E Josue Ruiz, Adan Pinto-Fernandez ... Axel Behrens
Deletion and small-molecule inhibition of ubiquitin-specific protease 28 destabilizes the oncogenes c-MYC, c-JUN, and Δp63, and elicits regression of squamous cell lung carcinoma, a major cancer type with currently limited treatment options.
In addition to its cytoplasmic role for translation, the seryl-tRNA synthetase also antagonizes the c-Myc transcription factor in the nucleus to transcriptionally repress the growth factor VEGFA and ensure proper development of the vasculature in vertebrates.
Protein kinase A-driven increases in c-MYC protein expression and tumor cell proliferation can be blocked by eIF4A inhibitors, suggesting a potential new treatment option for patients with oncogenic PKA activation.
A c-Myc-transcribed long noncoding RNA namely LAST (LncRNA-assisted stabilization of transcripts) collaborates with a cellular factor CNBP to promote the stability of CCND1/cyclin D1 mRNA post-transcriptionally, ensuring the proper G1/Sphase transition of the cell cycle.
The central immune modulator interferon-gamma downregulates the proto-oncogene c-Myc to shut down host cell metabolism and interfere with infection of epithelial cells by obligate intracellular pathogenic Chlamydia trachomatis.
L Michelle Lewis, Meredith C Edwards ... Reproducibility Project: Cancer Biology
Editors' Summary: This Replication Study has reproduced important parts of the original paper, but it also contains results that are not consistent with some parts of the original paper.
The transcription factor c-Myc amplifies the transcription of many growth-related genes in cancer cells, but its role as an oncogene is not fully understood.
PHAROH lncRNA is upregulated in hepatocellular carcinoma and functions by sequestering the translational suppressor TIAR via a 71 nucleotide hairpin to regulate c-MYC translation.