Phosphorylation of c-Myc at Ser62 via the protein kinase activity of acetaldehyde dehydrogenase 18A1 promotes tumor growth.

The oncoprotein c-Myc is a prominent target in cancer therapy, and modulating its stability is a promising potential treatment strategy. Phosphorylation at Ser62 is the primary mechanism by which c-Myc degradation is suppressed, which extends its half-life. Consequently, identifying kinases that regulate the phosphorylation of c-Myc at Ser62 may pave the way for novel intervention strategies.

The microenvironment cell index is a novel indicator for the prognosis and therapeutic regimen selection of cancers.

Background: It is worthwhile to establish a prognostic prediction model based on microenvironment cells (MCs) infiltration and explore new treatment strategies for triple-negative breast cancer (TNBC).

Methods: The xCell algorithm was used to quantify the cellular components of the TNBC microenvironment based on bulk RNA sequencing (bulk RNA-seq) data. The MCs index (MCI) was constructed using the least absolute shrinkage and selection operator Cox (LASSO-Cox) regression analysis.