The pro-survival transcription factor myocyte enhancer factor 2D (MEF2D) is identified to exhibit pro-tumor effects based on clinical and experimental studies. However, the detailed mechanisms underlying IGF-1-MEF2D pathway-induced tumor biology in cardiac myxoma (CM) was not clear. Here, we investigated the role of MEF2D in CM tissues and cells using RT-PCR, western blot, gene silencing, et al. Our findings revealed MEF2D was significantly increased in CM tissues compared with adjacent normal tissues and closely related to tumor size. In vitro assay demonstrated that IGF-1 enhanced CM cell proliferation in a time-dependent fashion. However, knockdown of MEF2D reversed the IGF-1-induced proliferative effects on CM cells in a time-dependent fashion and further resulted in cell cycle arrest. Based on the molecular level, IGF-1 enhanced the expression of epidermal growth factor receptor (EGFR) and matrix metalloprotein 9 (MMP9) in CM cells, whereas knockdown of MEF2D was able to reduce the expression of EGFR and MMP9 compared with vector control. Furthermore, we found knockdown of MEF2D directly affected G1/S transition in cultured CM cells. In conclusion, MEF2D regulates IGF-1-induced proliferation and apoptosis in CM development, indicating IGF-1-MEF2D pathway may be a useful target for treatment.
Keywords: Biology; CM; IGF-1; MEF2D.