LINC00958 promotes the proliferation of TSCC via miR-211-5p/CENPK axis and activating the JAK/STAT3 signaling pathway.

BACKGROUND: Tongue squamous cell carcinoma (TSCC) is one of the most common oral tumors. Recently, long intergenic noncoding RNA 00958 (LINC00958) has been identified as an oncogene in human cancers. Nevertheless, the role of LINC00958 and its downstream mechanisms in TSCC is still unknown. METHODS: The effect of LINC00958 on TSCC cells proliferation and growth were assessed by CCK-8, colony formation, 5-Ethynyl-2'-deoxyuridline (EdU) assay and flow cytometry assays in vitro and tumor xenograft model in vivo. Bioinformatics analysis was used to predict the target of LINC00958 in TSCC, which was verified by RNA immunoprecipitation and luciferase reporter assays. RESULTS: LINC00958 was increased in TSCC tissues, and patients with high LINC00958 expression had a shorter overall survival. LINC00958 knockdown significantly decreased the growth rate of TSCC cells both in vitro and in vivo. In mechanism, LINC00958 acted as a ceRNA by competitively sponging miR-211-5p. In addition, we identified CENPK as a direct target gene of miR-211-5p, which was higher in TSCC tissues than that in adjacent normal tissues. Up-regulated miR-211-5p or down-regulated CENPK could abolish LINC00958-induced proliferation promotion in TSCC cells. Furthermore, The overexpression of CENPK promoted the expression of oncogenic cell cycle regulators and activated the JAK/STAT3 signaling. CONCLUSIONS: Our findings suggested that LINC00958 is a potential prognostic biomarker in TSCC.

Interleukin-6 released by oral lichen planus myofibroblasts promotes angiogenesis.

Oral lichen planus (OLP), defined as a potential for malignant transformation, is a chronic inflammatory disease in which abnormal angiogenesis serves a role in the malignant changes of the disease. OLP-associated fibroblasts (OLP-MFs), derived from the stroma of OLP tissues, are characterized by the presence of myofibroblasts and contribute to the secretion of pro-inflammatory cytokines, which may be involved in the molecular pathogenesis of OLP. However, the associated mechanisms of angiogenesis in OLP remain unknown. The present study aimed to verify the expression of intercellular adhesion molecular 1, vascular cell adhesion molecule 1, VEGF and CD34 in OLP, and to investigate whether IL-6 secreted by OLP-MFs promoted OLP angiogenesis and the effect of its corresponding antibody inhibition. The results of the experiments demonstrated that inflammation was present and OLP upregulated the secretion of IL-6 by OLP stromal fibroblasts, thereby enhancing OLP angiogenesis. Anti-IL-6 receptor antibody inhibited OLP-stroma IL-6 signaling and suppressed OLP angiogenesis. The antibody inhibited the inflammatory response by inhibiting the secretion of inflammatory factors, including IL-6, to suppress angiogenesis and reduce disease progression, thus indicating that this could be a potential target to develop a treatment for OLP.

[Synovial chondromatosis in the temporomandibular joint: analysis of 5 cases].

Five patients with synovial chondromatosis in the temporomandibular joint were treated in our hospital between August, 2011 and August, 2014. All the patients underwent preoperative imaging examinations for clinical diagnosis and determining the involvement of the lesions. Surgeries were performed and the lesions were confirmed as synovial chondromatosis by pathological diagnosis. The clinical manifestations, imaging features, diagnosis and treatment results were analyzed. All the 5 patients had pain in the joint region, 3 had limited mouth opening, and 3 had swelling in the joint region. X-ray film showed widening of the joint space in all the 5 cases and radiographic findings showed space-occupying lesions in the intra-articular space. Open joint surgeries was performed and completed successfully in all the cases. The postoperative imaging showed no residual lesions in the surgical area. As a rare clinical entity, synovial chondromatosis in the temporomandibular joint was poorly documented without specific clinical manifestations. The diagnosis of synovial chondromatosis relies on imaging, arthroscopic and pathological findings. Corpus liberum is an important feature of the disease occurring frequently in the joint cavity. Surgical intervention is the primary choice for treatment of synovial chondromatosis in the temporomandibular joint, in which the corpus liberum and the affected synovial membrane shall be removed after joint incision.