Background As the rate-limit enzyme of the pentose phosphate pathway, glucose-6-phosphate dehydrogenase (G6PD) plays important roles in tumour progression, but the exact mechanism through which G6PD controls cancer metastasis remains unclear. Methods G6PD expression in resected oral squamous cell carcinoma (OSCC) samples was analysed by immunohistochemistry. The effects and mechanism of G6PD suppression on OSCC cell lines were measured by transwell assay, wound healing assay, western and lectin blot, mass spectrometer analysis, ChIP-PCR, and luciferase reporter assay. BALB/c-nude mice were used to establish orthotopic xenograft model. Results G6PD expression in the tumours of 105 OSCC patients was associated with lymphatic metastasis and prognosis. In vitro cellular study suggested that G6PD suppression impaired cell migration, invasion, and epithelial-mesenchymal transition. Furtherly, G6PD knockdown activated the JNK pathway, which then blocked the AKT/GSK-3β/Snail axis to induce E-Cadherin expression and transcriptionally regulated MGAT3 expression to promote bisecting GlcNAc-branched N-glycosylation of E-Cadherin. An orthotopic xenograft model further confirmed that dehydroepiandrosterone reduced lymphatic metastatic rate of OSCC, which was partially reversed by JNK inhibition. Conclusions Suppression of G6PD promoted the expression and bisecting GlcNAc-branched N-glycosylation of E-Cadherin via activating the JNK pathway, which thus acted on OSCC metastasis.

Objectives:  To investigate the relationship between maximum standardized uptake value (SUVmax) of 18F-FDG PET/CT and clinicopathological features of oral squamous cell carcinoma (OSCC), in order to formulate a better clinical guideline. Methods:  In 104 patients with OSCC confirmed by pathology, there were 67 males and 37 females (age, 33–76 years; mean age, 56 years).18FDG, 18-fludeoxyglucose (18F-FDG) PET/CT manifestations and the clinicopathological features of the 104 patients were retrospectively analysed. Single-factor analysis and multiple regression analysis were conducted on possible factors influencing primary tumour SUVmax, including gender, age, smoking history, tumour location, tumour size, histological differentiation, TNM stage, T stage, N stage. Diagnostic performance of SUVmax for invading peri-tissue of OSCC was measured by the area under receiver operating characteristic curve, and sensitivity and specificity were determined at the Youdons index. Results:  The single-analysis results showed that SUVmax was correlated with the histological differentiation, tumour size, TNM stage, T stage, N stage(p < 0.05), yet it was not correlated with gender, age, smoking history, tumour location (p > 0.05). Multivariate liner regression analysis showed that tumour size, TNM stage were influencing factors independent of primary tumour SUVmax (p < 0.05). Primary tumour SUVmax had predictive value for invading peri-tissue of OSCC. When the cutoff value was 7.98, the diagnostic efficiency was the highest, with the sensitivity being 90.0％ and the specificity being 76.2%. Conclusions:  OSCC 18F-FDG PET/CT SUVmax is higher among patients with larger tumour size, poorer stage, and that primary tumour SUVmax is of important significance in predicting invading peri-tissue.

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