Oleic acid (OA), a main ingredient of Brucea javanica oil (BJO), is widely known to have anticancer effects in many tumors. In this study, we investigated the anticancer effect of OA and its mechanism in tongue squamous cell carcinoma (TSCC). We found that OA effectively inhibited TSCC cell proliferation in a dose- and time-dependent manner. OA treatment in TSCC significantly induced cell cycle G0/G1 arrest, increased the proportion of apoptotic cells, decreased the expression of CyclinD1 and Bcl-2, and increased the expression of p53 and cleaved caspase-3. OA also obviously induced the formation of autolysosomes and decreased the expression of p62 and the ratio of LC3 I/LC3 II. The expression of p-Akt, p-mTOR, p-S6K, p-4E-BP1 and p-ERK1/2 was significantly decreased in TSCC cells after treatment with OA. Moreover, tumor growth was significantly inhibited after OA treatment in a xenograft mouse model. The above results indicate that OA has a potent anticancer effect in TSCC by inducing apoptosis and autophagy via blocking the Akt/mTOR pathway. Thus, OA is a potential TSCC drug that is worthy of further research and development.

MTFR2 is an oncogene involved in the progression of cancer, its' potential mechanism in oral squamous carcinoma remains unknown. The aim of this study was to uncover the bio-function and the mechanism of MTFR2 in the progression of oral squamous carcinoma. We scanned TCGA database to identify MTFR2 as dysregulated genes. qRT-PCR and Western blotting assays were applied to detect the expression pattern of MTFR2 in oral squamous carcinoma. We next established stable MTFR2-overexpressing and MTFR2 knocking down cell lines. A series of experiments were applied and the results indicated that MTFR2 was upregulated in cancer tissue and negatively correlated with the overall survival (OS) of patients in both the TCGA database and our inhouse database. Following experiments showed that MTFR2 promotes proliferation, migration and invasion in an oral squamous carcinoma cell line by switching OXPHOS to glycolysis.

Previous evidence has indicated an increased cancer risk in individuals with diabetes mellitus (DM). The aim of this study was to investigate the relationship between DM (high glucose) and tongue squamous cell carcinoma (TSCC) and how high glucose mediated the metastatic potential of TSCC. The relationship between DM and TSCC was assessed in a retrospective study. The role and its mechanism of high glucose on the proliferation, metastatic potential of TSCC were investigated in vitro and in vivo. The prevalence rate of DM in patients with TSCC was 12.84%, which was significantly higher than that (9.7%) in the general population in China. Although no significant difference was observed in the overall survival (OS) rate, TSCC patients with DM have a 1.38-fold increase in relative risk affecting 5-year OS compared to patients without DM. High glucose enhanced the TSCC cell proliferation, migration, invasion and upregulated PKM2 (pyruvate kinase M2) expression. Whereas, these effect was abolished after knockdown of PKM2 in TSCC cells. High glucose promoted tumour growth and lung metastasis of TSCC in a DM animal model. Our results confirm DM as a risk factor for the development of TSCC. High glucose enhances the metastatic potential of TSCC through stimulation of the PKM2 pathway.

electroacupuncture (ea) has been documented as a form of therapy for chronic sinusitis (crS). The present study aimed to assess the effects of ea combined with interleukin-10 (il-10) overexpression on crS in mice, and to investigate the associated mechanisms. a mouse model of crS was established by the administration of ovalbumin (oVa), and overexpression of il-10 was induced using virus-encoded il-10. The experimental groups were as follows: i) control group; ii) oVa group; iii) oVa + ea group; iv) oVa + empty vector group; v) oVa + vector + ea group; vi) oVa + il-10 group; and vii) oVa + il-10 + ea group. Pathological changes and nasal mucus were analyzed using hematoxylin and eosin staining. interferon-γ (iFn-γ) and il-10 were detected via reverse-transcription quantitative Pcr and western blot analyses. The pseudostratified epithelium of the mucosa of the nasal sinus was impaired following the induction of crS. Treatment with ea and/or il-10 reversed the injury. combination treatment with ea and il-10 induced synergistic effects. No infiltration of inflammatory cells was observed in the submucosa following ea and il-10 treatment. compared with the control group, the expression of iFn-γ and il-10 in the oVa group was reduced. By contrast, ea or the overexpression of il-10 inhibited this reduction. Furthermore, the combined application of EA and IL-10 had a significantly more potent inhibitory effect on the reduction of iFn-γ expression, but not il-10. collectively, ea combined with il-10 induced specific effects on CRS in mice, likely through the upregulation of iFn-γ and il-10. The current study presented mechanistic implications for the application of ea as an alternative treatment for crS.