Explore chapters and articles related to this topic
Mitigation of Obesity: A Phytotherapeutic Approach
Published in Amit Baran Sharangi, K. V. Peter, Medicinal Plants, 2023
A.B. Sharangi, Suddhasuchi Das
Adipocytes release fatty acid, which are used as fuel by organs in times of limited glucose. These fatty acids are the outcomes from triacylglycerol breakdown, which contain more energy per unit mass compared to carbohydrates. Lipid homeostasis and energy balance is centrally regulated by adipocytes. According to changing energy demands they release free fatty acids from stored triglycerides. The hyperplasia and hypertrophy of adipocytes both are involved with adipocyte tissue growth, which led to the development of natural products which helps in anti-obesity therapy that exclusively target adipogenesis inhibition. Some research has also proposed that through blockade of several transcription factors like C/EBP_ (CCAAT/enhancer-binding protein beta) and PPAR (peroxisome proliferator-activated receptor-gamma) adipocyte differentiation could be inhibited (Kang et al., 2013).
Anaplastic Large Cell Lymphoma
Published in Wojciech Gorczyca, Atlas of Differential Diagnosis in Neoplastic Hematopathology, 2014
The prognosis of ALK+ ALCL is favorable, except for cases with blood involvement, which are aggressive. ALCL without ALK expression occurs in older patients with similar distribution in male and female patients is associated with poor prognosis and lower incidence of stage III and IV disease and extranodal involvement. Supervised analysis with microarray gene expression profiling showed that ALK+ ALCL and ALK− ALCL have different gene expression profiles, further confirming that they are different entities [6]. Among the most significantly differentially expressed genes between ALK+ and ALK− samples, Lamant et al. [6] found BCL6, PTPN12, CEBPB, and SERPINA1 genes to be overexpressed in ALK+ ALCL. It is therefore suggested that ALK− lymphomas with anaplastic features may represent a variant of CD30+ peripheral T-cell lymphoma (PTCL).
The S100A7/8/9 Proteins: Novel Biomarker and Therapeutic Targets for Solid Tumor Stroma
Published in Surinder K. Batra, Moorthy P. Ponnusamy, Gene Regulation and Therapeutics for Cancer, 2021
Sanjay Mishra, Dinesh Ahirwar, Mohd W. Nasser, Ramesh K. Ganju
To analyze the potential of S100A8/A9 as prognostic biomarkers in PCa, the researchers have analyzed S100A8/A9 levels in benign prostate hyperplasia (BPH) and PCa patient samples. It was found that both S100A8 and S100A9 were highly expressed in patients with aggressive disease and shorter recurrence-free time. S100A8/A9 levels correlated positively with expression levels obtained from tissue staining [71]. Using a doxycycline regulated S100A8/A9 overexpression system, it was observed that increased expression of S100A8/A9 in prostate cancer (PCa) cells enhances their ability to grow as tumors in mice and invade surrounding tissue by recruiting immune cells, especially neutrophils [72]. In addition, intra-cardiac injection of S100A8/A9 overexpressing prostate cancer cells resulted in higher colonization of tumor cells into the lungs compared to control cells [72]. Oncogenic molecule, such as Prostaglandin E2 (PGE2), has been shown to induce the expression of S100A8 and S100A9 in prostate cancer cells [73]. PGE2 is a member of prostaglandin lipids, which are lipid mediators and are known to be involved in diverse physiological and pathological processes, including pain, inflammation, renal functions and cancer progression [74]. Transcription factor binding sequence analysis revealed that PGE2 induced overexpression of S100A8 by enhancing the binding of CCAAT/enhancer-binding-protein-beta transcription factor to S100A8 promotor [73]. In addition to lipid mediators, hypoxia also induces expression of S100A8/A9 in prostate cancer cells [75]. Furthermore, overexpression of hypoxia-inducing factor-1α (HIF-1α) increased mRNA expression as well as secretion [75]. Chromatin immunoprecipitation experiments confirmed the binding of HIF-1α to S100A8 and S100A9 promotors. A direct correlation of S100A8/A9 expression with HIF-1 expression was also observed in prostate cancer patient samples [75]. These studies suggest that various tumor inducing factors activate different transcription factors to enhance the expression of S100A8/A9 which results in enhanced tumor cell proliferation, recruitment of immune-suppressive cells, and increased production of cytokine/chemokine which all together support tumor progression.
The role of myeloid-derived suppressor cells in the pathogenesis of rheumatoid arthritis; anti- or pro-inflammatory cells?
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Misagh Rajabinejad, Farhad Salari, Ali Gorgin Karaji, Alireza Rezaiemanesh
The factors that induce proliferation of MDSCs include: macrophage colony-stimulating factor (M-CSF), stem-cell factor (SCF), vascular endothelial growth factor (VEGF), granulocyte colony-stimulating factor (G-CSF), granulocyte/macrophage CSF (GM-CSF), IL-1β, IL-6, IL-17, TNF-α, high mobility group box protein 1 (HMGB1), oestrogens, and polyunsaturated fatty acids [24–27]. Moreover, the transcriptional factors/regulators, such as signal transducer activator of transcription (STAT) 3, interferon regulatory factor (IRF) 8, STAT5, NOTCH, and CCAAT/enhancer-binding protein beta isoform b (C/EBP-β) have a critical role in this process [28]. Other factors involved in this process include adenosine receptor A2b, retinoblastoma protein 1 (RB1), cytoplasmic receptor NLRP3, and calprotectin (S100A9, S100A8) [27,29].
Combined effect of retinoic acid and calcium on the in vitro differentiation of human adipose-derived stem cells to adipocytes
Published in Archives of Physiology and Biochemistry, 2018
Farjam Goudarzi, Arash Sarveazad, Maryam Mahmoudi, Adel Mohammadalipour, Reza Chahardoli, Obeid M. Malekshah, Shiva Karimi Gorgani, Ali Akbar Saboor-Yaraghi
Among them, various transcriptional factors such as CCAAT-enhancer-binding protein alpha (C/EBPA) and CCAAT-enhancer-binding protein beta (C/EBPB) are important to regulate all pro-adipogenic cell signaling pathways and differentiation of the preadipocytes into the mature cells (Morrison and Farmer 2000, Guo et al. 2015). Their regulatory function is accomplished with the participation of genes such as peroxisome proliferator-activated receptor gamma (PPARG), a master regulator of adipogenesis (Tzameli et al. 2004).