RESUMEN
Breast cancer is the second most prevalent cancer in women worldwide. Long noncoding RNAs (lncRNAs) have been identified as important regulators of tumorigenesis and tumor metastasis. lncRNA FGD5AS1 has been previously reported as a carcinogenic gene, however its role in breast cancer has yet to be investigated. The present study aimed to understand the function of lncRNA FGD5AS1 in breast cancer and examine the underlying molecular mechanisms. Sample tissues for downstream gene expression profiling were collected from patients with breast cancer (n=23). The effect of FGD5AS1 overexpression on cell viability, invasion and migration has been studied in breast cancer cells (MDAMB231). Changes in glycolysis were monitored by comparing glucose consumption, lactate production and ATP levels. Using StarBase and TargetScan databases a putative interaction between FGD5AS1, miR1955p and SNF1like kinase 2 (NUAK2) was predicted in silico. Expression levels of FGD5AS1, hasmiR1955p and NUAK2 were validated by reverse transcriptionquantitative PCR and interactions were validated using dualluciferase reporter assays and RNA pulldown. High expression of lncRNA FGD5AS1 was detected in breast cancer tissue samples and disease model cell lines. Silencing of FGD5AS1 led to decreased cell proliferation, migration and invasion. It was identified that at a molecular level FGD5AS1 serves as a sponge of miR1955p and alters the expression of its downstream target gene NUAK2. In breast cancer lncRNA FGD5AS1 serve a key role in glycolysis and tumor progression via the miR1955p/NUAK2 axis. The findings of the present study indicated FGD5AS1 as a candidate target for intervention in patients with breast cancer.