BackgroundDiabetes mellitus (DM) has been identified to be both a risk factor and a prognostic factor in a variety of malignancies, but its association with the risk and outcome of nasopharyngeal carcinoma (NPC) is still unclear. To elucidate this issue, we systematically reviewed the evidence concerning the association between DM status and NPC.Materials and methodsWe identified studies by a literature search of PubMed, Embase, and ISI Web of Knowledge through May 31, 2017, and by searching the reference lists of pertinent articles. Odds ratios (ORs) and hazard ratios (HRs) with 95% CIs were used to estimate the effect size. Heterogeneity across studies was evaluated by the Cochran’s Q and I2 statistics.ResultsA total of nine studies were included. Four studies with a total sample size of 221,611 reported the effect of DM on NPC risk, and the other five studies with a sample size of 9,442 reported the impact of DM on survival in NPC patients. All included studies were retrospective, and mostly conducted in Asian populations. Meanwhile, condition of metformin usage was not considered in all studies. A pooled OR of 0.65 (95% CI: 0.43–0.98, P=0.04) revealed an inverse association between DM and NPC. Additionally, pooled analyses of studies investigating the prognosis value of DM revealed that preexisting DM had no effect on overall survival (HR =1.17, 95% CI: 0.94–1.46, P=0.16), local recurrence-free survival (HR =1.16, 95% CI: 0.80–1.67, P=0.44), and distant metastasis-free survival (HR =1.14, 95% CI: 0.92–1.40, P=0.22).ConclusionOur results suggested that DM patients might have decreased NPC risk, and have little impact on prognosis of NPC patients. This conclusion should be limited to Asian population. Our results also suggest that more attention should be paid to metformin medication in further studies in order to clarify whether the effects of DM on NPC risk and prognosis are influenced by the anticancer effect of metformin.

The current experiment was performed to investigate whether luteolin affects the proliferation and apoptosis of keloid fibroblasts by regulating the expression of FRAT1 gene. Keloid fibroblasts were treated with luteolin at different concentrations. MTT method, western blot, flow cytometry, and real-time quantitative PCR (qPCR) were used to detect cell proliferation, cyclin D1 (CyclinD1), p21, B-cell lymphoma / leukemia-2 (Bcl-2), Bcl-2 related X protein (Bax), FRAT1 protein expression, apoptosis and ARHI mRNA expression. Keloid fibroblasts were transfected with si-FRAT1, or pcDNA-FRAT1 and treated with luteolin to observe their roles in cell proliferation and apoptosis. Compared with the control group, luteolin significantly reduced the keloid fibroblast activity, CyclinD1, Bcl-2, and FRAT1 protein levels, and obviously improved the cell apoptosis rate, p21 and Bax protein expression (P<0.05). The expression of FRAT1 mRNA and protein in keloid fibroblasts was greatly increased (P<0.05). Inhibition of FRAT1 expression evidently decreased cell viability at 24 h, 48 h, and 72 h, CyclinD1, and Bcl-2 protein expression of keloid fibroblasts, while-dramatically enhanced cell apoptosis, p21, and Bax protein levels (P<0.05). FRAT1 overexpression reversed the inhibitory effect of luteolin on keloid fibroblast activity, FRAT1, CyclinD1, and Bcl-2 protein expression, and promotion of apoptosis, p21 and Bax protein expression. Luteolin can inhibit the proliferation and induce apoptosis of keloid fibroblasts by regulating the expression of FRAT1 gene.

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