Abstract
As previously reported, long intergenic non‑protein‑coding RNA 1006 (LINC01006) plays crucial roles in prostate, pancreatic and gastric cancers. However, whether it plays important roles in cervical cancer remains unclear. The present study thus aimed to determine the precise role of LINC01006 in cervical cancer and elucidate its regulatory mechanisms. The expression of LINC01006 in cervical cancer was examined by reverse transcription‑quantitative polymerase chain reaction. Cell proliferation assay, flow cytometric analysis, Transwell migration and invasion assays, and tumor xenograft model experiments were performed to elucidate the roles of LINC01006 in cervical cancer. Bioinformatics analysis, luciferase reporter assay, RNA immunoprecipitation and rescue experiments were performed for mechanistic analyses. The expression of LINC01006 was found to be upregulated in cervical cancer and to be associated with a poor prognosis. The absence of LINC01006 inhibited the proliferation, migration and invasion of cervical cancer cells, whereas it promoted cell apoptosis in vitro. The downregulation of LINC01006 impeded tumor growth in vivo. LINC01006 was verified as an endogenous 'sponge' that competed for microRNA‑28‑5p (miR‑28‑5p), which resulted in the upregulation of the miR‑28‑5p target P21‑activated kinase 2 (PAK2). Rescue experiments revealed that the suppression of miR‑28‑5p expression or the overexpression of PAK2 abrogated the effects of LINC01006 downregulation on malignant cellular functions in cervical cancer. On the whole, the present study demonstrates that LINC01006 exhibits tumor‑promoting functions in cervical cancer via the regulation of the miR‑28‑5p/PAK2 axis. These findings may provide the basis for the identification of LINC01006‑targeted clinical therapy.