• BMB Reports
• /
• v.54 no.7
• /
• pp.344-355
• /
• 2021

Mucins are high molecular-weight epithelial glycoproteins and are implicated in many physiological processes, including epithelial cell protection, signaling transduction, and tissue homeostasis. Abnormality of mucus expression and structure contributes to biological properties related to human cancer progression. Tumor growth sites induce inhospitable conditions. Many kinds of research suggest that mucins provide a microenvironment to avoid hypoxia, acidic, and other biological conditions that promote cancer progression. Given that the mucus layer captures growth factors or cytokines, we propose that mucin helps to ameliorate inhospitable conditions in tumor-growing sites. Additionally, the composition and structure of mucins enable them to mimic the surface of normal epithelial cells, allowing tumor cells to escape from immune surveillance. Indeed, human cancers such as mucinous carcinoma, show a higher incidence of invasion to adjacent organs and lymph node metastasis than do non-mucinous carcinoma. In this mini-review, we discuss how mucin provides a tumor-friendly environment and contributes to increased cancer malignancy in mucinous carcinoma.

• Korean Circulation Journal
• /
• v.48 no.11
• /
• pp.951-963
• /
• 2018

HMG-CoA reductase inhibitors, i.e. statins, are effective in reducing cardiovascular disease events but also in cardiac-related and overall mortality. Statins are in general well-tolerated, but currently the concerns are raised if statins may increase the risk of new-onset diabetes mellitus (NOD). In this review, the possible effects of statins on organs/tissues being involved in glucose metabolism, i.e. liver, pancreas, adipose tissue, and muscles, had been discussed. The net outcome seems to be inconsistent and often contradictory, which may be largely affected by in vitro experimental settings or/and in vivo animal conditions. The majority of studies point out statin-induced changes of regulations of isoprenoid metabolites and cellassociated cholesterol contents as predisposing factors related to the statin-induced NOD. On the other hand, it should be considered that dysfunctions of isoprenoid pathway and mitochondrial ATP production and the cholesterol homeostasis are already developed under (pre)diabetic and hypercholesterolemic conditions. In order to connect the basic findings with the clinical manifestation more clearly, further research efforts are needed.

• Journal of Yeungnam Medical Science
• /
• v.38 no.2
• /
• pp.107-117
• /
• 2021

MicroRNAs (miRNAs) are a class of noncoding RNAs that negatively regulate target messenger RNAs. In multicellular eukaryotes, numerous miRNAs perform basic cellular functions, including cell proliferation, differentiation, and death. Abnormal expression of miRNAs weakens or modifies various apoptosis pathways, leading to the development of human cancer. Cell death occurs in an active manner that maintains tissue homeostasis and eliminates potentially harmful cells through regulated cell death processes, including apoptosis, autophagic cell death, and necroptosis. In this review, we discuss the involvement of miRNAs in regulating cell death pathways in cancers and the potential therapeutic functions of miRNAs in cancer treatment.

• Proceedings of the PSK Conference
• /
• 2002.10a
• /
• pp.378.1-378.1
• /
• 2002

Prostaglandins (PGs) and nitric oxide (NO) are essential to maintain homeostasis and defensa systems in human beings. However. overproduced PGs and NO by inducible cyclooxygenase (COX-2) and inducible nitric oxide synthase (iNOS), respectively. cause tissue damages. chronic inflammation. and carcinogenesis. In this view. the potential COX-2 or iNOS inhibitors have been considered as anti-inflammatory or cancer chemopreventive agents. (omitted)

• BMB Reports
• /
• v.56 no.1
• /
• pp.2-9
• /
• 2023

Hair follicles in the skin undergo cyclic rounds of regeneration, degeneration, and rest throughout life. Stem cells residing in hair follicles play a pivotal role in maintaining tissue homeostasis and hair growth cycles. Research on hair follicle aging and age-related hair loss has demonstrated that a decline in hair follicle stem cell (HFSC) activity with aging can decrease the regeneration capacity of hair follicles. This review summarizes our understanding of how age-associated HFSC intrinsic and extrinsic mechanisms can induce HFSC aging and hair loss. In addition, we discuss approaches developed to attenuate ageassociated changes in HFSCs and their niches, thereby promoting hair regrowth.

