AKR1B10 promotes breast cancer cell proliferation and migration via the PI3K/AKT/NF-?B signaling pathway

Abstract Background Aberrant expression of Aldo-Keto reductase family 1 member B10 (AKR1B10) was associated with tumor size and metastasis breast cancer in our published preliminary studies. However, little is known about the detailed function underlying molecular mechanism AKR1B10 pathological process cancer. Methods The relationship between elevated overall survival disease-free patients analyzed by Kaplan–Meier Plotter database. Breast cell lines overexpressing (MCF-7/AKR1B10) knockdown (BT-20/shAKR1B10) were constructed to analyze impact on proliferation migration levels detected compared tissues RT-qPCR, western blot immunohistochemistry. cells monitored CCK8 assay, invasion observed scratch test transwell assay. proliferation- EMT-related proteins including cyclinD1, c-myc, Survivin, Twist, SNAI1, SLUG, ZEB1, E-cadherin, PI3K, p-PI3K, AKT, p-AKT, IKB?, p-IKB?, NF-?B p65, p-NF-?B p65 cells. MCF-7/AKR1B10 treated LY294002, a PI3K inhibitor, consider overexpression PI3K/AKT/NF-?B signal cascade presence nuclear. In vivo xenograft experiments used observe role growth mice. Results significantly greater tissue paired non-cancerous tissue. positively correlated lymph node metastasis, size, Ki67 expression, p53 but inversely rates. Gene Ontology analysis showed that activity contributes proliferation. Overexpression facilitated MCF-7 cells, induced vitro association induction epithelial-mesenchymal transition (EMT). Conversely, inhibited these effects BT-20 Mechanistically, activated nuclear translocation proliferation-related downregulated E-cadherin silencing reduced phosphorylation migration-related attenuated p65. confirmed promoted Conclusions promotes proliferation, via signaling pathway represents novel prognostic indicator as well potential therapeutic target