BUD31 (BUD31 Homolog)

Mutant cells lacking the cwf14 gene showed cell size and division defects, altered stress response, rapamycin sensitivity, enhanced chronological aging, and increased sporulation tendency...In silico experiments have revealed that BUD31 orthologous genes are found from yeast to humans, are evolutionarily conserved with a high degree of sequence identity, conserved motifs, and structures. Since the human gene partially complemented the mutant phenotype of S. pombe cells, indicating functional homology, our data can help better understand pathological mechanisms observed in human cancer cells.

BUD31 is upregulated in various tumors and is associated with poor outcomes, increased genomic instability, and a suppressed immune microenvironment in ccRCC. BUD31 promotes cell cycle progression via alternative splicing, suggesting it as a prognostic biomarker and potential therapeutic target in ccRCC.

Our in vitro results showed BUD31 knockdown promotes cell proliferation and migration of prostate cancer cells via activation of p-AKT and vimentin. These results support the clinical data, where low expression of BUD31 was correlated to more advanced stages of PCa.

In the case of STAT1, CASP3, PARP1, and PRKDC proteins, a transient increase in their content was observed at early time points (3-12 h) after the ATRA treatment. Obtained data on nuclear proteome composition and dynamics during granulocytic differentiation could be beneficial for the development of new treatment approaches for leukemias with the mutated p53 gene.