BACKGROUND Necrotizing enterocolitis(NEC)of the newborn is a frequently occurring clinical disease in infants.The mortality rate of NEC in premature infants is as high as 50%,and the morbidity rate is on the rise.NEC ...BACKGROUND Necrotizing enterocolitis(NEC)of the newborn is a frequently occurring clinical disease in infants.The mortality rate of NEC in premature infants is as high as 50%,and the morbidity rate is on the rise.NEC has already caused serious impacts on newborn survival and poses serious threats to both children and families.AIM To investigate the expression and significance of mucin 1(MUC1)and interleukin-11(IL-11)in the intestinal mucosa of infants with neonatal NEC after surgery.METHODS Forty-eight postoperative intestinal mucosal specimens from children with NEC(NEC group)and twenty-two intestinal mucosal specimens from children with congenital intestinal atresia(control group)were collected in our hospital.Immunohistochemical staining and Western blot analysis were used to examine the protein expression of MUC-1 and IL-11 in the two groups.The serum levels of tumor necrosis factor-α(TNF-α)and IL-1βin the two groups were measured by enzyme-linked immunosorbent assay,and the relationship between MUC-1 and IL-11 protein expression and serum TNF-αand IL-1βlevels was analyzed by the linear correlation method.RESULTS The protein expression of MUC-1 and IL-11 in the NEC group was significantly lower than that in the control group,and the difference was statistically significant(P<0.05).The levels of serum TNF-αand IL-1βin the NEC group were significantly higher than those in the control group(P<0.05).The protein expression of MUC-1 and IL-11 in the NEC group negatively correlated with serum TNF-αand IL-1βlevels(P<0.05).There was a significant negative correlation between the protein expression of MUC-1 and IL-11 and the levels of serum TNF-αand IL-1βin the NEC group.CONCLUSION The protein expression of MUC1 and IL-11 in the intestinal mucosa of children with NEC is significantly downregulated after surgery.This downregulation may be involved in the pathogenesis of this disease and has a certain correlation with inflammatory response factors in children with NEC.展开更多
Objective To investigate the effect of mucin 1(MUC1)on the proliferation and apoptosis of nasopharyngeal carcinoma(NPC)and its regulatory mechanism.Methods The 60 NPC and paired para-cancer normal tissues were collect...Objective To investigate the effect of mucin 1(MUC1)on the proliferation and apoptosis of nasopharyngeal carcinoma(NPC)and its regulatory mechanism.Methods The 60 NPC and paired para-cancer normal tissues were collected from October 2020 to July 2021 in Quanzhou First Hospital.The expression of MUC1 was measured by real-time quantitative PCR(qPCR)in the patients with PNC.The 5-8F and HNE1 cells were transfected with siRNA control(si-control)or siRNA targeting MUC1(si-MUC1).Cell proliferation was analyzed by cell counting kit-8 and colony formation assay,and apoptosis was analyzed by flow cytometry analysis in the 5-8F and HNE1 cells.The qPCR and ELISA were executed to analyze the levels of TNF-αand IL-6.Western blot was performed to measure the expression of MUC1,NFкB and apoptosis-related proteins(Bax and Bcl-2).Results The expression of MUC1 was up-regulated in the NPC tissues,and NPC patients with the high MUC1 expression were inclined to EBV infection,growth and metastasis of NPC.Loss of MUC1 restrained malignant features,including the proliferation and apoptosis,downregulated the expression of p-IкB、p-P65 and Bcl-2 and upregulated the expression of Bax in the NPC cells.Conclusion Downregulation of MUC1 restrained biological characteristics of malignancy,including cell proliferation and apoptosis,by inactivating NF-κB signaling pathway in NPC.展开更多
Background::Non-coding RNAs have attracted considerable attention for their vital role in cancer.The purpose of this study was to determine the effects of non-coding RNAs on hepatocellular carcinoma(HCC)and reveal the...Background::Non-coding RNAs have attracted considerable attention for their vital role in cancer.The purpose of this study was to determine the effects of non-coding RNAs on hepatocellular carcinoma(HCC)and reveal their regulatory mechanism in the pathophysiological process.Methods::We measured the expression of mucin 1(MUC1)and miR-485-5p in tissues from 15 HCC patients and in liver cancer cell lines by quantitative real-time polymerase chain reaction and Western blot,screened for aberrantly expressed microRNAs(miRNAs)by miRNA microarrays.Bioinformatics tools were used to find the miRNA and circular RNA that regulated MUC1,which were validated by RNA immunoprecipitation assay and luciferase reporter assay.Cell counting kit-8,Transwell assays,and flow cytometry were used to conduct functional experiments.Proteins were examined by western blot and immunohistochemical staining assays.Significant differences between groups were estimated using the one-way analysis of variance.A P<0.05 was considered statistically significant.Results::MUC1 was overexpressed in HCC tissues compared with that in paratumor tissues(normal vs.tumor,1.007±0.215 vs.75.213±18.403,t=18.401,P<0.001)while miR-485-5p was down-regulated(normal vs.tumor,4.894±0.684 vs.1.586±0.398,t=16.191,P<0.001).Inhibition of miR-485-5p promoted cell proliferation(73.33%±5.13%vs.41.33%±3.51%,t=8.913,P<0.001),migration(102±8 cells vs.46±8 cells,t=8.681,P<0.001),invasion(59±7 cells vs.28±2 cells,t=8.034,P<0.01),and suppressed apoptosis(22.64%±6.97%vs.36.33%±3.96%,t=2.958,P<0.05)of HepG2 cells with which MUC1 is knocked down.Mechanically,miR-485-5p binds to MUC1,while circHECTD1 binds to miR-485-5p,resulting in the indirect up-regulation of the MUC1 level.Conclusions::Our findings reveal that circHECTD1 facilitates HCC progression by sponging miR-485-5p to up-regulate MUC1.展开更多
基金Suzhou Science and Technology Program,No.SLT202005Suzhou Municipal Commission of Health and Family Planning,No.LCZX202031+1 种基金Suzhou New District Science and Technology Plan,No.2019Z009Independent Innovation Project of National High Tech Development Zone Hospital,No.SGY2018C03.
