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Abstract Breast cancer (BC) poses a huge threat to women's health. Growing evidence has shown lncRNAs play critical roles in BC progression. However, the effect of LINC00536 in BC remains unknown. LINC00536, miR‐4282, and centromere protein F (CENPF) expressions in BC cells were determined using qPCR assay. Colony formation assay was employed to evaluate the cell proliferation of BC cells. Besides, cell migration and invasion were evaluated using the transwell assay. FISH assay was employed to analyze LINC00536 and miR‐4282 locations in BC cells. Additionally, dual luciferase reporter gene assay was performed to verify the binding relationships between LINC00536 and miR‐4282, miR‐4282 and CENPF. Here, our results displayed that LINC00536 and CENPF were overexpressed in BC cells, while miR‐4282 was downregulated. LINC00536 could negatively regulate miR‐4282 expression via directly binding to miR‐4282. LINC00536 silence suppressed the proliferation, migration, and invasion of BC cells, which was abolished by miR‐4282 inhibition. Additionally, miR‐4282 could negatively regulate CENPF expression via directly binding to CENPF. MiR‐4282 overexpression suppressed BC development, which was abolished by CENPF overexpression. Finally, we proved that LINC00536 silencing suppressed BC growth via regulating the miR‐4282/CENPF axis in vivo. Our research displayed that LINC00536 acted as an oncogene in BC. LINC00536‐enhanced BC cell proliferation, migration, and invasion. Moreover, LINC00536 functioned as a ceRNA to exert malignant characteristics in BC via the miR‐4282–CENPF axis. Collectively, our results demonstrated that the LINC00536–miR‐4282–CENPF axis was a critical player in BC development and was a promising target for BC therapy.

Abstract Osteosarcoma (OS) is the second most common primary malignant bone tumors in adolescents that causes cancer‐related deaths. Previous studies have confirmed the promoting role of lncRNA HCP5 in the development of OS, but the specific mechanism is still not well understood. MiRNA levels were measured via RT‐qPCR and protein expression was detected via western blotting. Cell proliferation was analyzed by CCK‐8 assays and colony formations assay were conducted to measure colony formation ability. Dual‐luciferase reporter assay was performed to detect the targeting relationship between HCP5 and miR‐29b‐3p, and between miR‐29b‐3p and LOXL2. Wound healing assays and Transwell assays were conducted to verify the migration and invasion abilities of OS cells. Correlations between the levels of HCP5 and miR‐29b‐3p, and between miR‐29b‐3p and LOXL2 were determined by Pearson correlation coefficient analysis. MiR‐29b‐3p expression was decreased and HCP5 and LOXL2 levels were increased in OS tissues and cell lines. MiR‐29b‐3p could directly act on LOXL2 and knockdown of LOXL2 restrained the proliferation, migration, and invasion of OS cells. Moreover, transfection with sh‐HCP5‐1 and sh‐HCP5‐2 suppressed the malignant biological behavior of OS cells. HCP5 directly targeted miR‐29b‐3p, and promoted OS proliferation, migration, and invasion via the miR‐29b‐3p/LOXL2 axis. The lncRNA HCP5 may upregulate LOXL2 expression by targeting miR‐29b‐3p, thereby promoting OS proliferation, migration, and invasion.