• IMMUNE NETWORK
• /
• v.20 no.3
• /
• pp.24.1-24.14
• /
• 2020

Eosinophils are terminally differentiated cytotoxic effector cells that have a role in parasitic infections and allergy by releasing their granule-derived cytotoxic proteins. However, an increasing number of recent observations indicate that eosinophils are not only associated with the pathogenesis of a wide range of diseases, but also contribute to the maintenance of homeostatic responses in previously underappreciated diverse tissues, such as the gastrointestinal (GI) tract and adipose tissue. In this review, we describe biological characteristics of eosinophils, as their developmental properties, permissive proliferation and survival, degranulation activity, and migration properties enable them to distribute to both homeostatic and inflamed tissues. We describe pathologic aspects of eosinophils with a role in asthma and in various GI diseases, including eosinophilic GI disorders, inflammatory bowel disease, and radiation-induced enteropathy. Finally, we discuss the beneficial role of eosinophils, which contribute to the resolution of pathogenic conditions and to the modulation of homeostatic biologic responses.

• IMMUNE NETWORK
• /
• v.20 no.1
• /
• pp.4.1-4.17
• /
• 2020

Tregs have a role in immunological tolerance and immune homeostasis by suppressing immune reactions, and its therapeutic potential is critical in autoimmune diseases and cancers. There have been multiple studies conducted on Tregs because of their roles in immune suppression and therapeutic potential. In tumor immunity, Tregs can promote the development and progression of tumors by preventing effective anti-tumor immune responses in tumor-bearing hosts. High infiltration of Tregs into tumor tissue results in poor survival in various types of cancer patients. Identifying factors specifically expressed in Tregs that affect the maintenance of stability and function of Tregs is important for understanding cancer pathogenesis and identifying therapeutic targets. Thus, manipulation of Tregs is a promising anticancer strategy, but finding markers for Treg-specific depletion and controlling these cells require fine-tuning and further research. Here, we discuss the role of Tregs in cancer and the development of Treg-targeted therapies to promote cancer immunotherapy.

• IMMUNE NETWORK
• /
• v.20 no.3
• /
• pp.22.1-22.21
• /
• 2020

In the progression of atherosclerosis, macrophages are the key immune cells for foam cell formation. During hyperlipidemic condition, phagocytic cells such as monocytes and macrophages uptake oxidized low-density lipoproteins (oxLDLs) accumulated in subintimal space, and lipid droplets are accumulated in their cytosols. In this review, we discussed the characteristics and phenotypic changes of macrophages in atherosclerosis and the effect of cytosolic lipid accumulation on macrophage phenotype. Due to macrophage plasticity, the inflammatory phenotypes triggered by oxLDL can be re-programmed by cytosolic lipid accumulation, showing downregulation of NF-κB activation followed by activation of anti-inflammatory genes, leading to tissue repair and homeostasis. We also discuss about various in vivo and in vitro models for atherosclerosis research and next generation sequencing technologies for foam cell gene expression profiling. Analysis of the phenotypic changes of macrophages during the progression of atherosclerosis with adequate approach may lead to exact understandings of the cellular mechanisms and hint therapeutic targets for the treatment of atherosclerosis.

• Endocrinology and Metabolism
• /
• v.37 no.1
• /
• pp.9-25
• /
• 2022

Evidence for involvement of the central nervous system (CNS) in the regulation of glucose metabolism dates back to the 19th century, although the majority of the research on glucose metabolism has focused on the peripheral metabolic organs. Due to recent advances in neuroscience, it has now become clear that the CNS is indeed vital for maintaining glucose homeostasis. To achieve normoglycemia, specific populations of neurons and glia in the hypothalamus sense changes in the blood concentrations of glucose and of glucoregulatory hormones such as insulin, leptin, glucagon-like peptide 1, and glucagon. This information is integrated and transmitted to other areas of the brain where it eventually modulates various processes in glucose metabolism (i.e., hepatic glucose production, glucose uptake in the brown adipose tissue and skeletal muscle, pancreatic insulin and glucagon secretion, renal glucose reabsorption, etc.). Errors in these processes lead to hyper- or hypoglycemia. We here review the current understanding of the brain regulation of glucose metabolism.

• Korean Journal of Psychosomatic Medicine
• /
• v.7 no.2
• /
• pp.149-157
• /
• 1999

Food intake and body weight are determined by a complex interaction of regulatory pathways. Leptin, the product of the ob gene, is a recently discovered hormone secreted by adipocytes, that signals the amount of adipose tissue energy stores to the brain and exerts major effects on energy homeostasis and neuroendocrine function. In addition, leptin has recently been shown to affect reproductive function in rodents and humans. The study of leptin and its effectors in the hypothalamus may provide important insights with respect to the interplay of several hypothalamic neuropeptides in regulating feeding as well as the interaction of genetics and environment in the regulation of energy homeostasis. In this review we summarise the action of leptin in the regulation of food intake and highlight a working model of the effects of environmental factors on the leptin system.