Dysregulation of microRNAs (miRNAs) influences diverse hallmarks of cancer, including proliferative signaling, metastasis, and resistance to cell death. We explored the contribution of miR-92b-3p in oral squamous cell carcinoma (OSCC) and its potential as a monitoring biomarker. Analysis of TCGA, GEO, and our own cohort revealed dysregulation of miR-92b-3p in OSCC, which correlated with aggressive tumor characteristics. miR-92b-3p overexpression augmented proliferation and the epithelial-mesenchymal transition in both YD8 and SCC25 cell lines and xenograft models. Mechanically, augmented miR-92b-3p expression suppressed ATXN1 and CPEB3, activating the Notch signaling pathway and thereby promoting metastasis and cisplatin resistance. In our cohort, serum miR-92b-3p expression reflected the disease status, including relapse. Our results suggest that miR-92b-3p might be an onco-miR involved in OSCC through regulating the ATXN1/CPEB3/Notch pathway. These findings provide novel insights for treating and monitoring OSCC.
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http://dx.doi.org/10.1038/s41388-025-03306-2 | DOI Listing |
Med Res Rev
March 2025
Biochemistry and Molecular Biology, Primeasia University, Banani, Dhaka, Bangladesh.
The development of standard drugs for some unusual cancers, including estrogen-nonresponsive breast cancer, is somewhat difficult within a very short time. So, considering the current situation, phytoestrogen may be a potential candidate for unraveling chemotherapeutics agents. The reason for this review article is to manifest overall information regarding the effects of phytoestrogen on triple-negative breast cancer (TNBC), along with its related cellular and molecular pathways in different TNBC models.
View Article and Find Full Text PDFFront Vet Sci
February 2025
Key Laboratory of Reproductive Regulation and Breeding of Grassland Livestock, School of Life Sciences, Inner Mongolia University, Hohhot, China.
Secondary hair follicles (SHFs) in cashmere goats produce high-value cashmere fibers, which cyclic regulation is critical for optimizing cashmere yield and quality. This study explores the phenotypic changes and differential protein expression profiles involved in the telogen-to-anagen transition of SHFs. Through histological observations, proteomic analyses, and immunohistochemical validation, we identified key molecular features and regulatory pathways underlying SHF cyclic renewal.
View Article and Find Full Text PDFBMC Musculoskelet Disord
March 2025
Department of Neurosurgery, Ningbo Key Laboratory of Neurological Diseases and Brain Function, The First Affiliated Hospital of Ningbo University, Ningbo, China.
Fractures will impair or disrupt angiogenesis, resulting in delayed union or non-union. Exploring angiogenic signaling molecules and related pathways can promote fracture healing. In this study, the roles of different endothelial cell (EC) subsets in fracture healing were observed using single-cell RNA sequencing (scRNA-seq).
View Article and Find Full Text PDFNat Commun
March 2025
Division of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
The vertebrate segmentation clock drives periodic somite segmentation during embryonic development. Her1 and Her7 clock proteins generate oscillatory expression of their own genes as well as that of deltaC in zebrafish. In turn, DeltaC and DeltaD ligands activate Notch signaling, which then activates transcription of clock genes in neighboring cells.
View Article and Find Full Text PDFJ Adv Res
March 2025
Department of Hepatobiliary Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China. Electronic address:
Introduction: Neutrophils are initial responders in inflammation and contribute to non-alcoholic fatty liver disease (NAFLD) progression to steatohepatitis (NASH). Neutrophil extracellular traps (NETs) are implicated in liver injury, yet their precise mechanisms in NASH progression remains unclear.
Objectives: This study investigates how NETs drive NASH progression by disrupting hepatocyte lipotoxicity and explore the regulatory mechanism of NETs formation and its downstream effects on liver pathology.
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