HOTAIR may regulate proliferation, apoptosis, migration and invasion of MCF-7 cells through regulating the P53/Akt/JNK signaling pathway.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

PubMedID: 28407576

Yu Y, Lv F, Liang D, Yang Q, Zhang B, Lin H, Wang X, Qian G, Xu J, You W. HOTAIR may regulate proliferation, apoptosis, migration and invasion of MCF-7 cells through regulating the P53/Akt/JNK signaling pathway. Biomed Pharmacother. 2017;90555-561.
Breast cancer is a common malignancy, and it is the second leading cause of cancer-related death among women worldwide. The pathogenesis of breast cancer is poorly understood, leading to unsatisfactory efficacy of current anti-PC therapies. THE AIM
of this study is to investigate the role of LncRNA HOTAIR in proliferation, apoptosis, migration and invasion of human breast cancer cell line MCF-7.MCF-7 cells were cultured and transfected with HOTAIR siRNA, and the proliferation rate of cells was determined using MTT and colony-forming assay; moreover, the apoptosis as well as cell cycles were determined using annexin V/propidium iodide staining methods and analyzed using flow cytometery; furthermore, cell scratch and transwell assays have been performed to examine the migration and invasion of MCF-7 cells; Next, cells were collected, and RT-qPCR as well as western blotting assay were performed to examine the expression of P53, MDM2, AKT, JNK, MMP-2 and MMP-9. We discovered that knockdown of HOTAIR induced significant decrease in proliferation and increase in apoptosis of MCF-7 cells, and the cell cycles of HOTAIR siRNA transfected cells have been arrested at G1 phase (p<0. 01); moreover, knockdown of HOTAIR lead to marked decrease in the migration and invasion ability of MCF-7 cells; finally, knockdown of HOTAIR induced significant decrease in the expression of P53/Akt/JNK (p<0. 01), and significant increase in the expression of P53 in MCF-7 cells (p<0. 01). In conclusion, our results proved that HOTAIR may regulate proliferation, apoptosis, migration and invasion of MCF-7 cells through regulating the P53/Akt/JNK signaling pathway.