Increasing evidence indicates that circular RNAs (circRNAs) play a crucial role in regulating microRNAs (miRs) and mRNAs during breast cancer (BC) progression. Based on the in silico analysis of circRNA/miR/mRNA in BC, we aim to define an important role of circRNA_000554 in BC in relation to miR-182 and zinc finger protein 36 (ZFP36). Low expression of circRNA_000554 and ZFP36, and high miR-182 expression were determined in the clinical BC tissues. CircRNA_000554 acted as a sponge of miR-182, and miR-182 directly targeted ZFP36. After that, in order to evaluate the effects of circRNA_000554, miR-182, and ZFP36 on cellular process, we evaluated in vitro epithelial-mesenchymal transition (EMT) and in vivo tumor growth after delivering a series of overexpression plasmids, mimic, inhibitor, or shRNAs into BC cells. Increasing circRNA_000554 suppressed EMT, cell invasion and migration during BC by depleting miR-182 and increasing ZFP36. The inhibitory effect of circRNA_000554 on tumor growth was validated in vivo. Taken together, the present study confirms that circRNA_000554 functioned as an inhibitor of EMT in BC and suggests a molecular mechanism that circRNA_000554 bound to miR-182 to upregulate ZFP36 in this process.
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http://dx.doi.org/10.1096/fj.201903047R | DOI Listing |
Clin 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.
Am J Reprod Immunol
January 2025
Department of Obstetrics and Gynecology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu, China.
Problem: Endometriosis (EM) is known as a common estrogen-dependent chronic inflammatory disease. Elevated levels of Forkhead box L2 (FOXL2) have been observed in uterine diseases, including EM. However, the molecular mechanism of FOXL2 in EM needs to be further illustrated.
View Article and Find Full Text PDFHead Neck Pathol
January 2025
Department of Oral Pathology, School of Dentistry, University of São Paulo, São Paulo, Brazil.
Purpose: Oral squamous cell carcinoma (OSCC) is a significant public health challenge associated with high mortality rates primarily due to its invasive and metastatic behavior. This study aimed to evaluate the expression patterns of five critical biomarkers: β-catenin, E-cadherin, podoplanin (PDPN), CXCR4, and p53 in OSCC tissues and to investigate their correlations with clinicopathologic features and patient outcomes.
Methods: We conducted an immunohistochemical analysis utilizing tissue microarrays (TMAs) from 95 patients diagnosed with primary OSCC.
FASEB J
January 2025
Department of Medicine, Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island, USA.
Bromodomain-containing protein 4 (BRD4) plays a vital role in fibrosis of various organs. However, the underlying mechanism of BRD4 in renal fibrosis remains unclear. To construct in vitro and in vivo models of renal fibrosis, TCMK-1 cells were subjected to TGF-β1 treatment and mice were subjected to UUO surgery and adenine induction.
View Article and Find Full Text PDFPLoS One
December 2024
Department of Biology, College of Chemistry & Life Science, Beijing University of Technology, Chaoyang, Beijing, China.
Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer, characterized by a high incidence in late stages, high mortality rate, and poor prognosis. Src Homology 2 Domain Containing Protein 5 (SH2D5) is a mammalian-specific, uncharacterized scaffolding protein, and its role in LUAD remains unclear. In the present study, we investigated the function and potential mechanisms of SH2D5 in the progression of LUAD.
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