3-only regulators, FOXO-dependent transcription, BAX/BAK activation, mitochondrial outer membrane permeabilization, cytochrome c release, and caspase activation. Non-canonical mechanisms involving redox homeostasis, metabolic stress, c-Myc regulation, and autophagy further determine whether FGFR inhibition produces transient adaptation or irreversible cell death. FGFR alterations may also shape the immune contexture of selected tumors by influencing inflammatory signaling, PD-L1 regulation, antigen-presentation pathways, tumor-stromal interactions, and susceptibility to immune-mediated elimination. These effects are strongly dependent on tumor lineage, genomic background, bypass receptor tyrosine kinase signaling, mitochondrial priming, and the local immune microenvironment. We further synthesize preclinical and emerging clinical evidence for combining FGFR-targeted therapies with immune checkpoint blockade and discuss the biomarkers and limitations that may determine therapeutic benefit. By linking apoptotic regulation, immune evasion, and therapeutic resistance, this review provides a framework for mechanism-based treatment strategies in FGFR-aberrant cancers. - Source: PubMed
Publication date: 2026/09/17
Hu YinanZhang XinmiaoLiu WenWei YuqingXue JingliMa XiaowenCao YuanLi Peifeng - The MYC oncogene is dysregulated in nearly 70% of human cancers and plays a central role in tumor initiation and progression. However, direct targeting of c-MYC remains challenging because of its "undruggable" nature. Stabilization of DNA G-quadruplex (G4) structures within the c-MYC promoter offers an alternative strategy to suppress c-MYC transcription. Here, we report the synthesis and biological evaluation of a series of styryl quinolinium ligands, identifying PQB-4 as a selective c-MYC DNA G4-binder (K <1.0 µM). PQB-4 exhibited marked antiproliferative activity against pancreatic cancer cell lines, including MIA PaCa-2 (IC = 2.9 µM), PANC-1 (IC = 4.5 µM), and gemcitabine-resistant PANC-1 cells (IC = 5.0 µM), while showing substantially lower toxicity toward noncancerous HK-2 cells (IC = 40.1 µM). Mechanistically, PQB-4 stabilized c-MYC DNA G4-structures, suppressed c-MYC mRNA and protein expression, induced G0/G1 cell-cycle arrest, and activated a p53-dependent DNA damage response. PQB-4 also promoted telomere damage, cellular senescence, mitochondrial dysfunction, ferroptosis, and mitophagy, while inhibiting cancer cell migration, proliferation, and survival. Notably, PQB-4 synergized strongly with gemcitabine in resistant PANC-1 cells (CI = 0.027). In a PANC-1 xenograft model, PQB-4 reduced tumor weight by 44%. These findings highlight c-MYC DNA G4 targeting by PQB-4 as a feasible therapeutic strategy for pancreatic cancer, particularly in gemcitabine-resistant disease. - Source: PubMed
Publication date: 2026/10/02
Zheng Bo-XinWang Ya-KunChen Ze-XinMeng Yi-WenShe Meng-TingDong Jia-PengZheng YingyingZeng Yao-XunZheng Wen-DeLong WeiWong Wing-Leung - BRIP1 (BRCA1-interacting protein 1) or FANCJ is a 5'-3' DNA helicase that plays critical roles in the maintenance of genome stability through its involvement in DNA repair, replication stress responses, and the resolution of DNA secondary structures or non-B DNAs. Defects in the BRIP1 helicase gene are associated with an increased risk of various cancers. It has been shown that BRIP1-deficient mice are predisposed to B-cell lymphoma. Because activation-induced cytidine deaminase (AID)-dependent genomic instability resulting from its mistargeting to non-immunoglobulin genes is a major hallmark of B-cell lymphoma, and non-B DNA structures, including G-quadruplexes (G4) and RNA-DNA hybrids (R-loops), are implicated in AID-induced genomic instability, we asked whether BRIP1 helicase limits these secondary structures to suppress AID-mediated oncogenesis. - Source: PubMed
Publication date: 2026/09/30
Mahboob AishaAhmad HaleemaFatma NishatBegum Nasim AHusain Afzal - - Source: PubMed
Publication date: 2026/10/01
Wiman Klas G