Oncogenic Long Noncoding RNA Linc01287 Promotes IGF1R Expression by Sponging miR-98 in Breast Cancer

Long noncoding RNA (LncRNA) dysregulation has been shown to exhibit a regulatory effect in various cancers. However, the effect of LINC01287 on breast cancer (BC) has not been illustrated. The aim of this research was to explore the expression and function of LncRNA LINC01287 in BC. LINC01287 expression in clinical tissues and BC cell lines was detected. The luciferase reporter assay was performed to verify the correlation between LINC01287, microRNA 98 (miR-98), and the insulin-like growth factor 1 receptor (IGF1R). The CCK-8 assay was performed to examine cell viability. Cell invasion and migration capacity was determined by transwell and wound healing assays. The protein level of IGF1R, phosphorylated mitogen-activated protein kinase 1 and 2 (p-MEK1/2), and phosphorylated extracellular signal-regulated kinase 1 and 2 (p-ERK1/2) was analyzed by western blotting. LINC01287 expression markedly increased in BC cell lines. Subsequent studies identified LINC01287 as a downstream target of miR-98. In addition, LINC01287 knockdown and miR-98 overexpression significantly stagnated progression of BC cells. LINC01287 knockdown also downregulated IGF1R levels. Moreover, LINC01287 knockdown notably downregulated the phosphorylation of MEK1/2 and ERK1/2. The in vivo assay verified that LINC01287 can regulate tumorigenesis of BC. Our findings showed that LINC01287 was overexpressed in BC cells and tissues. LINC01287 promoted the malignant characteristics of BC cells and acted as an oncogene. Its regulatory effect may be associated with the miR-98/IGF1R/MEK/ERK signaling pathway. Therefore, LINC01287 has potential for use as a biomarker or therapeutic target for the treatment of BC.