Fig. 3.

DDX3X and cell cycle. DDX3X facilitates cyclin E1 translation by resolving the secondary structure in its 5′UTR during translation initiation. Moreover, it suppresses KLF4 expression by manipulating KLF4 mRNA alternative splicing. Therefore, by promoting cyclin E1 translation and suppressing KLF4 expression, DDX3X promotes G1/S transition. In lung cancer, P53 promotes DDX3X transcription. DDX3X synergistically enhances p53-activated P21 transcription by increasing the binding affinity of SP1 on the P21 promoter. In liver cancer, DDX3X directly interacts with SP1 to promote P21 transcription in a P53-independent manner, thus leading to tumour cell growth arrest