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.

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.

Editors' Summary: This Replication Study has reproduced important parts of the original paper.

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.