LINC00671 inhibits renal cell cancer progression via regulating miR-221-5p/SOCS1 axis

Background: Long non-coding RNA (IncRNA) has gradually received widespread attention due to its role in regulating tumor progression. However, in renal cell cancer (RCC), the exact function of IncRNA LINC00671 remains uncertain. Methods: Quantitative real-time polymerase chain reaction (qRT-PCR) was utilized for detecting LINC00671 and miR-221-5p expressions in RCC tissues and cell lines. Western blotting technique was utilized for detecting the expressions of epithelial-mesenchymal transition (EMT)-associated proteins (E-cadherin and N-cadherin) and suppressor of cytokine signaling 1 (SOCS1). The correlation between clinicopathological features and LINC00671 expression was also evaluated. RCC cell multiplication, migration and invasion were measured by CCK-8, EdU and Transwell assays, respectively. The targeted relationships between LINC00671 as well as the SOCS1 3'UTR and miR-221-5p were verified by RNA immunoprecipitation (RIP) and luciferase reporter gene assay. Results: LINC00671 expression in RCC tissues and cells was significantly reduced. Patients with low LINC00671 expression had relatively shorter disease-free survival and overall survival. Moreover, LINC00671 expression was linked to lymph node metastasis, tumor stage, and tumor size. In Caki-1 and 769-P cell lines, LINC00671 overexpression restrained the multiplication, migration, invasion, as well as the EMT process of RCC cells in vitro. In terms of mechanism, miR-221-5p was identified as a target of LINC00671, and LINC00671 could up-regulate SOCS1 by repressing miR-221-5p. Conclusion: LINC00671 regulates the miR-221-5p/SOCS1 axis as a tumor suppressor in RCC.