Emerging evidences suggest that miRNAs can be used as theranostic biomarkers for multiple cancers, including glioma. Thus, identification of novel miRNAs for glioma treatment and prognosis becomes necessary and urgent. Here, by analyzing miRNA expression profiles in the glioma and para-cancer tissues by miRNA microarray and verified by RT-PCR, we found that miR-133a was significantly downregulated in the cancerous tissues, and patients with low-expressed miR-133a levels predicted an unfavorable prognosis. The following functional experiments confirmed that overexpression of miR-133a restrained cell proliferation and colony formation abilities, and induced cell cycle arrest to restrain cancer progression in glioma cells. Then, the underlying mechanisms were uncovered, and the peroxisome proliferator-activated receptor γ (PPARγ, PPARG) was verified as the downstream target of miR-133a. Mechanistically, miR-133a negatively regulated PPARG expressions by binding to its 3' untranslated regions (3'UTR). The following rescuing experiments evidenced that miR-133a overexpression-induced anti-cancer effects in glioma cells were abrogated by upregulating PPARγ. Interestingly, we noticed that the promoter region of miR-133a was hypermethylated, and removal of DNA methylation by 5-Azacytidine (AZA) significantly increased the expression levels of miR-133a in glioma cells. Taken together, we concluded that DNA-methylation-induced miR-133a silence contributed to cancer progression in glioma through upregulating PPARγ, and firstly identified the DNA-methylation-regulated miR-133a/PPARG axis as the novel indicators for glioma treatment and prognosis.
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http://dx.doi.org/10.1016/j.slasd.2022.08.004 | DOI Listing |
Theranostics
January 2025
Institute for Innovation in Imaging, Department of Radiology, Massachusetts General Hospital, Charlestown, Massachusetts, 02129, MA.
The mannose receptor (CD206, expressed by the gene ) is a surface marker overexpressed by anti-inflammatory and pro-tumoral macrophages. As such, CD206 macrophages play key roles in the immune response to different pathophysiological conditions and represent a promising diagnostic and therapeutic target. However, methods to specifically target these cells remain challenging.
View Article and Find Full Text PDFClin Transl Oncol
January 2025
UPMC Hillman Cancer Center, University of Pittsburgh, Pittsburgh, PA, USA.
Background: Small extracellular vesicles (sEV) released by tumor cells (tumor-derived sEV; TEX) mediate intercellular communication between tumor and non-malignant cells and were shown to impact disease progression. This study investigates the relationship between the expression levels of the vesiculation-related genes linked to sEV production and the tumor microenvironment (TME).
Methods: Two independent gene sets were analyzed, both previously linked to sEV production in various non-malignant or malignant cells.
Sci Rep
January 2025
Research Division, JIMRO Co., Ltd., Takasaki, Japan.
This study investigated whether intravenous administration of tumor cells killed by photodynamic therapy (PDT) with 5-aminolevulinic acid (5-ALA) had antitumor effects on distal tumors. Furthermore, a novel extracorporeal blood circulating 5-ALA/PDT system was developed. 5-ALA/PDT- (low or high irradiation) or anticancer drug-treated cells were intravenously administered to rats in a glioma cancer model.
View Article and Find Full Text PDFNat Med
January 2025
Seattle Children's Therapeutics, Seattle, WA, USA.
Diffuse intrinsic pontine glioma (DIPG) is a fatal central nervous system (CNS) tumor that confers a median survival of 11 months. As B7-H3 is expressed on pediatric CNS tumors, we conducted BrainChild-03, a single-center, dose-escalation phase 1 clinical trial of repetitive intracerebroventricular (ICV) dosing of B7-H3-targeting chimeric antigen receptor T cells (B7-H3 CAR T cells) for children with recurrent or refractory CNS tumors and DIPG. Here we report results from Arm C, restricted to patients with DIPG.
View Article and Find Full Text PDFNat Commun
January 2025
The Intellectual and Developmental Disabilities Research Center, The Semel Institute for Neuroscience and Human Behavior, and The Broad Stem Cell Research Center, The Jonsson Comprehensive Cancer Center, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Extensive neovascularization is a hallmark of glioblastoma (GBM). In addition to supplying oxygen and nutrients, vascular endothelial cells provide trophic support to GBM cells via paracrine signaling. Here we report that Endocan (ESM1), an endothelial-secreted proteoglycan, confers enhanced proliferative, migratory, and angiogenic properties to GBM cells and regulates their spatial identity.
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