Published online May 6, 2016. doi: 10.5315/wjh.v5.i2.51
Peer-review started: August 13, 2015
First decision: November 6, 2015
Revised: November 19, 2015
Accepted: January 21, 2016
Article in press: January 22, 2016
Published online: May 6, 2016
Multiple myeloma (MM) is a malignant disease caused by clonal proliferation of plasma cells that result in monoclonal gammopathy and severe end organ damage. Despite the uniform clinical signs, the disease is very diverse in terms of the nature and sequence of the underlying molecular events. Multiple cellular processes are involved in helping the malignant cells to remain viable and maintain proliferative properties in the hypoxic microenvironment of the bone marrow. Specifically, the process of angiogenesis, triggered by the interactions between the malignant MM cells and the stroma cells around them, was found to be critical for MM progression. In this review we highlight the current understanding about the epigenetic regulation of the proliferation and apoptosis of MM cells and its dependency on angiogenesis in the bone marrow that is carried out by different microRNAs.
Core tip: The pathogenesis of multiple myeloma (MM) requires that malignant cells remain viable and proliferate. Therefore, genes relating to the regulation of apoptosis, proliferation and angiogenesis are tightly regulated. Specifically, angiogenesis, which is driven by the interactions between the malignant cells and stroma cell surrounding them, is critical for MM progression. In this review we summarize the current knowledge about the regulation of the expression of genes related to apoptosis, proliferation and angiogenesis, through the activity of specific microRNAs.