Results 61 to 70 of about 278,570 (263)

Recent advances in searching c-Myc transcriptional cofactors during tumorigenesis

Journal of Experimental & Clinical Cancer Research, 2018
Background The mechanism by which c-Myc exerts its oncogenic functions is not completely clear and different hypotheses are still under investigation. The knowledge of the capacity of c-Myc to bind exclusively E-box sequences determined the discrepancy ...
Matteo Caforio, Cristina Sorino, Stefano Iacovelli, Maurizio Fanciulli, Franco Locatelli, Valentina Folgiero   +5 more
doaj   +1 more source

USP29‐regulated noncanonical stabilization of the hypoxia‐inducible factor‐α in aggressive prostate cancer

Molecular Oncology, EarlyView.
We identify USP29 as the only DUB mirroring CA9 expression, a marker of hypoxia and HIF pathway activation associated with PCA aggressiveness. USP29 stabilizes HIF‐1α and HIF‐2α via a noncanonical mechanism that is independent of PHD/pVHL activity yet relies on proteasomal regulation, establishing USP29 as a previously unrecognized regulator of hypoxic
Amelie S Schober, Leire Moreno‐Cugnon, Laura Martínez‐Pérez, Amaia Ercilla, Amaia Zabala‐Letona, Adrián Vicente‐Barrueco, Maider Fagoaga‐Eugui, Saioa Garcia‐Longarte, Blanca Calle‐Ciborro, Encarnación Pérez‐Andrés, Onintza Carlevaris, Sara Pozo, Isabel Mendizabal, Ugo Mayor, Arkaitz Carracedo, Violaine Sée, Edurne Berra   +16 more
wiley   +1 more source

PA2G4 Functions as a Cofactor for MYC Family Oncoproteins in MYC-Driven Malignancies

Cells
MYCN and c-MYC are critical driver oncogenes in several childhood cancers, including neuroblastoma. Currently, the clinical development of MYC inhibitors has been hindered by the intrinsically disordered structure of MYC proteins, which lack well-defined
Sukriti Krishan, Jessica Koach, Taylor Lim, Kenny Yeo, Faith Cheong, Jie-Si Luo, Hassina Massudi, Xiaomian Gao, Sopheakwealthy Heangsarath, Andrew J. Kueh, Marco J. Herold, Belamy B. Cheung, Glenn M. Marshall   +12 more
doaj   +1 more source

Therapeutic Potential of the Cyclin-Dependent Kinase Inhibitor Flavopiridol on c-Myc Overexpressing Esophageal Cancer

Frontiers in Pharmacology, 2021
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, Md Sazzad Hassan, Nicholas Cwidak, Chloe Johnson, Silvio Däster, Serenella Eppenberger-Castori, Niranjan Awasthi, Niranjan Awasthi, Jun Li, Jun Li, Margaret A. Schwarz, Margaret A. Schwarz, Urs von Holzen, Urs von Holzen, Urs von Holzen, Urs von Holzen   +15 more
doaj   +1 more source

MITF maintains genome stability in nonmelanocyte lineages

Molecular Oncology, EarlyView.
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, Adrián López García de Lomana, Thejus B. Venkatesh, Kritika Kirty, Snaevar Sigurdsson, Linda Vidarsdottir, Ramile Dilshat, Erla Sveinbjornsdottir, Snaedis Ragnarsdottir, Daniel H Magnusson, Maria R. Bustos, Eirikur Steingrimsson, Thorkell Gudjonsson, Stefan Sigurdsson   +13 more
wiley   +1 more source

Nucleolar localization of hepatic c-Myc: a potential mechanism for c-Myc regulation

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research, 2005
The c-myc proto-oncogene encodes a transcription factor that is involved in cell proliferation, growth, differentiation, and apoptosis. Previous studies on the regulation of hepatic c-myc have focused on control of its mRNA expression, which generally correlates with hepatocyte proliferation during both liver development and liver regeneration. However,
Sanders, Jennifer A., Gruppuso, Philip A.   +1 more
openaire   +2 more sources

Nucleophosmin interacts directly with c-Myc and controls c-Myc-induced hyperproliferation and transformation [PDF]

Proceedings of the National Academy of Sciences, 2008
The transcription factor c-Myc is essential for cellular proliferation and is one of the most frequently activated oncogenes, but the molecular mechanism mediating its critical role in transformation is unclear. Like c-Myc, multifunctional nucleophosmin (NPM) is tightly regulated during proliferation and is overexpressed in several different types of ...
Zhaoliang, Li, David, Boone, Stephen R, Hann   +2 more
openaire   +2 more sources

Epigenetic heterogeneity and plasticity in therapy‐induced tumor states through single‐cell multi‐omics

Molecular Oncology, EarlyView.
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, Hwiyeong Lee, Jin Hong, Daechan Park   +3 more
wiley   +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

PAK1 activation drives divergent resistance mechanisms to aromatase inhibition and tamoxifen in a luminal: A breast cancer model

Molecular Oncology, EarlyView.
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, Janina Müller, Efstathios‐Iason Vlachavas, Lukas Beumers, Lena Fleischhacker, Sara Burmester, Angelika Wörner, Sabine Karolus, Dominic Helm, Cindy Körner, Stefan Wiemann   +10 more
wiley   +1 more source