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Functions of Aurora kinase C in meiosis and cancer.

Quartuccio SM, Schindler K - Front Cell Dev Biol (2015)

Bottom Line: While Aurora kinase A (AURKA) and B (AURKB) are found in cells throughout the body, significant protein levels of Aurora kinase C (AURKC) are limited to cells that undergo meiosis (sperm and oocyte).Despite its discovery nearly 20 years ago, we know little about the function of AURKC compared to that of the other 2 Aurora kinases.Here, we consolidate and update what is known about AURKC signaling in meiotic cells to better understand why it has oncogenic potential.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics, Rutgers, The State University of New Jersey Piscataway, NJ, USA.

ABSTRACT
The mammalian genome encodes three Aurora kinase protein family members: A, B, and C. While Aurora kinase A (AURKA) and B (AURKB) are found in cells throughout the body, significant protein levels of Aurora kinase C (AURKC) are limited to cells that undergo meiosis (sperm and oocyte). Despite its discovery nearly 20 years ago, we know little about the function of AURKC compared to that of the other 2 Aurora kinases. This lack of understanding can be attributed to the high sequence homology between AURKB and AURKC preventing the use of standard approaches to understand non-overlapping and meiosis I (MI)-specific functions of the two kinases. Recent evidence has revealed distinct functions of AURKC in meiosis and may aid in our understanding of why chromosome segregation during MI often goes awry in oocytes. Many cancers aberrantly express AURKC, but because we do not fully understand AURKC function in its normal cellular context, it is difficult to predict the biological significance of this expression on the disease. Here, we consolidate and update what is known about AURKC signaling in meiotic cells to better understand why it has oncogenic potential.

No MeSH data available.


Related in: MedlinePlus

Aberrations in AURKC levels results in altered cell phenotypes. Diagram summarizing cell phenotypes observed when AURKC expression is disrupted in mitotic and meiotic cells.
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Figure 2: Aberrations in AURKC levels results in altered cell phenotypes. Diagram summarizing cell phenotypes observed when AURKC expression is disrupted in mitotic and meiotic cells.

Mentions: AURKC is oncogenic because its overexpression transforms NIH 3T3 cells into tumors (Khan et al., 2011). AURKC is overexpressed in many cancer cell lines, including NB1RGB, MDA-MB-453, HEPG2, HeLa, and HuH7 (Kimura et al., 1999), and in cancer of the reproductive tract (Tsou et al., 2011). Overexpression increases cellular proliferation and migration and enhances xenograft tumor growth (Tsou et al., 2011). Kinase-dead AURKC decreases proliferation of HeLa cells while expression of the constitutively active AURKC (Spengler, 2007a; Khan et al., 2012) leads to more aggressive tumors (Khan et al., 2011; Tsou et al., 2011). Other carcinogenic genes are also located in the telomeric region of human Chromosome 19 (Bernard et al., 1998), a genomic region susceptible to translocations and deletions (Bernard et al., 1998; Kimura et al., 1999). Although some plasticity exists between the Aurora kinase family members allowing for functional compensation; some roles are kinase specific and maintaining the correct balance is necessary for genomic stability (Figure 2).


Functions of Aurora kinase C in meiosis and cancer.

Quartuccio SM, Schindler K - Front Cell Dev Biol (2015)

Aberrations in AURKC levels results in altered cell phenotypes. Diagram summarizing cell phenotypes observed when AURKC expression is disrupted in mitotic and meiotic cells.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4542505&req=5

Figure 2: Aberrations in AURKC levels results in altered cell phenotypes. Diagram summarizing cell phenotypes observed when AURKC expression is disrupted in mitotic and meiotic cells.
Mentions: AURKC is oncogenic because its overexpression transforms NIH 3T3 cells into tumors (Khan et al., 2011). AURKC is overexpressed in many cancer cell lines, including NB1RGB, MDA-MB-453, HEPG2, HeLa, and HuH7 (Kimura et al., 1999), and in cancer of the reproductive tract (Tsou et al., 2011). Overexpression increases cellular proliferation and migration and enhances xenograft tumor growth (Tsou et al., 2011). Kinase-dead AURKC decreases proliferation of HeLa cells while expression of the constitutively active AURKC (Spengler, 2007a; Khan et al., 2012) leads to more aggressive tumors (Khan et al., 2011; Tsou et al., 2011). Other carcinogenic genes are also located in the telomeric region of human Chromosome 19 (Bernard et al., 1998), a genomic region susceptible to translocations and deletions (Bernard et al., 1998; Kimura et al., 1999). Although some plasticity exists between the Aurora kinase family members allowing for functional compensation; some roles are kinase specific and maintaining the correct balance is necessary for genomic stability (Figure 2).

Bottom Line: While Aurora kinase A (AURKA) and B (AURKB) are found in cells throughout the body, significant protein levels of Aurora kinase C (AURKC) are limited to cells that undergo meiosis (sperm and oocyte).Despite its discovery nearly 20 years ago, we know little about the function of AURKC compared to that of the other 2 Aurora kinases.Here, we consolidate and update what is known about AURKC signaling in meiotic cells to better understand why it has oncogenic potential.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics, Rutgers, The State University of New Jersey Piscataway, NJ, USA.

ABSTRACT
The mammalian genome encodes three Aurora kinase protein family members: A, B, and C. While Aurora kinase A (AURKA) and B (AURKB) are found in cells throughout the body, significant protein levels of Aurora kinase C (AURKC) are limited to cells that undergo meiosis (sperm and oocyte). Despite its discovery nearly 20 years ago, we know little about the function of AURKC compared to that of the other 2 Aurora kinases. This lack of understanding can be attributed to the high sequence homology between AURKB and AURKC preventing the use of standard approaches to understand non-overlapping and meiosis I (MI)-specific functions of the two kinases. Recent evidence has revealed distinct functions of AURKC in meiosis and may aid in our understanding of why chromosome segregation during MI often goes awry in oocytes. Many cancers aberrantly express AURKC, but because we do not fully understand AURKC function in its normal cellular context, it is difficult to predict the biological significance of this expression on the disease. Here, we consolidate and update what is known about AURKC signaling in meiotic cells to better understand why it has oncogenic potential.

No MeSH data available.


Related in: MedlinePlus