Long non‑coding RNA PCAT1 sponges miR‑134‑3p to regulate PITX2 expression in breast cancer.

Abstract

Breast cancer (BC) is the most prevalent cancer among women. Long non‑coding (lnc)RNAs and microRNAs (miRs) both regulate the expression of key genes in tumorigenesis. The present study aimed to explore the molecular mechanism of the prostate cancer‑associated transcript 1 (PCAT1)/miR‑134‑3p/pituitary homeobox 2 (PITX2) in BC. Reverse transcription‑quantitative PCR was performed to examine the expression of miR‑134‑3p. Cell proliferation, viability, cell cycle, apoptosis and migration were analyzed using Cell Counting Kit‑8, colony formation, flow cytometry, wound healing and Transwell assays. Protein expression levels were determined by western blotting. The present study demonstrated that PCAT1 was significantly highly expressed in BC cells. Knockdown of PCAT1 significantly inhibited cell proliferation, migration and invasion, but promoted apoptosis in human BC cell lines. The results of the dual‑luciferase assay showed that PCAT1 targeted miR‑134‑3p, and PITX2 was a potential target of miR‑134‑3p. Western blotting results demonstrated that PCAT1 knockdown significantly reduced the protein expression levels of anti‑apoptotic protein Bcl‑2, and significantly upregulated the protein expression levels of proapoptotic proteins, Bax, cleaved caspase‑3 and cleaved caspase‑9. Furthermore, the effect of a miR‑134‑3p inhibitor on BC progression was rescued by the knockdown of PITX2 in cells transfected with short hairpin RNA‑lncRNA PCAT1. To conclude, the results of the present study indicated that the PCAT1/miR‑134‑3p/PITX2 axis could be a promising therapeutic target in BC treatment.