Abstract
The cell cycle is a series of events by which cellular components are accurately segregated into daughter cells, principally controlled by the oscillating activities of cyclin-dependent kinases (CDKs) and their co-activators. In eukaryotes, DNA replication is confined to a discrete synthesis phase while chromosome segregation occurs during mitosis. During mitosis, the chromosomes are pulled into each of the two daughter cells by the coordination of spindle microtubules, kinetochores, centromeres, and chromatin. These four functional units tie chromosomes to the microtubules, send signals to the cells when the attachment is completed and the division can proceed, and withstand the force generated by pulling the chromosomes to either daughter cell. Protein ubiquitination is a post-translational modification that plays a central role in cellular homeostasis. E3 ubiquitin ligases mediate the transfer of ubiquitin to substrate proteins determining their fate. One of the largest subfamilies of E3 ubiquitin ligases is the family of the tripartite motif (TRIM) proteins, whose dysregulation is associated with a variety of cellular processes and directly involved in human diseases and cancer. In this review we summarize the current knowledge and emerging concepts about TRIMs and their contribution to the correct regulation of cell cycle, describing how TRIMs control the cell cycle transition phases and their involvement in the different functional units of the mitotic process, along with implications in cancer progression.
Highlights
Cell Cycle and MitosisPrecise replication of genetic material and its equal distribution into daughter cells are essential to maintain genome stability
TRIM29 knockdown increases the level of JAK2 and STAT3 phosphorylation, while TRIM8 interacts with and promotes STAT3 transcriptional activity with a consequent deregulation of STAT3 target genes that are directly involved in cell cycle progression [25,32]
TRIM59 protein levels are significantly high in non-small cell lung carcinoma (NSCLC) [29] and its expression is significantly elevated in cervical cancers, epithelial ovarian cancer (EOC), cholangiocarcinoma (CCA)
Summary
Precise replication of genetic material and its equal distribution into daughter cells are essential to maintain genome stability. Different phases of the cell cycle require different cyclins and the transition through the cell cycle phases is governed by the respective checkpoints that prevent the entry into the phase until cellular or genetic defects are repaired [1,2] (Figure 1a). Different phases of the cell cycle require different cyclins and the coordination between. Among the different phases of the cell cycle, delicateevent event that must be executed with high fidelity to ensure genomic stability, since genetic material has to be duplicated and eacheach with high fidelity to ensure genomic stability, since genetic material has to be duplicated and chromosome must be segregated into two daughter cells. When all of the chromosomes are bi-oriented and aligned, the cell is in metaphase, with sister kinetochores attached to microtubules from opposite spindle poles (bipolar attachment). In mammalian cells abscission fails if chromosomes are pulled apart erroneously or if the anaphase spindle midzone is not properly formed, leading to regression of the cleavage furrow and the formation of multinucleated cells [6,7,8]
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