Long non‑coding RNA nuclear paraspeckle assembly transcript 1 interacts with microRNA‑107 to modulate breast cancer growth and metastasis by targeting carnitine palmitoyltransferase‑1.

Abstract

Previous studies revealed that the long non‑coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) exhibits abnormal expression in numerous cancer types, including breast cancer (BC); however, the regulatory mechanism of NEAT1 in BC remains unclear. In the present study, the effect of NEAT1 on the progression of BC and its regulation mechanism was investigated. The expression levels of NEAT1 and microRNA‑107 (miR‑107) in BC cells were analyzed using the reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR). NEAT1 was knocked down in BC cells, and mimics‑miR‑107 or inhibitor‑miR‑107 were transfected into BC cells. Subsequently, cell proliferation, invasion and migration, apoptosis and cell cycle distribution were determined. The regulatory mechanism of NEAT1, miR‑107 and carnitine palmitoyltransferase‑1 (CPT1A) was analyzed using a luciferase reporter assay system, western blotting and RT‑qPCR. NEAT1 expression was increased in BC cells, whereas miR‑107 expression was decreased, compared with normal mammary gland cells. NEAT1 promoted the progression of BC cells through inhibiting apoptosis‑associated genes and promoting cell cycle‑ and invasion‑associated gene expression, whereas miR‑107 served the opposite function. Furthermore, NEAT1 promoted the expression of CPT1A, which was mediated by miR‑107. The results of the present study indicate that NEAT1 promotes the expression of CPT1A by inhibiting miR‑107 to improve the progression of BC cells; therefore, NEAT1 is a potential therapeutic target of BC.