Abstract
Breast cancer is a major contributor leading to cancer death in females worldwide. The aim of the present study was to investigate the effects of microRNA-98 (miR-98) on the processes of cell proliferation, invasion, migration and apoptosis by binding to high-mobility group AT-hook 2 (HMGA2) in breast cancer. Breast cancer tissues and adjacent normal tissues were collected from 112 patients suffering from breast cancer. The target relationship between miR-98 and HMGA2 was verified by in connection with the bioinformatics website as well as a dual-luciferase reporter assay, both of which provided evidence indicating that HMGA2 was a target gene of miR-98. Human breast cancer MDA-MB-231 cells were treated with miR-98 mimics, miR-98 inhibitors, siRNA-HMGA2 or miR-98 inhibitors + siRNA-HMGA2. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry methods were performed to determine cell proliferation, cell cycle and apoptosis, respectively, while a Transwell assay was employed to detect cell migration and invasion. Breast cancer tissues exhibited decreased miR-98 expression, while increased expression levels of HMGA2 were recorded. The mRNA and protein expressions of HMGA2, cell proliferation, cells at the S phase, cell migration, invasion, expressions of matrix metalloproteinase (MMP)2 as well as MMP9 were all reduced in response to miR-98 mimics or siRNA-HMGA2, while a contradictory trend was observed in the miR-98 inhibitors group. In conclusion, the results of the study demonstrate that miR-98 inhibits cell proliferation, migration and invasion, while acting to promote apoptosis by negatively regulating HMGA2 in breast cancer.
Highlights
Driven by multiple genetic or epigenetic alterations and molecular events, breast cancer is a molecularly heterogeneous disease representing the most common type of cancer and a primary cause of mortality among women worldwide [1,2,3]
Based on the exploration of literature as well as the current situation regarding the treatment of breast cancer, the central objective of the current study was to investigate whether miR-98 could suppress the cell proliferation, invasion and migration of breast cancer via binding to HMGA2 in a bid to discover a potential biomarker for improved breast cancer treatment
Positive expression rate of HMGA2 is higher in the breast cancer tissues
Summary
Driven by multiple genetic or epigenetic alterations and molecular events, breast cancer is a molecularly heterogeneous disease representing the most common type of cancer and a primary cause of mortality among women worldwide [1,2,3]. In spite of the distinct progress in the clinical diagnosis, prognosis and treatment of breast cancer the survival rate of patients with metastatic breast cancer is still limited [6]. This is largely due to the complexity and poorly understood underlying cellular and molecular mechanisms associated with the occurrence of the disease. The effect of microRNA (miRNA) dysregulation on breast cancer has been extensively investigated c 2018 The Author(s)
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