Metabolic Shift of an Isogenic Strain of Enterococcus faecalis 14, Deficient in Its Own Bacteriocin Synthesis, as Revealed by a Transcriptomic Analysis
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Breast cancer is the most common cancer among women. Adiposity generally accompanies immune cell infiltration and cytokine secretion, which is ideal for tumor development. Aspirin is a chemopreventive agent against several types of cancer. The aim of this study was to investigate whether aspirin inhibits the growth of 4T1 breast cancer cells by inhibiting the inflammatory response and regulating the metabolomic profile of 3T3-L1 adipocytes. 3T3-L1 adipocyte-conditioned medium (Ad-CM) was used to mimic the obese adipose tissue microenvironment in 4T1 cells. The results revealed that aspirin inhibited macrophage chemoattractant protein (MCP-1), interleukin (IL-6), IL-1β, and plasminogen activator inhibitor (PAI-1) production in 3T3-L1 adipocytes stimulated by tumor necrosis factor-alpha (TNF-α) and lipopolysaccharide (LPS). In the obesity-associated model, Ad-CM significantly promoted 4T1 cell growth and migration, which were attenuated after aspirin treatment. The results of metabolic analyses using Ad-CM showed that amino acid metabolites and oxidative stress were increased in mature 3T3-L1 adipocytes compared to those in fibroblasts. Aspirin treatment modified metabolites involved in suppressing lipogenesis, oxidative stress, and neoplastic formation. In the relative fatty acid quantitation analysis of Ad-CM, aspirin diminished fatty acid contents of C16:1, C18:1, C18:2, C20:4, and C24:1. This study is the first to show that aspirin modifies the metabolomics and fatty acid composition of 3T3-L1 adipocytes and inhibits obesity-associated inflammation that contributes to obesity-related breast cancer cell growth and migration.
Cancer is defined as a group of neoplastic cells that grow uncontrollably and destroy the body’s healthy physiology. Breast cancer is one of the most frequent and ubiquitous cancers throughout every region of the world. In 2018, World Health Organization (WHO) statistics indicated that breast cancer affects 2.1 million women every year and encompasses approximately 15% of all cancer-related mortality amongst women [1]. Epidemiological evidence shows that 30–50% of all cancers are preventable, mainly through changes in lifestyle, environment, and diet [1]. Prevention is considered to be the most effective and economically advantageous strategy in controlling several diseases, especially cancer [1].
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Overweight and obesity have become significant impairments to public health, leading to several pathological developments. In 2016, the WHO estimated that over 650 million adults worldwide were overweight or obese, comprising approximately 39% and 13% of the global population, respectively [2]. The main characteristic of adiposity is the hyperaccumulation of fat accompanied by chronic low-grade inflammation. In the adipose tissue microenvironment, several types of immune cells demonstrate increased infiltration into adipose tissue, setting off a series of proinflammatory cytokine secretions, for example, interleukin-6 (IL-6), leptin, and tumor necrosis factor-alpha (TNF-α) [3].
Corroborating evidence exists showing that obesity is associated with cancer development and progression due to chronic inflammation, hormonal imbalances, and metabolic abnormalities [4]. Obesity is recognized as a significant risk for breast cancer development, with obese breast cancer patients shown to have overall lower survival rates and higher risk of recurrence regardless of whether therapeutic interventions are sought [5, 6]. Carcinogenesis progression involves the participation of endothelial cells, stromal fibroblasts, tumor cells, and infiltrating immune cells. The recruitment of immune cells, such as macrophages and leukocytes, generates reactive oxygen species (ROS). Along with ROS production, several cytokines contribute to neoplastic transformation, angiogenesis, invasion, and metastasis [4, 7].
Metabolomics is a field of science that studies the metabolites generated from blood, body fluids, cells, and tissues through metabolic processes [8]. The number of metabolites in humans is estimated to be in the range of 5000 to 20, 000; the majority of these metabolites are not well understood. The pattern of metabolites within subjects was shown to vary due to factors such as environment, heredity, nutrition, sex, and overall physiology. In addition to animal studies, metabolite analyses of cell lines provided better understanding regarding the metabolomics and metabolic pathways of specific cells under different conditions. The contribution of metabolite analyses to preclinical data while minimizing interfering factors has allowed metabolomics analysis of cell lines to be one of the more advanced and innovative preclinical applications for future research [9].
