Results 71 to 80 of about 14,797,528 (308)
BackgroundProto-oncogenes are abnormally activated in nearly all types of tumors. However, the epigenetic mechanism of proto-oncogene activation has not yet been well elucidated.MethodsThe present study involved the construction of a double-stranded cDNA
Xuming Hu +19 more
doaj +1 more source
Tumors with elevated c-Myc expression often exhibit a highly aggressive phenotype, and c-Myc amplification has been shown to be frequent in esophageal cancer.
Md Sazzad Hassan +15 more
doaj +1 more source
Direct Activation of HSP90A Transcription by c-Myc Contributes to c-Myc-induced Transformation [PDF]
The c-myc proto-oncogene encodes a ubiquitous transcription factor involved in the control of cell growth and differentiation and implicated in inducing tumorigenesis. Understanding the function of c-Myc and its role in cancer depends upon the identification of c-Myc target genes.
Teng, Shu-Chun +6 more
openaire +2 more sources
MITF maintains genome stability in nonmelanocyte lineages
MITF is essential for melanocyte survival and acts as an oncogene in 10%–20% of melanomas. We show that MITF depletion causes genome instability in nonmelanocytic cells, leading to LATS2‐mediated P53 activation, cell cycle arrest, and apoptosis. This study highlights the role of MITF as a genome maintenance factor beyond the melanocyte lineage. Created
Drifa H. Gudmundsdottir +13 more
wiley +1 more source
Nucleophosmin is essential for c-Myc nucleolar localization and c-Myc-mediated rDNA transcription [PDF]
The transcription factor c-Myc has a critical role in cell proliferation and growth. The control of ribosome biogenesis by c-Myc through the regulation of transcription mediated by all three RNA polymerases is essential for c-Myc-driven proliferation. Specifically, in the nucleolus, c-Myc has been shown to be recruited to ribosomal DNA and activate RNA
Z, Li, S R, Hann
openaire +2 more sources
Single‐cell multi‐omics reveals epigenetic heterogeneity across therapy‐adaptive tumor states, including quiescent/dormant, drug‐tolerant persister, and EMT‐like phenotypes. By linking regulatory features with state‐associated biomarkers, these approaches inform biomarker‐guided therapeutic strategies for evolving tumors.
Hee Jung Kim +3 more
wiley +1 more source
c-Myc Inhibition Induces an Additive Effect with Cyclophosphamide in Acute Lymphoblastic Leukemia [PDF]
Background: Cellular-myelocytomatosis (c-Myc), an oncoprotein and a transcription factor, is involved in several essential cellular processes. The c-Myc expression level is highly regulated in normal cells.
Mohammad Sadeghi +8 more
doaj +1 more source
Domain-specific c-Myc ubiquitylation controls c-Myc transcriptional and apoptotic activity [PDF]
The oncogenic transcription factor c-Myc causes transformation and tumorigenesis, but it can also induce apoptotic cell death. Although tumor suppressors are necessary for c-Myc to induce apoptosis, the pathways and mechanisms are unclear.
Qin, Zhang +5 more
openaire +2 more sources
Breast cancer remains a major cause of cancer death in women, frequently developing endocrine therapy resistance. This study demonstrates that upregulated p21‐activated kinase 1 (PAK1) activity drives resistance to tamoxifen and long‐term estrogen deprivation in ER+ breast cancer models.
Luisa Schwarzmüller +10 more
wiley +1 more source
Additional file 2: Figure S2. RNF180 silencing contributed to the expression of C-myc through inhibiting its ubiquitination. A and B. Western blot was used to examine the protein level of C-myc in siNC and siRNF180 transfecting H292 and A549 with or ...
Yi Ding (172783) +4 more
core +1 more source

