Results 51 to 60 of about 282,710 (262)

In vivo inhibition of c-MYC in myeloid cells impairs tumor-associated macrophage maturation and pro-tumoral activities. [PDF]

PLoS ONE, 2012
Although tumor-associated macrophages (TAMs) are involved in tumor growth and metastasis, the mechanisms controlling their pro-tumoral activities remain largely unknown.
Oscar M Pello, Raphael Chèvre, Damya Laoui, Alba De Juan, Fidel Lolo, María Jesús Andrés-Manzano, Manuel Serrano, Jo A Van Ginderachter, Vicente Andrés   +8 more
doaj   +1 more source

ABL kinase‐dependent phosphorylation of SH proteins promotes their direct interaction with CRK family SH2 domains

FEBS Letters, EarlyView.
CT10 regulator of kinase (CRK) and CRK‐Like (CRKL) are signaling adaptors driving cell adhesion, motility, differentiation, and proliferation. SH2‐domain containing (SH) proteins are enriched in YXXP motifs which when phosphorylated create preferred binding sites for CRK family SH2 domains.
Phoebe M. Cousens, Brendan W. Chandler, Anna M. Schmoker, Jaye L. Weinert, Charlotte A. Kearns, Warren T. Yacawych, Amila Šemić, Alicia M. Ebert, Bryan A. Ballif   +8 more
wiley   +1 more source

Mechanisms of c-myc degradation by nickel compounds and hypoxia.

PLoS ONE, 2009
Nickel (Ni) compounds have been found to cause cancer in humans and animal models and to transform cells in culture. At least part of this effect is mediated by stabilization of hypoxia inducible factor (HIF1a) and activating its downstream signaling ...
Qin Li, Thomas Kluz, Hong Sun, Max Costa
doaj   +1 more source

siRNA directed against c-Myc inhibits proliferation and downregulates human telomerase reverse transcriptase in human colon cancer Colo 320 cells

Journal of Experimental & Clinical Cancer Research, 2008
The c-Myc and human telomerase reverse transcriptase gene (hTERT) gene are frequently deregulated and overexpressed in malignancy. hTERT activity is induced by c-Myc and strategies designed to inhibit c-Myc expression in cancer cells may have ...
Guofu Huang, Wen Su, Xiong Wei, Lei Fu, Nancai Yu, Hao Huang, yanxia Wu, Hanju Huang, Qian Liu, Hong Xiao   +9 more
doaj   +1 more source

Epigenetic reprogramming of lineage switching in cancer

FEBS Letters, EarlyView.
Cancer cells rarely commit to a single identity. Epigenetic mechanisms and tumor microenvironment cues push epithelial cells toward flexible, hybrid states that can shift into mesenchymal, neuroendocrine, or stem‐like fates, driving metastasis, drug resistance, and tumor heterogeneity. Targeting the epigenetic regulators behind these transitions, using
Ezgi Boyvatlı, Burcu Akman, Ezgi Bağırsakçı, Nese Atabey, Serap Erkek‐Ozhan   +4 more
wiley   +1 more source

PDCD11 Stabilizes C‐MYC Oncoprotein by Hindering C‐MYC‐SKP2 Negative Feedback Loop to Facilitate Progression of p53‐Mutant Breast and Colon Malignancies

Advanced Science
C‐MYC is a proto‐oncoprotein whose dysregulation triggers tumorigenesis and tumor progression in ≈70% of cancer cases. It is presently demonstrated that aberrantly upregulated MYC is caused by the overexpressed and “extra‐nucleolar” PDCD11 in p53‐mutant ...
Li Ding, Wei Ni, Yichao Ma, Lin Xu, Zhiping Zhang, Kai Liao, Jingwen Li, Xinyu Mei, Zhun Wang, Huiqian Ge, Jiajia Li, Dong Tang, Xinyue Zhang   +12 more
doaj   +1 more source

Inhibition of c-Myc overcomes cytotoxic drug resistance in acute myeloid leukemia cells by promoting differentiation. [PDF]

PLoS ONE, 2014
Nowadays, drug resistance still represents a major obstacle to successful acute myeloid leukemia (AML) treatment and the underlying mechanism is not fully elucidated. Here, we found that high expression of c-Myc was one of the cytogenetic characteristics
Xiao-Na Pan, Jia-Jie Chen, Le-Xun Wang, Ruo-Zhi Xiao, Ling-Ling Liu, Zhi-Gang Fang, Quentin Liu, Zi-Jie Long, Dong-Jun Lin   +8 more
doaj   +1 more source

Golgi enzymes are retrieved from the plasma membrane to the trans‐Golgi network

FEBS Letters, EarlyView.
Golgi enzymes are traditionally considered resident proteins retained within the Golgi apparatus. Here, we demonstrate that a subset transiently reaches the cell surface and is subsequently retrieved to the trans‐Golgi network via retrograde transport. Using a nanobody‐based toolkit, we uncover a dynamic trafficking cycle of several Golgi enzymes.
Dominik P. Buser, Tina Junne
wiley   +1 more source

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

Ligand‐dependent transcriptional heterogeneity in cell cycle gene expression delays G1/S entry

FEBS Letters, EarlyView.
EGF and HRG induce distinct G1/S progression programs in ErbB2‐amplified BT474 breast cancer cells. Despite activating the potent ErbB2–ErbB3 heterodimer, HRG does not accelerate cell‐cycle entry. Instead, EGF promotes earlier restriction‐point passage via ERK–FOS signaling, whereas HRG activates the AKT–MYC axis, driving transcriptional heterogeneity ...
Ririn Rahmala Febri, Ayaka Nagasato‐Ichikawa, Keita Iida, Shuhei Kimura, Akira Imamoto, Mariko Okada   +5 more
wiley   +1 more source