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Aspirin (i.e., acetylsalicylic acid) is one of many nonsteroidal anti-inflammatory drugs (NSAIDs) that is widely used for anti-inflammatory, antipyretic, and coronary heart disease protective reasons [10]. Breast cancer tumorigenesis is associated with the inflammatory pathway and overexpression of cyclooxygenase-2 (COX-2). Thus, a possible mechanism of aspirin as a chemopreventive agent in breast cancer may be the inhibition of COX-2, which blocks inflammatory reactions [11]. Recently, aspirin was shown to interfere in the communication between macrophages and 4T1 breast cancer cells, thus suppressing breast cancer cell growth [12]. Accumulated evidence from epidemiological studies, animal experiments, and cell models showed that aspirin exerts chemopreventive properties, especially in breast cancer [13, 14]. However, there are still few studies regarding aspirin treatment for breast cancer development induced by obesity.
This work aimed to investigate the mechanism of aspirin chemoprevention in obesity-related breast cancer. The effect of aspirin on the inflammatory response, metabolomic profile, and fatty acid composition in 3T3-L1 adipocytes is tested and the inhibitory effects on the growth and migration of 4T1 breast cancer cells are investigated.
In our previous study, a high dose of 5 mM aspirin demonstrated significant cellular toxicity, whereas 2 mM of aspirin did not affect cell numbers but decrease lipid drop accumulation in 3T3-L1 adipocytes [15]. Thus, dosages of 0.5, 1, and 2 mM of aspirin were used in this experiment. Proinflammatory cytokine-, adipokine-, and angiogenesis-related mediators were analyzed in supernatants of 3T3-L1 adipocytes to evaluate the chemopreventive properties of aspirin, as shown in Figure 1. 3T3-L1 cells, in which inflammation was induced by TNF-α and lipopolysaccharide (LPS) stimulation, were treated with various doses of aspirin for 24 h. Subsequently, the culture supernatants were collected and assayed. In the aspirin-treated TNF-α model of 3T3-L1 cells, significant decreases were observed in interleukin-6 (IL-6), IL-1β, macrophage chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor-1 (PAI-1), and vascular endothelial growth factor (VEGF) secretion (p < 0.05) compared to the vehicle control. Upon LPS stimulation, cells treated with aspirin revealed decreases in the levels of cytokines IL-6, MCP-1, and PAI-1 in a dose-dependent manner (p < 0.05) compared to the vehicle control. In inflammatory models of 3T3-L1 adipocytes, aspirin decreased the secretion of proinflammatory cytokines and angiogenesis mediators. However, aspirin treatment did not affect the secretion of adipokines, such as leptin and adiponectin.
Does Menopause Cause You Anxiety 4046998.jpg
Cultured media were collected for analysis by LC-MS to investigate whether adipocyte differentiation and aspirin intervention caused metabolic changes in 3T3-L1 cells. Metabolite profiling was performed using conditioned media of 3T3-L1 fibroblasts (Fb), mature adipocytes (Ad), and 3T3-L1 fibroblasts treated with 1 mM aspirin during the differentiation process (AdA) (Figure 2).
In LC-MS analysis, a total 49 metabolites were identified in the Fb, with 45 metabolites identified in the Ad and 59 metabolites identified in the AdA. A total of 28 metabolites were identified in both the Ad and AdA groups and 36 metabolites were identified in both the Ad and AdA groups. The same metabolites that were identified in the Fb, Ad, and AdA groups are shown in Supplementary Table S1. Figure 2a shows the principal component analysis (PCA) score plots of the Fb, Ad, and AdA groups. During fibroblast differentiation into adipocytes, a clear separation between Fb and Ad revealed metabolite profiles that were distinct between these two groups. As the AdA group moved closer to the Fb group, the results indicated that the aspirin treatment reversed the metabolic change in the Ad group.
One-way ANOVA was further used to identify the significant metabolites between the three groups. Twelve metabolites showed significant differences among the three groups (p < 0.05); these metabolites are listed in Figure 2b. Additionally, the least significant difference (LSD) test was used to identify metabolites with significant differences between the two groups; the fold changes and involved pathways of significant metabolites are shown in Table 1. These metabolites are associated with branched-chain amino acid (BCAA) metabolism, alanine metabolism, urea acid/arginine biosynthesis, leucine biosynthesis, phenylalanine metabolism, fatty acid metabolism, and arginine metabolism.
