Metabolomic Analysis Reveals that SPHK1 Promotes Oral Squamous Cell Carcinoma Progression through NF-κB Activation.

Background: Metabolic disorders are significant in the occurrence and development of malignant tumors. Changes of specific metabolites and metabolic pathways are molecular therapeutic targets. This study aims to determine the metabolic differences between oral squamous cell carcinoma (OSCC) tissues and paired adjacent noncancerous tissues (ANT) through liquid chromatography-mass spectrometry (LC-MS).

experimental study on the formation of microRNA-34a loaded exosomes and their inhibitory effect in oral squamous cell carcinoma.

Studies have shown the inhibitory effect of microRNA-34a on proliferation, migration, and invasion of oral squamous cell carcinoma. However, the lack of a safe and effective delivery system limits the clinical application of microRNA-34a in oral cancer treatment. An exosome is a small extracellular vesicle that mediates intercellular communication by delivering proteins, nucleic acids, and other contents, and functions as a natural drug delivery carrier.

Exosomal microRNA-23b-3p promotes tumor angiogenesis and metastasis by targeting PTEN in salivary adenoid cystic carcinoma.

MicroRNA (miR)-23b-3p is known to target various genes that are involved in cancer-related pathways. Exosomes are emerging intercellular communication agents. Exosomes secreted by cancer cells can deliver active molecules to the surrounding stromal cells, thereby influencing the recipient cells and promoting the development of cancers.

Follistatin-like 1 suppresses osteoblast differentiation of bone marrow mesenchymal cells during inflammation.

Objective: The current study aimed to explore the effect of Follistatin-like 1 (FSTL1) on osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) in an inflammatory environment.

Design: Animal models of FSTL1-deficiency and wild-type mice were used, and the micro-CT images of the femoral head were evaluated. Mouse bone marrow mesenchymal stem cells were treated with various concentrations of recombinant FSTL1 (rFSTL1) in an inflammatory environment in vitro.

Identification of pivotal microRNAs involved in the development and progression of salivary adenoid cystic carcinoma.

Background: miRNAs and mRNAs have been significantly implicated in tumorigenesis and served as promising prognostic biomarkers for human cancer. Hence, this study was aimed to develop the pivotal miRNA biomarkers-based prognostic signature for salivary adenoid cystic carcinoma.

Methods: The miRNA and mRNA expression data were integrated from the gene expression omnibus database to study their involvement in salivary adenoid cystic carcinoma development and progression.

Sphk1 promotes salivary adenoid cystic carcinoma progression via PI3K/Akt signaling.

The progression of salivary adenoid cystic carcinoma (SACC) is closely related to abnormal gene expression. Herein, the role of Sphk1 in SACC was explored. Sphk1 was overexpressed in SACC tissues.

Evaluation of autofluorescence visualization system in the delineation of oral squamous cell carcinoma surgical margins.

Introduction: Delineating the margins of Oral squamous cell carcinoma (OSCC) is a critical step for optimaltumor resection. The aim of this study was to evaluate the accuracy of lesion surgical margin identification using autofluorescence visualization.

Materials And Methods: Thirty patients with OSCC were included in this study.

SATB2 overexpression promotes oral squamous cell carcinoma progression by up-regulating NOX4.

While atypical expression of special AT-rich sequence-binding protein 2 (SATB2) has been approved associated with tumor progression, metastasis and unfavourable prognosis in various carcinomas. However, in oral squamous cell carcinoma (OSCC), both the expressive state and associated functions of SATB2's are still undefined. Here we show that, in clinical samples from a retrospective cohort of 58 OSCC patients, high expression of SATB2 is associated with poor prognosis of OSCC patients.

Toll‑like receptor 4 activates the NLRP3 inflammasome pathway and periodontal inflammaging by inhibiting Bmi‑1 expression.

Overproduction of pro‑inflammatory cytokines in the aged, which is called inflammaging, leads to the deterioration of periodontitis. Toll‑like receptor 4 (TLR4) plays a role in the regulation of cellular senescence, and its expression increases with age. However, there has been limited research into the molecular mechanisms underlying the onset of periodontal inflammaging, and the interplay between TLR4 and inflammaging.

P16 played a critical role in exacerbating acute tubular necrosis in acute kidney injury.

Acute kidney injury (AKI) is a common clinical syndrome with high morbidity and mortality, which is mostly caused by acute tubular necrosis (ATN). AKI is associated with many factors, including cell senescence, inflammatory infiltration, apoptosis and excessive accumulation of reactive oxygen species (ROS). P16 (hereafter termed p16) inhibits cell cycle, and the absence of can significantly slow the progression of cell senescence.