Long noncoding RNA PDIA3P promotes breast cancer development by regulating miR-183/ITGB1/FAK/PI3K/AKT/ß-catenin signals.

Aberrantly expressed long noncoding RNAs (lncRNAs) play crucial roles in the process of breast cancer (BC). This research aims to dig the possible roles and regulatory mechanism of lncRNA protein disulfide isomerase family A member 3 pseudogene 1 (PDIA3P1) in BC. The mRNA level of PDIA3P both in BC tissues and in cells were determined, followed by the investigation of the effects of PDIA3P suppression on cell biological processes including the viability, apoptosis, migration and invasion. Furthermore, whether PDIA3P modulated the expression of integrin ß1 (ITGB1) expression by competitively sponging miR-183 and then regulated the activation of FAK/PI3K/AKT/ß-catenin pathway was explored. PDIA3P was discovered as up-regulated in BC tissues and cells. PDIA3P suppression markedly decreased cell viability, promoted apoptosis, and inhibited migration and invasion in MCF-7 cells. In addition, PDIA3P was found to be negatively interacting with miR-183, and PDIA3P regulated tumor growth and metastasis through negatively regulating miR-183. Moreover, ITGB1 was targeted by miR-183 and involved in tumor growth and metastasis. Lastly, PDIA3P suppression markedly inhibited the activation of FAK/PI3K/AKT/ß-catenin pathway, which was significantly reversed after simultaneous inhibition of miR-183. Our results reveal that PDIA3P may forpromote BC development by sponging miR-183 to regulate ITGB1, thus inducing the activation of FAK/PI3K/AKT/ß-catenin signals. PDIA3P may serve as a promising biomarker or target for the detection or treatment of BC.