Abstract
Serine/threonine kinase 31 (STK31) is one of the novel cancer/testis antigens for which its biological functions remain largely unclear. Here, we demonstrate that STK31 is overexpressed in many human colorectal cancer cell lines and tissues. STK31 co-localizes with pericentrin in the centrosomal region throughout all phases of the cell cycle. Interestingly, when cells undergo mitosis, STK31 also localizes to the centromeres, central spindle, and midbody. This localization behavior is similar to that of chromosomal passenger proteins, which are known to be the important players of the spindle assembly checkpoint. The expression of STK31 is cell cycle-dependent through the regulation of a putative D-box near its C-terminal region. Ectopically-expressed STK31-GFP increases cell migration and invasive ability without altering the proliferation rate of cancer cells, whereas the knockdown expression of endogenous STK31 by lentivirus-derived shRNA results in microtubule assembly defects that prolong the duration of mitosis and lead to apoptosis. Taken together, our results suggest that the aberrant expression of STK31 contributes to tumorigenicity in somatic cancer cells. STK31 might therefore act as a potential therapeutic target in human somatic cancers.
Highlights
Cell division in mammalian cells is regulated by a number of protein kinases that control progression through various phases of the cell cycle
The expression of Serine/threonine kinase 31 (STK31) mRNA was further evaluated in many colorectal cancer cells compared with AZ521
The same result occurred in human clinical colorectal tissues, which expressed high levels of STK31 in cancerous tissues relative to normal tissues from the same person (Figure 1C)
Summary
Cell division in mammalian cells is regulated by a number of protein kinases that control progression through various phases of the cell cycle. Previous studies indicated that misregulation of cell cycle kinases might result in the unlimited proliferation and aberrant division of cells leading to genomic instability, both of which are the hallmarks of carcinogenesis [1,2]. Accumulated evidence indicates that mitotic kinases are responsible for protecting cells from chromosome aberrations and aneuploidy. Mitotic kinases like Polo-like kinases (Plks) and Aurora kinases are involved in regulating the centrosome cycle and mitotic spindle formation. Alterations in signaling pathways involved in these mitotic kinases can result in an exit from mitosis with a aberrant chromosome number, leading to aneuploidy and eventually cancer [3]
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