Results 61 to 70 of about 278,661 (263)

Distinct functions of transforming growth factor-β signaling in c-MYC driven hepatocellular carcinoma initiation and progression

Cell Death and Disease, 2021
Dysregulation of transforming growth factor-beta (TGFβ) signaling has been implicated in liver carcinogenesis with both tumor promoting and inhibiting activities.
Haichuan Wang, Pan Wang, Meng Xu, Xinhua Song, Hong Wu, Matthias Evert, Diego F. Calvisi, Yong Zeng, Xin Chen   +8 more
doaj   +1 more source

AID Is Required for the Chromosomal Breaks in c-myc that Lead to c-myc/IgH Translocations [PDF]

Cell, 2008
Chromosomal translocation requires formation of paired double-strand DNA breaks (DSBs) on heterologous chromosomes. One of the most well characterized oncogenic translocations juxtaposes c-myc and the immunoglobulin heavy-chain locus (IgH) and is found in Burkitt's lymphomas in humans and plasmacytomas in mice.
Robbiani, Davide F., Bothmer, Anne, Callen, Elsa, Reina-San-Martin, Bernardo, Dorsett, Yair, Difilippantonio, Simone, Bolland, Daniel J., Chen, Hua Tang, Corcoran, Anne E., Nussenzweig, André, Nussenzweig, Michel C.   +10 more
openaire   +2 more sources

Inhibition of cyclin‐dependent kinases 12/13 using CT7439 as a treatment for colorectal cancer with CDK12 upregulation

Molecular Oncology, EarlyView.
The proposed mechanism of action for the CDK12/13 inhibitor and cyclin K degrader, CT7439. CDK12/13 inhibition interrupts transcription elongation, leading to increased DNA damage that results in cell death. This agent is a potentially novel treatment option for patients with colorectal cancer. Created in BioRender. Cyclin‐dependent kinase (CDK) 12 and
Wylie K. Watlington, Divya L. Dayanidhi, Mohammad Zokaasadi, John B. Mantyh, Pelumi D. Olawuni, Gabrielle Rupprecht, Jeremy M. Force, Shannon McCall, Ashwani K. Bahl, David S. Hsu, Jason A. Somarelli   +10 more
wiley   +1 more source

A novel mechanism by which c-MYC is aberrantly activated by epigenetic silencing of its antisense lncRNA in colon cancer

Frontiers in Genetics
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, Xuming Hu, Xuming Hu, Ye Wei, Meiying Zhang, Chunfeng Dou, Liping Wang, Gul Zaib, Huixian Wu, Wang Guo, Xiaoyuan Wang, Shihao Chen, Qi Xu, Qi Xu, Qi Xu, Mingzhou Guo, Hengmi Cui, Hengmi Cui, Hengmi Cui, Hengmi Cui   +19 more
doaj   +1 more source

C-MYC aberrations as prognostic factors in diffuse large B-cell lymphoma: a meta-analysis of epidemiological studies.

PLoS ONE, 2014
ObjectivesVarious studies have investigated the prognostic value of C-MYC aberrations in diffuse large B-cell lymphoma (DLBCL). However, the role of C-MYC as an independent prognostic factor in clinical practice remains controversial. A systematic review
Kuangguo Zhou, Danmei Xu, Yang Cao, Jue Wang, Yunfan Yang, Mei Huang   +5 more
doaj   +1 more source

SCP1 regulates c-Myc stability and functions through dephosphorylating c-Myc Ser62 [PDF]

Oncogene, 2015
Serine 62 (Ser62) phosphorylation affects the c-Myc protein stability in cancer cells. However, the mechanism for dephosphorylating c-Myc is not well understood. In this study, we identified carboxyl-terminal domain RNA polymerase II polypeptide A small phosphatase 1 (SCP1) as a novel phosphatase specifically dephosphorylating c-Myc Ser62.
W, Wang, P, Liao, M, Shen, T, Chen, Y, Chen, Y, Li, X, Lin, X, Ge, P, Wang   +8 more
openaire   +2 more sources

ZW4864‐mediated inhibition of the β‐catenin/BCL9/BCL9L complex reveals therapeutic potential in bladder cancer

Molecular Oncology, EarlyView.
BCL9 and BCL9L drive bladder cancer progression by enhancing β‐catenin signaling, promoting proliferation, migration, invasion, and organoid growth. Genetic depletion of BCL9(L) suppresses malignant phenotypes, while pharmacological disruption of the β‐catenin/BCL9(L) complex with ZW4864 inhibits canonical Wnt signaling and tumor‐associated cellular ...
Roland Kotolloshi, Mandy Berndt‐Paetz, Eileen Lerner, Gregoire Najjar, Anca Azoitei, Krishna Pal Singh, Shailendra Kumar Gupta, Olaf Wolkenhauer, Cagatay Günes, Otmar Huber, Marc‐Oliver Grimm, Daniel Steinbach   +11 more
wiley   +1 more source

Nucleophosmin is essential for c-Myc nucleolar localization and c-Myc-mediated rDNA transcription [PDF]

Oncogene, 2012
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

Targeting transcription factors associated with hemoglobinopathies: Lessons from successful interventions and implications for cancer

Molecular Oncology, EarlyView.
This review summarizes the transcription factors, repressive chromatin‐modifying complexes, and epigenetic mechanisms that control fetal hemoglobin repression. Notably, many regulators of γ‐globin silencing also function in transcriptional and epigenetic networks that drive cancer, highlighting opportunities to translate advances in hemoglobinopathy ...
Meigen Yu, Puspa Das, Xing Zhang, Xiaodong Cheng   +3 more
wiley   +1 more source

Glutathione Depletion Induced by c-Myc Downregulation Triggers Apoptosis on Treatment with Alkylating Agents

Neoplasia: An International Journal for Oncology Research, 2004
Here we investigate the mechanism(s) involved in the c-Myc-dependent drug response of melanoma cells. By using three M14-derived c-Myc low-expressing clones, we demonstrate that alkylating agents, cisplatin and melphalan, trigger apoptosis in the c-Myc ...
Annamaria Biroccio, Barbara Benassi, Francesco Fiorentino, Gabriella Zupi   +3 more
doaj   +1 more source