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Aspirin (i.e., acetylsalicylic acid) is one of many nonsteroidal anti-inflammatory drugs (NSAIDs) that is widely used for anti-inflammatory, antipyretic, and coronary heart disease protective reasons [10]. Breast cancer tumorigenesis is associated with the inflammatory pathway and overexpression of cyclooxygenase-2 (COX-2). Thus, a possible mechanism of aspirin as a chemopreventive agent in breast cancer may be the inhibition of COX-2, which blocks inflammatory reactions [11]. Recently, aspirin was shown to interfere in the communication between macrophages and 4T1 breast cancer cells, thus suppressing breast cancer cell growth [12]. Accumulated evidence from epidemiological studies, animal experiments, and cell models showed that aspirin exerts chemopreventive properties, especially in breast cancer [13, 14]. However, there are still few studies regarding aspirin treatment for breast cancer development induced by obesity.
This work aimed to investigate the mechanism of aspirin chemoprevention in obesity-related breast cancer. The effect of aspirin on the inflammatory response, metabolomic profile, and fatty acid composition in 3T3-L1 adipocytes is tested and the inhibitory effects on the growth and migration of 4T1 breast cancer cells are investigated.
In our previous study, a high dose of 5 mM aspirin demonstrated significant cellular toxicity, whereas 2 mM of aspirin did not affect cell numbers but decrease lipid drop accumulation in 3T3-L1 adipocytes [15]. Thus, dosages of 0.5, 1, and 2 mM of aspirin were used in this experiment. Proinflammatory cytokine-, adipokine-, and angiogenesis-related mediators were analyzed in supernatants of 3T3-L1 adipocytes to evaluate the chemopreventive properties of aspirin, as shown in Figure 1. 3T3-L1 cells, in which inflammation was induced by TNF-α and lipopolysaccharide (LPS) stimulation, were treated with various doses of aspirin for 24 h. Subsequently, the culture supernatants were collected and assayed. In the aspirin-treated TNF-α model of 3T3-L1 cells, significant decreases were observed in interleukin-6 (IL-6), IL-1β, macrophage chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor-1 (PAI-1), and vascular endothelial growth factor (VEGF) secretion (p < 0.05) compared to the vehicle control. Upon LPS stimulation, cells treated with aspirin revealed decreases in the levels of cytokines IL-6, MCP-1, and PAI-1 in a dose-dependent manner (p < 0.05) compared to the vehicle control. In inflammatory models of 3T3-L1 adipocytes, aspirin decreased the secretion of proinflammatory cytokines and angiogenesis mediators. However, aspirin treatment did not affect the secretion of adipokines, such as leptin and adiponectin.
Does Menopause Cause You Anxiety 4046998.jpg
Cultured media were collected for analysis by LC-MS to investigate whether adipocyte differentiation and aspirin intervention caused metabolic changes in 3T3-L1 cells. Metabolite profiling was performed using conditioned media of 3T3-L1 fibroblasts (Fb), mature adipocytes (Ad), and 3T3-L1 fibroblasts treated with 1 mM aspirin during the differentiation process (AdA) (Figure 2).
In LC-MS analysis, a total 49 metabolites were identified in the Fb, with 45 metabolites identified in the Ad and 59 metabolites identified in the AdA. A total of 28 metabolites were identified in both the Ad and AdA groups and 36 metabolites were identified in both the Ad and AdA groups. The same metabolites that were identified in the Fb, Ad, and AdA groups are shown in Supplementary Table S1. Figure 2a shows the principal component analysis (PCA) score plots of the Fb, Ad, and AdA groups. During fibroblast differentiation into adipocytes, a clear separation between Fb and Ad revealed metabolite profiles that were distinct between these two groups. As the AdA group moved closer to the Fb group, the results indicated that the aspirin treatment reversed the metabolic change in the Ad group.
One-way ANOVA was further used to identify the significant metabolites between the three groups. Twelve metabolites showed significant differences among the three groups (p < 0.05); these metabolites are listed in Figure 2b. Additionally, the least significant difference (LSD) test was used to identify metabolites with significant differences between the two groups; the fold changes and involved pathways of significant metabolites are shown in Table 1. These metabolites are associated with branched-chain amino acid (BCAA) metabolism, alanine metabolism, urea acid/arginine biosynthesis, leucine biosynthesis, phenylalanine metabolism, fatty acid metabolism, and arginine metabolism.
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