miR-29a regulated ER-positive breast cancer cell growth and invasion and is involved in the insulin signaling pathway

Abstract

Increasing amounts of evidence show that insulin can activate different insulin signaling pathways to promote breast cancer growth and invasion. miR-29a plays crucial roles in decreasing glucose-stimulated insulin secretion, as well as in regulating breast cancer cell proliferation and EMT. However, the mechanism responsible for the regulatory effects of miR-29a on breast cancer growth and invasion and the relationship between these effects and insulin signaling remains unclear. Herein, we showed that human insulin increased miR-29a expression in ER-positive breast cancer cells and that miR-29a facilitated the ability of insulin to promote breast cancer cell proliferation and migration. We found that miR-29a-induced cell proliferation and metastasis acceleration occurred primarily through ERK phosphorylation. The IGF-1R is the upstream target gene of miR-29a, while CDC42 and p85α are the downstream target genes of miR-29a. These results have provided us with information regarding the molecular mechanisms by which hyperinsulinemia promotes breast cancer occurrence and development and thus leads to a poor prognosis in breast cancer patients and indicate that miR-29a plays an important role in breast cancer development and invasion.

MicroRNA‑320a suppresses tumor cell growth and invasion of human breast cancer by targeting insulin‑like growth factor�1 receptor

“…IGF-1R is markedly and excessively expressed in breast cancer cells compared with normal breast epithelium and benign tumor tissues. Moreover, research has indicated that the IGF-1R expression level is related to the recurrence, metastasis and prognosis of breast cancer (15). The present study also revealed that overexpression of microRNA-320a suppressed IGF-1R, p-Akt and cyclin D1 protein expression, and induced Bax protein expression in MDA-MB-231 cells.…”

Anticancer effect of HOTTIP regulates human pancreatic cancer via the metabotropic glutamate receptor 1 pathway

“…Caspase promotes apoptosis, reconstructing the cytoskeleton, terminating DNA repair, destroying DNA and nuclear structure and reducing formation of the apoptotic body (23). Certain studies in biological chemistry and genetics have indicated that the caspase protease family has important functions at every stage of apoptosis (23,24). The results of the present study demonstrated that the downregulated expression of HOTTIP reduced cell viability, induced apoptosis, promoted caspase-3 and caspase-8 activity, and increased Bax expression in pancreatic cancer cells.…”

Alternative Polyadenylation Regulates Patient-specific Tumor Growth by Individualizing the MicroRNA Target Site Landscape

“…MRE stands for microRNA recognition element. E. IPA comparison analysis between gene targets by highly and lowly modified miRNAs for pathways implied for cancer progression and migration, NFAT [59], Axonal Guidance [60], MYC Mediated Apoptosis [61], Protein kinase A [44], Pigment epithelium-derived factor (PEDF) [62], Thrombin [63], CXCR4 [43], Erythropoietin [64], Insulin receptor [65], FAK [66], STAT3 [67].…”