Fig. 3

Probable mechanisms related to the CDC27 dysregulation in cancer and their effects on tumorigenesis and prognosis. The mechanisms which alter CDC27 gene function in cancer are classified as genetic and epigenetic events at different levels of DNA, RNA and protein. In genetic events, missense mutations usually change the amnioacid sequence of protein which subsequently leads to an abnormal protein function. Large deletions and promoter mutation decrease the level of transcription. In mutations with Premature Termination Codon (PTC), usually the level of mRNA decreases by Nonsense Mediated Decay (NMD). Epigenetic events including CpG island methylation changes, Histone modifications, gene specific miRNAs and alterations in transcription factor levels can change the level of gene expression. Collectively increased CDC27 is associated to cell cycle progression, EMT and stemness which may increase tumorigenesis. On the other hand, decreased activity of CDC27 is associated to cell cycle arrest, increased efferocytosis and cancer cell survival which may lead to increased chemoresistancy and decreased radiosensitivity. Therefore, dysregulation of CDC27 activity (both increased and decreased) is related to tumorigenesis and poor prognosis and may decrease patient’s survival