Bioinformatics analysis predicted that annexin A4 was a potential target gene of miR-203. Next luciferase reporter assay confirmed that miR-203 could directly target annexin A4.
ANXA4 expression was increased at both the mRNA and protein level in the drugresistant ovarian cancer cells and ANXA4 contained a Lewis(y) structure. ANXA4 overexpression can abnormally activate signaling pathways and regulate the expression of a numbers of factors forming a positive feedback loop to induce the chemoresistance of ovarian cancer cells.
Taken together these data indicate that up-regulation of ANXA4 leads to activation of the NF-kappaB pathway and its target genes in a feedback regulatory mechanism via the p65 subunit resulting in tumor growth in GBC.
Upregulation and nuclear translocation of ANXA4 have been observed in the progression of colorectal cancer and ovarian serous carcinoma. Knockdown of ANXA4 attenuated migration in ovarian cancer and breast cancer cells. In contrast knockdown of ANXA4 increased susceptibility to platinum in ovarian cancer and malignant mesothelioma cells. Review.
Data shows that CYTB and ANXA4 overexpression may be involved in carcinogenesis and histopathological differentiation of ovarian clear cell carcinoma and suggest they may serve as a potential diagnostic biomarkers.
These findings indicate that the calcium-binding site in the ANXA4 repeat induces chemoresistance to the platinum-based drug by elevating the intracellular chloride concentration.
This study showed that overexpression and nuclear localization of annexin A4 are related to chemoresistance and poor survival in patients with serous papillary ovarian carcinomas.
Lower expression of annexin A4 during window of implantation in infertile patients with endometriosis might be associated with the decrease of endometrial receptivity.
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