The clinical relevance of MBL2 gene polymorphism and sepsis

Objective:To detect the clinical relevance of mannose-binding lectin 2(MBL2) gene polymorphism and sepsis in Chinese lived in Hainan island.Methods: Blood samples from 57 patients with sepsis and 69 patients without sepsis were collected in the ICU of several large hospitals in Hainan province. Genomic DNA was extracted from whole blood and then PCR purification product was sequenced and typed by 3730 sequencing analyzer. The concentration of MBIL2 in serum was detected by ELISA.Results: We found that genotype and allele distributions in two groups were in accordance with the Hardy-Weinberg Equilibrium. The frequency of GA genotype was significantly higher than that in non-sepsis group(P=0.013). A allele frequency in sepsis group was also much higher than that in non-sepsis group(P=0.028).Logister regression analysis showed that the patients who carried A allele were more prone to get sepsis than G allele carrier(P=0.014, OR=2,550, 95%CI=1.207-5.386). The MBL2 level in serum of sepsis patients with genotype GG and GA was significantly lower than that in non-sepsis group(P<0.05). In sepsis group, the MBL2 serum level of patients with genotype GA was obviously lower than that in patients with genotype GG(P<0.05).Conclusions: The variation of rs 1800450 G→A increased the incidence of sepsis and decreased the level of MBL2 in serum.

Association of MBL2 gene polymorphisms with sepsis in children and adult

Sepsis is a syndrome characterized by systemic inflammatory response caused by infection or toxin, with high morbidity and mortality. Different infection microflora and environment have great influence on the occurrence, development and prognosis of sepsis, but individual genetic factors also play an extremely important role. It was reported that the polymorphisms of mannose-binding lectin 2 gene were closely relevant to the occurrence and development of sepsis, but the conclusions in different studies were inconsistent. Therefore, we performed this reviews on the relevance of mannose-binding lectin 2 gene polymorphisms and sepsis.

ZNF582 hypermethylation promotes metastasis of nasopharyngeal carcinoma by regulating the transcription of adhesion molecules Nectin-3 and NRXN3

Background:Epigenetic regulation plays an important role in the development and progression of nasopharyngeal carcinoma(NPC).However,the epigenetic mechanisms underlying NPC metastasis remains poorly understood.We aimed to find functional genes which regulate the metastasis of NPC and identify therapeutic targets for NPC treatment.Methods:Bisulfite pyrosequencing was used to analyze zinc finger protein 582(ZNF582)methylation in NPC tissues and cell lines.Quantitative reverse transcription-polymerase chain reaction(qRT-PCR)and Western blotting were used to determine the expression of ZNF582.In vitro and in vivo experiments were performed to evaluate the biological function of ZNF582 in NPC.ZNF582-targeting genes were identified by chromatin immunoprecipitation sequencing(ChIP-seq)and were confirmed by ChIP-qPCR and luciferase assay.Results:ZNF582 promoter was hypermethylated in NPC,and both the mRNA and protein levels of ZNF582 were down-regulated in NPC tissues and cell lines.The restoration of ZNF582 inhibited NPC migration,invasion,and metastasis,while the knockdown of ZNF582 promoted NPC migration,invasion,and metastasis in vitro and in vivo.ZNF582 directly regulated the transcription and expression of adhesion molecules Nectin-3 and NRXN3.Both Nectin-3 and NRXN3 were identified as functional targets of ZNF582,and the restoration or abrogation of these genes reversed the tumor suppressor effect of ZNF582 in NPC metastasis.Conclusions:ZNF582 acts as a tumor suppressor gene in NPC by regulating the transcription and expression of adhesion molecules Nectin-3 and NRXN3,which may provide novel therapeutic targets for NPC treatment.

Correction to: ZNF582 hypermethylation promotes metastasis of nasopharyngeal carcinoma by regulating the transcription of adhesion molecules Nectin-3 and NRXN3

Following publication of this article[1],the authors noticed that the mismatched images were inadvertently included in Figure 5(migration assays of SUNE1-shNRXN3-#2 group in Figure 5I)and Figure 6(invasion assays of SUNE1-ZNF582+Nectin3 group in Figure 6A).This error has now been corrected online.