Multiple studies have shown that protein kinase Bβ (AKT2) is involved in the development and progression of ovarian cancer, however, its precise role remains unclear.
We focused on examining the Akt2 expression, mainly because of its report as being overamplified in the aggressive variants of ovarian cancer, as well as TGFbeta-sensitivity of Akt2 that forms the key basis for metastasis initiation of most kinds of carcinoma.
Taken together, our study suggests that miR-29b regulates the Warburg effect in EOC via AKT2/AKT3 and may provide novel options for future treatments for EOC.
Despite the relatively high prevalence of ovarian cancer (1% of American women will develop this disease in their lifetime) and recent developments in its molecular genetic understanding (several proto-oncogenes, such as AKT2 and cKRAS, and tumor suppressor genes, such as BRCA1 and BRCA2, have been implicated), little is known about the presence of ovarian tumors and cancer in women already diagnosed with other familial multiple tumor syndromes.
The proliferation-related function of AKT2 and SEI-1 suggests that both genes are likely to be biological targets of an amplification event at 19q13.1 in ovarian cancer and to play important roles in ovarian tumorigenesis.
In addition, downstream effectors of PI3-kinase, AKT1 and AKT2, have been found to be amplified or activated in human tumours, including ovarian cancer.
In addition to AKT2, amplification and overexpression of other yet-unidentified genes in the 19q13.1-q13.2 region may contribute to ovarian carcinoma pathogenesis or progression.