Long non‑coding RNA PLK1S1 was associated with renal cell carcinoma progression by interacting with microRNA‑653 and altering C‑X‑C chemokine receptor 5 expression.

Renal cell carcinoma (RCC) is the most common type of renal cancer. Long non‑coding RNA (lncRNA) has been reported to play a vital role in the development and progression of various types of cancer type. However, the underlying molecular mechanisms of PLK1S1 in regulating RCC progression remain unclear. In the present study, PLK1S1 was upregulated in RCC tissues and cells, and PLK1S1 expression was also significantly elevated in stage IV RCC tissues. Kaplan‑Meier analysis showed that patients with high PLK1S1 expression had a shorter overall survival time compared with those with low PLK1S1 expression. Moreover, bioinformatics analysis and luciferase reporter assay demonstrated that PLK1S1 inhibited microRNA (miR)‑653 expression by direct interaction. Functional analyses demonstrated that a miR‑653 inhibitor promoted short hairpin PLK1S1‑attenuated cell proliferation, invasion and sorafenib resistance of RCC cells. In addition, C‑X‑C motif chemokine receptors 5 (CXCR5) was identified as an effector of PLK1S1/miR‑653‑mediated tumorigenesis and drug resistance in RCC cells. Lastly, xenograft experiments demonstrated that PLK1S1 knockdown inhibited tumor growth in vivo. Reverse transcription‑quantitative PCR and western blot analysis revealed that PLK1S1 knockdown upregulated the expression level of miR‑653, whilst downregulating the expression level of CXCR5. In conclusion, the present study revealed that PLK1S1 promoted tumor progression and sorafenib resistance in RCC through regulation of the miR‑653/CXCR5 axis, which may offer a novel treatment strategy for patients with RCC.