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      • Effects of electromagnetic fields on cell signaling and vitality

        Jayson M. Antonio 한국물학회 2021 한국물학회지 Vol.9 No.1

        Magnetotherapy is a treatment that uses magnetic and electrical forces to improve the physiological and functional state of the body. One of its modalities is pulsed electromagnetic field (PEMF) therapy, which has demonstrated promising results in restoring cellular homeostatic functions. Although the precise mechanisms of PEMF are unknown, numerous studies have demonstrated that it increases cell differentiation, viability, and proliferation, as well as activation of various cellular signaling, all of which are essential for cell vitality. It is imperative to recognize that the duration and intensity of PEMF are by far the most important variables of its therapeutic action. PEMF can induce differentiation in a variety of stem cell types when administered at the appropriate dose. Likewise, PEMF therapy boosts cellular resistance to oxidative damage by upregulating antioxidant machinery in immune, muscular, and intestinal cells. In preclinical and clinical investigations, PEMF has also been proven to suppress tumor formation and metastasis, improve wound healing, and stimulate bone formation. This presentation will examine the how PEMF affects cellular signaling of stem cells, immunocytes, and cancer, as well as its potential application in the development of better treatment strategies for aging, inflammation, and metabolic syndromes.

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        Peroxisome proliferator-activated receptor gamma as a theragnostic target for mesenchymal-type glioblastoma patients

        Tuyen N. M. Hua,오지웅,김소현,Jayson M. Antonio,Vu T. A. Vo,Jiyeon Om,최종환,Jeong-Yub Kim,Chan-Woong Jung,Myung-Jin Park,정양식 생화학분자생물학회 2020 Experimental and molecular medicine Vol.52 No.-

        Glioblastomas (GBMs) are characterized by four subtypes, proneural (PN), neural, classical, and mesenchymal (MES) GBMs, and they all have distinct activated signaling pathways. Among the subtypes, PN and MES GBMs show mutually exclusive genetic signatures, and the MES phenotype is, in general, believed to be associated with more aggressive features of GBM: tumor recurrence and drug resistance. Therefore, targeting MES GBMs would improve the overall prognosis of patients with fatal tumors. In this study, we propose peroxisome proliferator-activated receptor gamma (PPARγ) as a potential diagnostic and prognostic biomarker as well as therapeutic target for MES GBM; we used multiple approaches to assess PPARγ, including biostatistics analysis and assessment of preclinical studies. First, we found that PPARγ was exclusively expressed in MES glioblastoma stem cells (GSCs), and ligand activation of endogenous PPARγ suppressed cell growth and stemness in MES GSCs. Further in vivo studies involving orthotopic and heterotopic xenograft mouse models confirmed the therapeutic efficacy of targeting PPARγ; compared to control mice, those that received ligand treatment exhibited longer survival as well as decreased tumor burden. Mechanistically, PPARγ activation suppressed proneural–mesenchymal transition (PMT) by inhibiting the STAT3 signaling pathway. Biostatistical analysis using The Cancer Genomics Atlas (TCGA, n=206) and REMBRANDT (n=329) revealed that PPARγ upregulation is linked to poor overall survival and disease-free survival of GBM patients. Analysis was performed on prospective (n=2) and retrospective (n=6) GBM patient tissues, and we finally confirmed that PPARγ expression was distinctly upregulated in MES GBM. Collectively, this study provides insight into PPARγ as a potential therapeutic target for patients with MES GBM.

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