ABSTRACT
Editor's Note: this Article has been retracted; the Retraction Note is available at https://www.nature.com/articles/s41598-020-77203-x.
ABSTRACT
OBJECTIVE: The purpose of the study was to analyze the characteristics of elder patients with maxillofacial fracture. METHODS: We retrospectively analyzed the characteristics of maxillofacial fractures in the elder patients, who were treated from July 2010 to October 2017. The clinical characteristics of the etiology, fracture site, combined injury, systemic disease, and treatment method were analyzed. RESULTS: In the 198 elderly patients with maxillofacial fractures, the male-to-female ratio was 3.95︰1, and the mean age was 66.15 years old. Traffic accident injury (78 patients, 39.39%), fall injury (49 patients, 24.75%), high fall injury (33 patients, 16.67%) were the main factors of maxillofacial fracture in elderly patients. The most frequently observed fracture site was the mandible (120 patients). A total of 60 patients demonstrated associated injuries, in which limb injuries were the most prevalent (28 patients); whereas 66 patients had other systemic medical conditions, in which cardiovascular diseases was the most frequent (50 patients). The main treatment method of 198 patients was rigid internal fixation with small or micro-plates. CONCLUSIONS: Falling and traffic accidents are the main factors of maxillofacial fracture in elderly patients. Thus, interference measures should be observed for the prevention of maxillofacial fractures in elderly patients.
Subject(s)
Maxillofacial Injuries , Accidental Falls , Accidents, Traffic , Aged , Female , Fracture Fixation, Internal , Humans , Male , Retrospective StudiesABSTRACT
In this study, we investigated the effects of microRNA-542-3p (miR-542-3p) on ILK/TGF-ß1/Smad2/3 signaling and oral squamous cell carcinoma (OSCC) progression. Levels of miR-542-3p were lower in OSCC tissues (n=108) than adjacent normal tissues, whereas levels of ILK, TGF-ß1 and Smad2/3 were higher. Patients with undifferentiated tumors, advanced TNM stage and lymph node metastasis showed low miR-542-3p levels. This was accompanied by high ILK expression and poor survival. Dual luciferase reporter assays of SCC-9 cells showed that miR-542-3p inhibited ILK gene expression by binding to its 3'UTR at 233-240 bp. SCC-9 cells transfected with miR-542-3p mimics exhibited elevated miR-542-3p and decreased ILK, TGF-ß1 and Smad2/3 expression. They also showed reduced self-renewal (fewer CD44+ cells and tumor-spheres), invasiveness, migration, proliferation and survival. Conversely, miR-542-3p inhibitors promoted increased self-renewal (more CD44+ cells and tumor-spheres), invasiveness, migration, proliferation and survival. In xenograft experiments with nude mice, SCC-9 cells transfected with miR-542-3p mimics or siRNA-ILK yielded tumors with smaller volumes and weights than control tumors. These results demonstrate that miR-542-3p is a tumor suppressor that inhibits ILK/TGF-ß1/Smad2/3 signaling, thereby inhibiting OSCC progression.
ABSTRACT
This study aimed to elucidate how microRNA27a-3p (miR-27a-3p) modulates the Wnt/ß-catenin signaling pathway to promote the epithelial-mesenchymal transition (EMT) in oral squamous carcinoma stem cells (OSCSCs) by targeting secreted frizzled-related protein 1 (SFRP1). Flow cytometry was used to sort OSCSCs from the SCC-9 and Tca8113 cell lines. The OSCSCs were randomly assigned into the miR-27a-3p inhibitors group, the miR-27a-3p inhibitors-NC group, the si-SFRP1 group, the si-SFRP1 + miR-27a-3p inhibitors group and the blank group. A luciferase reporter, immunofluorescence and Transwell assays were performed to detect luciferase activity, SFRP1, and cell migration and invasion, respectively. The mRNA expression of miR-27a-3p, SFRP1 and EMT markers (E-cadherin, N-cadherin, vimentin and ZEB1) were detected using qRT-PCR. The protein expression of SFRP1, EMT markers and the proteins of the Wnt/ß-catenin signaling pathway was detected by Western blotting. OSCSCs showed up-regulated miR-27a-3p, Wnt/ß-catenin signaling pathway-related proteins, vimentin, N-cadherin and ZEB1 and down-regulated SFRP1 and E-cadherin. MiR-27a-3p targeted SFRP1. Down-regulated miR-27a-3p resulted in increased E-cadherin and SFRP1 but decreased vimentin, N-cadherin, ZEB1, the Wnt/ß-catenin signaling pathway-related proteins, and invasive and migratory cells. Silenced SFRP1 reversed this effect. We found that miR-27a-3p modulated the Wnt/ß-catenin signaling pathway to promote EMT in OSCSCs by down-regulating SFRP1.