**5. ABCA7 and Cancers**

As mentioned previously, due to the GWAS studies, ABCA7 functions were mainly studied in AD mouse models and in AD samples. This is noteworthy because ABC transporters have been closely linked to the MDR phenotype observed in cancer cells in the most recent studies of ABCA7 in cancer. Finally, no relation with the MDR phenotype has been observed, but a possible involvement in the epithelial to mesenchymal transition (EMT process) was reported, in particular in ovarian cancers (OC) [93]. In EMT, cells lose their epithelial markers and express more mesenchymal markers in order to acquire capacities like migration, invasion and proliferation, characteristics of malignancies and metastatic cancers. In this study, authors demonstrated that ABCA7 was upregulated in ovarian cancer (OC) cells from patients when compared to adjacent non-cancer tissues [93]. This upregulation was associated with poor survival rates in OC patients. When ABCA7 expression is suppressed, OC cell lines showed a decrease in migration and an increase in epithelial marker expression such as E-cadherin, correlated with a decrease of the mesenchymal marker, N-cadherin [93,94]. Interestingly, ABCA7 knockdown decreased the TGF beta transcription factor SMAD-4, a key regulator for EMT [93].

Additionally, regulation of ABCA7 in cancer cells was reported to be modulated by the micro-RNA tumor suppressor called Mir-197-3p. This is found downregulated in OVACAR-3 cells as well as in other types of cancer cells such as hepatocarcinoma cells [94], suggesting a potential implication of ABCA7 in other types of cancers. Further investigations for the ABCA7 role in cancer are needed for a better understanding of this transporter functions and for a better diagnosis and prognosis. They will also determine if targeting ABCA7 expression might be a promising approach to prevent or cure certain types of cancers.
