Objective: Amongst noncoding RNAs, competing endogenous RNAs (ceRNAs) are popular and interesting regulatory mechanisms involved in oncogenesis and tumour progression. LncRNA FGD5-AS1, also known as miR-5590-3p, is involved in the regulatory role of ceRNA in many cancers. However, the roles of lncRNA FGD5-AS1 or miR-5590-3p in renal cell carcinoma (RCC) remain unclear. We investigated how FGD5-AS1 and miR-5590-3p regulated clear cell proliferation and metastasis in RCC.
Patients and methods: Real Time-quantitative PCR (RT-qPCR) was used to detect the expression of FGD5-AS1 in tumour issues and renal cancer cell lines. MTT, scratch test and transwell assay were performed to confirm the effect of FGD5-AS1 on the proliferation, migration or invasion of the above cell lines. RNA pull-down and Luciferase assays were used to detect the target site between FGD5-AS1 and miR-5590-3p. In addition, we examined the proteins related to ERK/AKT signalling related via Western blot analysis. Finally, we used the RT-qPCR method to detect the mRNA levels of E-cadherin and vimentin.
Results: LncRNA FGD5-AS1 was highly expressed in renal cancer tissues, especially in patients with metastasis. This effect facilitated the proliferation, migration, epithelial-mesenchymal transition and invasion of renal cancer cells. Silencing the expression of FGD5-AS1 with FGD5-AS1 siRNA significantly inhibited the malignancy of tumour cells. RNA pull-down and Luciferase assays demonstrated that FGD5-AS1 targeted miR-5590-3p to interact with miR-5590-3p negatively. Furthermore, miR-5590-3p inhibitors could eliminate the FGD5-AS1 siRNA-induced upregulation of E-cadherin and downregulation of vimentin.
Conclusions: Mechanistically, lncRNA FGD5-AS1 can competitively interact with miR-5590-3p and regulate the downstream signalling of ErkAKT to enhance the malignancy of tumours. This lncRNA could become a potential target molecule for treating and diagnosing RCC.