Synthetic miR-145 mimic inhibits multiple myeloma cell growth in vitro and in vivo

Abstract

Multiple myeloma (MM) is a disease with an adverse outcome and new therapeutic strategies are required to combat this disease. It is well known that tumor‑suppressor microRNA (miRNA) acts as a new potential anticancer agent. Accumulating evidence showed that microRNA-145 (miR-145) is a candidate tumor suppressor miRNA. However, whether miR-145 is involved in the development and progression of MM reamins to be determined. In the present study, we investigated the therapeutic potential of synthetic miR-145 against human MM cells in vitro and in vivo. The results showed that miR-145 was reduced in MM tissues and cell lines. Enforced expression of miR-145 by transfection with miR-145 mimics inhibited cell proliferation, migration, and the invasion abilities of H929 cells. Furthermore, our results demonstrated that the enforced expression of miR-145 in H929 cells profoundly decreased the levels of p-AKT and p-PI3K, which may contribute to some extent to the inhibition of MM cell proliferation and survival. The enforced expression of miR-145 in a xenograft mouse model suppressed tumor growth. In conclusion, our findings suggested that miR-145 may act as a tumor suppressor and contributes to the progression of MM. Additionally, miR-145 mimics is a potential therapeutic agent for the treatment of MM.

MicroRNA-145 inhibits the activation of the mTOR signaling pathway to suppress the proliferation and invasion of invasive pituitary adenoma cells by targeting AKT3 in vivo and in vitro

“…PI3K, a heterodimer, includes both catalytic subunit (p110) and regulatory subunit (p85) 32. The AKT/PI3K pathway is stated to be oncogenic, which influences cell proliferation and cell apoptosis in cancers, and has been found to be downregulated by overexpressed miR-145 to inhibit cell growth and promote cell apoptosis in tumor development 33. This study found that with increased miR-145 in IPA, there were decreased mRNA and protein expressions of PI3K and AKT3, where IPA cell proliferation, migration and invasion were inhibited while cell apoptosis was promoted.…”

MicroRNA‑145 inhibits migration and induces apoptosis in human non‑small cell lung cancer cells through regulation of the EGFR/PI3K/AKT signaling pathway

“…The results of the present study demonstrated that the EGFR inhibitor suppressed the EGFR/PI3K/AKT signaling pathway and increased the anticancer effects of miR-145 upregulation in A549 cells. Zhang et al (26) reported that synthetic miR-145 expression inhibits multiple myeloma cell growth through the PI3K/AKT signaling pathway. The present study only investigated the effect of the EGFR inhibitor on miR-145 upregulation in A549 cells, therefore future studies should also explore the effect of miR-145 inhibitors combined with EGFR inhibitors in A549 cells.…”

MicroRNA-145-3p suppresses proliferation and promotes apotosis and autophagy of osteosarcoma cell by targeting HDAC4

“…It has been shown that miR-145-5p can regulate apoptosis of osteosarcoma cells and play a therapeutic role, suggesting that miR-145 is a potential therapeutic target to interfere with the invasion, proliferation, apoptosis and other biological processes of the disease [9,10]. MiR-145-3p expression levels and the possibility of being a diagnosis and prognosis marker are not particularly clear in osteosarcoma [11]. The regulation of apoptosis and autophagy has yet to be defined.…”