Overexpression of microRNA-96-5p inhibits autophagy and apoptosis and enhances the proliferation, migration and invasiveness of human breast cancer cells

Abstract

Abstract. MicroRNAs (miRNA/miR) are short non-coding RNAs that function in the endogenous regulation of genes. miRNAs serve important roles in cellular events such as apoptosis, cell proliferation, migration, invasion, autophagy and the cell cycle. They also control the genesis and progression of tumors. Autophagy is a self-digestive process that occurs as a response to stress, and serves two opposite roles in tumor promotion or inhibition that may result in resistance to therapy. A number of studies have revealed that miRNAs control autophagic activity by targeting autophagy-associated genes, particularly in cancer. These previous studies demonstrated that miR-96-5p is upregulated in several types of malignant tumors. However, other functions of miR-96-5p in breast cancer, particularly those that are associated with autophagy, remain unknown. miR-96-5p expression was demonstrated to be upregulated in breast cancer cells compared with in normal breast epithelial cells. The overexpression of miR-96-5p inhibited autophagy, particularly starvation-induced autophagy, in MCF-7 and MDA-MB-231 cells. In addition, this inhibitory effect may have resulted in the suppression of Forkhead box O1. Additionally, the overexpression of miR-96-5p may promote cell proliferation, migration and invasion and inhibit apoptosis in MCF-7 and MDA-MB-231 cells. These data indicate that miR-96-5p is involved in the progression of breast cancer cells and may represent a potential therapeutic target for the treatment of breast cancer.

miR-96-5p enhances cell proliferation and invasion via targeted regulation of ZDHHC5 in gastric cancer

“…Six miRNAs were identified in the present study, and the results showed that the levels of miR-96-5p, miR-222-5p, and miR-652-5p were overexpressed, while miR-125-5p, miR-145-3p, and miR-379-3p levels were down-regulated in GAC sample. Several studies have demonstrated that miR-96-5p is overexpressed in various cancers, including colorectal cancer [13], pancreatic carcinoma [14], prostate cancer [15], hepatocellular carcinoma [16], and breast cancer [17], and it is oncogene that promotes cell proliferation. It has been reported that miR-652-5p is associated with non-small cell lung cancer [18], esophageal adenocarcinoma [19], and breast cancer [20], while the mechanism of miR-652-5p was not elaborated.…”

MicroRNA Dysregulation Associated with Red Blood Cell Storage

“…As a consequence of that, miRNA-96 silencing induces an increase in γ-globin [32,33]. In addition, overexpression of miRNA-96-5p inhibits autophagy and apoptosis in human breast cancer cells [34]. Thus, although our results are referred to RBCs, this evidence could indicate that miRNA-96 decrease might be a sign of ongoing RBC autophagy and apoptosis.…”

Circular RNA HIPK3 contributes to hyperglycemia and insulin homeostasis by sponging miR-192-5p and upregulating transcription factor forkhead box O1

“…In consistent with these studies, the present study shows that miR-192-5p could target FOXO1, and its dysregulation was involved in hyperglycemia and insulin resistance. Indeed, it has been shown that the expression of FOXO1 and acetylated-FOXO1 is regulated by miR-96-5p in human breast cancer cell [13]. These studies suggest that the expression of FOXO1 is regulated by different miRNAs.…”

“…It has been documented that FOXO1 is regulated by miRNA. For example, it has been reported that miR-96-5p inhibited autophagy via downregulation of the expression of FOXO1 and acetylated-FOXO1 in human breast cancer cell [13]. However, the relationship between circHIPK3 and FOXO1/diabetes remains largely unknown.…”