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Silencing of tumor suppressor genes by hypermethylation in gene promoter regions is a crucial mechanism in carcinogenesis. Gene methylation may be reversible and evaluated easily, thus providing a promising substrate for the development of biomarkers for the detection and prevention of cancer, including colorectal cancer (CRC). In the present study, the protein expression and methylation status of smooth muscle protein 22α (SM22α) was investigated in 78 cases of CRC and adjacent normal tissue. The aim of the study was to investigate the function of SM22α in the pathogenesis of CRC and to identify a candidate biomarker for the early detection of CRC. The methylation status of promoter of SM22α gene was detected using methylation-specific polymerase chain reaction. The protein expression of SM22α was evaluated using western blot analysis. The results demonstrated a significant decrease of SM22α protein expression in 50 (68.5%) cases of CRC compared with that in adjacent normal tissues (P<0.001). The methylation status of SM22α promoter in CRC was significantly increased compared with that in adjacent normal tissues (P<0.001). Additionally, there was a negative correlation between the expression of SM22α protein and methylation levels of SM22α gene in CRC (P<0.001). Kaplan-Meier curves revealed that patients with CRC with an unmethylated promoter of SM22α gene exhibited an increased survival time (34.8±0.6 vs. 30.9±1.3 months; P=0.025) compared with that in patients with a methylated promoter of SM22α gene. The present study demonstrated that the protein expression of SM22α is downregulated in CRC tissues by hypermethylation of its promoter, and that the methylation of SM22 α promoter may be used as a biomarker for early detection, prognosis and prediction of CRC. [ABSTRACT FROM AUTHOR]

Early growth response 2 (Egr2) is a zinc-finger transcription factor that acts as an important modulator of a variety of physiological processes, such as cell differentiation, proliferation and apoptosis. Here we showed that Egr2 was downregulated by bone morphogenetic protein (BMP) signaling pathways during the commitment of C3H10T1/2 stem cells to adipocyte lineage. Overexpression of Egr2 completely prevented BMP4-induced adipocyte lineage commitment of C3H10T1/2 stem cells, while simultaneously stimulating early smooth muscle-like differentiation. We also demonstrated that Egr2-induced early smooth muscle-like differentiation is transforming growth factor β1-independent. Egr2 can activate the transcription of early smooth muscle cell specific genes smooth muscle protein 22α and calponin 1. Together, the results indicated a novel role for Egr2 in repressing adipocyte lineage commitment and promoting early smooth muscle-like cell differentiation., (Copyright © 2013 Elsevier Ltd. All rights reserved.)