Long non-coding RNA 01088 restrains breast cancer progression via regulating miR-498/PTEN axis

Abstract

Breast cancer (BC) is one of the most common tumors and the second leading cause of cancer-related death among women. Long non-coding RNA (lncRNA) is vital in regulating the progression of BC, however, its biological function in BC is inconclusive. Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to quantify the expressions of LINC01088, microRNA (miRNA) miR-498, phosphatase and tensin homologue deleted on chromosome 10 (PTEN) mRNA in BC tissues and cells. Cell counting kit-8 (CCK-8) and 5-Ethynyl-2’-deoxyuridine (EdU) assays were used to detect cell proliferation. The apoptosis was detected by flow cytometry. Moreover, PTEN protein expression was determined by Western blot. Dual-luciferase reporter gene assay and RNA immunoprecipitation (RIP) assay were used to verify the targeting relationships among LINC01088, miR-498, and PTEN. LINC01088 expression level was declined in BC tissues and cells, which was related to higher TNM stage. LINC01088 overexpression significantly inhibited the growth of BC cells, induced apoptosis, promoted Bax and cleaved-caspase-3 expressions, and restrained Bcl-2 expression; LINC01088 knockdown worked oppositely. MiR-498 was confirmed as the target of LINC01088. PTEN expression was negatively modulated by miR-498 and positively regulated by LINC01088 in BC cells. LINC01088 up-regulates the expression of PTEN by targeting miR-498 and has the potential to repress the progression of BC.