ORAOV1 Human

ORAOV1 was first identified by Huang and his colleagues, who noted its significant role in the amplification of the 11q13 chromosomal region . This gene was found to be a primary driving force behind the amplification and was considered a candidate oncogene due to its involvement in the development and progression of various SCCs .

Recent studies have shown that ORAOV1 plays a crucial role in the tumorigenesis of SCCs by regulating cell growth and tumor angiogenesis . In particular, ORAOV1 has been implicated in the regulation of the cell cycle and apoptosis in cancer cells. For example, in cervical cancer HeLa cells, silencing ORAOV1 led to downregulation of Cyclin A, Cyclin B1, and Cdc2, resulting in cell cycle arrest at the S phase . Additionally, the knockdown of ORAOV1 activated both extrinsic and intrinsic apoptotic pathways, leading to apoptosis through the modulation of proteins such as P53, Bcl-2, Caspase-3, Caspase-8, Caspase-9, and cytochrome c .

The expression level of ORAOV1 has been tightly correlated with prognosis-related clinicopathological parameters and clinical grades in several SCCs, including esophageal squamous cell carcinoma and oral squamous cell carcinoma (OSCC) . This makes ORAOV1 a valuable biological marker for these cancers. Its overexpression is associated with poor prognosis and higher clinical grades, suggesting its potential as a therapeutic target .

Human recombinant ORAOV1 is produced using recombinant DNA technology, which involves inserting the ORAOV1 gene into a suitable expression system, such as bacteria or yeast, to produce the protein in large quantities. This recombinant protein can be used in various research applications to study its function and role in cancer biology. It can also be utilized in drug development to screen for potential inhibitors that target ORAOV1, providing a basis for new cancer therapies.