AURKA inhibits p53 suppressor function by at least two things, it immediately phosphorylates p53 at Ser315 facilitating MDM 2 mediated degradation of p53 in cancer cells, and it also phosphorylates p53 at Ser215 to inactivate its transcriptional activity. Along with both of these mechanisms, our work indicates regulation of p53 through AKT/MDM 2 axis in gastric cancer cells. We also reported that ubiquitin conjugation AURKA over expression inhibits TAp73 in p53 deficient cancer cells. TAp73, a p53 family, member has considerable homology with p53 and plays an important role in apoptosis induced by cytotoxic agents. The tumefaction suppressor proteins p53 and p73 can trigger genetic programs that halt cell growth transiently or permanently or eliminate the cell completely. Regulation of p53 and p73 by AURKA over-expression can result in suppression of apoptosis of tumefaction cells. AKT is really a significant pro proliferative Plastid serine/threonine kinase that encourages cell survival in many different cell types and stops apoptosis induced by different apoptotic stimuli. We, and others, have noted that AURKA up regulates AKT phosphorylation at Ser473. We described the regulation of GSK 3fi and fi catenin by AURKA over-expression in gastric cancer cells. A schematic breakdown of possible AURKA connection is shown in Figure 3. AURKB AURKB guarantees faithful chromosome segregation and handles kinetochore microtubule attachment. It is over expressed in several human cancers like breast, colorectal, kidney, lung, and prostrate. A heightened degree of AURKB correlates with advanced stages of colorectal cancer. Its over expression leads to multiple nucleation and polyploidy in human cells, but, this phenotype is exacerbated in lack of p53. It’s also been reported that AURKB over expression triggers chromosomes lagging in metaphase, chromosome segregation error and mistakes in cytokinesis, and hence, playing a role in carcinogenesis. AURKB doesn’t change cells alone but is reported (-)-MK 801 to cause H Ras mediated transformation. AURKB over expression is reported to link with the level of genomic instability inside a tumefaction suggesting that it plays a part in the exchange of genetic changes critical for neoplastic transformation. AURKC AURKC is really a chromosome messenger protein expressed in the testis and not in somatic cells. But, it’s claimed to be highly expressed in cancer cells such as HepG2, HuH7, MDAMD 453, and HeLa cells. Almost no information can be obtained about the role of AURKC in tumors, further functional analysis must comprehend its role in molecular pathways in cancer. Their over-expression and association with genetic instability in tumors have made them the target of drug discovery. Because of the participation in a wide array of cell cycle activities, they attracted plenty of attention from pharmaceutical organizations to produce possible inhibitors against them.