Inflammasomes can identify endogenous danger signals as an inflammatory immune response. As the most common inflammasome, the NLR pyrin family domain containing 3 (NLRP3) inflammasome is associated with the pathogenesis of different tumors. However, the function of the NLRP3 inflammasome in esophageal cancer (EC) has rarely been reported. Herein, the expression levels of the components of NLRP3 inflammasome and Ki‑67 were analyzed by immunohistochemistry. Furthermore, correlations between the NLRP3 inflammasome and Ki‑67 along with the clinicopathological features of EC patients were evaluated. The components of the NLRP3 inflammasome were also assessed by western blot analysis and quantitative PCR. NLRP3 was silenced or overexpressed in different esophageal squamous cell carcinoma (ESCC) cell lines, and cell viability, migration and invasion were assessed by CCK‑8 and Transwell assays. The present results showed that high NLRP3 expression in the tumor specimens was significantly associated with TNM stage and T category. Spearman's correlation analysis revealed a positive correlation between NLRP3 and the Ki‑67 proliferation index. The mRNA and protein levels of NLRP3, apoptosis‑associated speck‑like protein containing a CARD (ASC), cleaved caspase‑1, and interleukin (IL)‑1β in tumor tissues were higher than those in non‑cancerous tissues. The level of secreted IL‑1β in tumor tissues was also increased, as compared to that in normal tissues. Silencing of NLRP3 in KYSE‑70 and TE13 cells strongly attenuated cell viability, decreased cell mobility in wound‑healing assays and greatly diminished the ability of cell migration and invasion in the Transwell system. Overexpression of NLRP3 in KYSE‑510 and EC9706 cells markedly promoted the proliferation, migration and invasion. Collectively, these results revealed that the the NLRP3 inflammasome is upregulated in human ESCC tissues and promotes ESCC progression. Hence, NLRP3 could be a promising new candidate diagnostic and prognostic target.

Cardiovascular diseases (CVDs) are the leading cause of morbidity and mortality worldwide, especially in developing countries. To date, several approaches have been proposed for the prevention and treatment of CVDs. However, the increased risk of developing cardiovascular events that result in hospitalization has become a growing public health concern. The pathogenesis of CVDs has been analyzed from various perspectives. Recent data suggest that regulatory RNAs play a multidimensional role in the development of CVDs. Studies have identified several mRNA modifications that have contributed to the functional characterization of various cardiac diseases. RNA methylation, such as N6-methyladenosine, N1-methyladenosine, 5-methylcytosine, N7-methylguanosine, N4-acetylcytidine, and 2'-O-methylation are novel epigenetic modifications that affect the regulation of cell growth, immunity, DNA damage, calcium signaling, apoptosis, and aging in cardiomyocytes. In this review, we summarize the role of RNA methylation in the pathophysiology of CVDs and the potential of using epigenetics to treat such disorders.

Expression of cytochrome P450s (CYPs) is regulated by epigenetic factors, such as DNA methylation, histone modifications, and non-coding RNAs through different mechanisms. Among these factors, long non-coding RNAs (lncRNAs) have been shown to play important roles in the regulation of gene expression; however, little is known about the effects of lncRNAs on the regulation of CYP expression. The aim of this study was to explore the role of lncRNAs in the regulation of CYP expression by using human liver tissues and hepatoma Huh7 cells. Through lncRNA microarray analysis and quantitative polymerase chain reaction in human liver tissues, we found that the lncRNA hepatocyte nuclear factor 1 alpha antisense 1 (HNF1α-AS1), an antisense RNA of HNF1α, is positively correlated with the mRNA expression of CYP2C8, 2C9, 2C19, 2D6, 2E1, and 3A4 as well as pregnane X receptor (PXR) and constitutive androstane receptor (CAR). Gain- and loss-of-function studies in Huh7 cells transfected with siRNAs or overexpression plasmids showed that HNF1α not only regulated the expression of HNF1α-AS1 and CYPs, but also regulated the expression of CAR, PXR, and aryl hydrocarbon receptor (AhR). In turn, HNF1α-AS1 regulated the expression of PXR and most CYPs without affecting the expression of HNF1α, AhR, and CAR. Moreover, the rifampicin-induced expression of CYPs was also affected by HNF1α and HNF1α-AS1. In summary, the results of this study suggested that HNF1α-AS1 is involved in the HNF1α-mediated regulation of CYPs in the liver at both basal and drug-induced levels.

Cardiovascular diseases (CVDs) are the leading cause of hospitalization and death worldwide, especially in developing countries. The increased prevalence rate and mortality due to CVDs, despite the development of several approaches for prevention and treatment, are alarming trends in global health. Chronic inflammation and macrophage infiltration are key regulators of the initiation and progression of CVDs. Recent data suggest that epigenetic modifications, such as DNA methylation, posttranslational histone modifications, and RNA modifications, regulate cell development, DNA damage repair, apoptosis, immunity, calcium signaling, and aging in cardiomyocytes; and are involved in macrophage polarization and contribute significantly to cardiac disease development. Cardiac macrophages not only trigger damaging inflammatory responses during atherosclerotic plaque formation, myocardial injury, and heart failure but are also involved in tissue repair, remodeling, and regeneration. In this review, we summarize the key epigenetic modifications that influence macrophage polarization and contribute to the pathophysiology of CVDs, and highlight their potential for the development of advanced epigenetic therapies.