文摘BACKGROUND Necrotizing enterocolitis(NEC)of the newborn is a frequently occurring clinical disease in infants.The mortality rate of NEC in premature infants is as high as 50%,and the morbidity rate is on the rise.NEC has already caused serious impacts on newborn survival and poses serious threats to both children and families.AIM To investigate the expression and significance of mucin 1(MUC1)and interleukin-11(IL-11)in the intestinal mucosa of infants with neonatal NEC after surgery.METHODS Forty-eight postoperative intestinal mucosal specimens from children with NEC(NEC group)and twenty-two intestinal mucosal specimens from children with congenital intestinal atresia(control group)were collected in our hospital.Immunohistochemical staining and Western blot analysis were used to examine the protein expression of MUC-1 and IL-11 in the two groups.The serum levels of tumor necrosis factor-α(TNF-α)and IL-1βin the two groups were measured by enzyme-linked immunosorbent assay,and the relationship between MUC-1 and IL-11 protein expression and serum TNF-αand IL-1βlevels was analyzed by the linear correlation method.RESULTS The protein expression of MUC-1 and IL-11 in the NEC group was significantly lower than that in the control group,and the difference was statistically significant(P<0.05).The levels of serum TNF-αand IL-1βin the NEC group were significantly higher than those in the control group(P<0.05).The protein expression of MUC-1 and IL-11 in the NEC group negatively correlated with serum TNF-αand IL-1βlevels(P<0.05).There was a significant negative correlation between the protein expression of MUC-1 and IL-11 and the levels of serum TNF-αand IL-1βin the NEC group.CONCLUSION The protein expression of MUC1 and IL-11 in the intestinal mucosa of children with NEC is significantly downregulated after surgery.This downregulation may be involved in the pathogenesis of this disease and has a certain correlation with inflammatory response factors in children with NEC.
文摘Objective To investigate the effect of mucin 1(MUC1)on the proliferation and apoptosis of nasopharyngeal carcinoma(NPC)and its regulatory mechanism.Methods The 60 NPC and paired para-cancer normal tissues were collected from October 2020 to July 2021 in Quanzhou First Hospital.The expression of MUC1 was measured by real-time quantitative PCR(qPCR)in the patients with PNC.The 5-8F and HNE1 cells were transfected with siRNA control(si-control)or siRNA targeting MUC1(si-MUC1).Cell proliferation was analyzed by cell counting kit-8 and colony formation assay,and apoptosis was analyzed by flow cytometry analysis in the 5-8F and HNE1 cells.The qPCR and ELISA were executed to analyze the levels of TNF-αand IL-6.Western blot was performed to measure the expression of MUC1,NFкB and apoptosis-related proteins(Bax and Bcl-2).Results The expression of MUC1 was up-regulated in the NPC tissues,and NPC patients with the high MUC1 expression were inclined to EBV infection,growth and metastasis of NPC.Loss of MUC1 restrained malignant features,including the proliferation and apoptosis,downregulated the expression of p-IкB、p-P65 and Bcl-2 and upregulated the expression of Bax in the NPC cells.Conclusion Downregulation of MUC1 restrained biological characteristics of malignancy,including cell proliferation and apoptosis,by inactivating NF-κB signaling pathway in NPC.
基金a grant from the Medical Health Science and Technology Program of Zhejiang Province(No.2019PY003).
文摘Background::Non-coding RNAs have attracted considerable attention for their vital role in cancer.The purpose of this study was to determine the effects of non-coding RNAs on hepatocellular carcinoma(HCC)and reveal their regulatory mechanism in the pathophysiological process.Methods::We measured the expression of mucin 1(MUC1)and miR-485-5p in tissues from 15 HCC patients and in liver cancer cell lines by quantitative real-time polymerase chain reaction and Western blot,screened for aberrantly expressed microRNAs(miRNAs)by miRNA microarrays.Bioinformatics tools were used to find the miRNA and circular RNA that regulated MUC1,which were validated by RNA immunoprecipitation assay and luciferase reporter assay.Cell counting kit-8,Transwell assays,and flow cytometry were used to conduct functional experiments.Proteins were examined by western blot and immunohistochemical staining assays.Significant differences between groups were estimated using the one-way analysis of variance.A P<0.05 was considered statistically significant.Results::MUC1 was overexpressed in HCC tissues compared with that in paratumor tissues(normal vs.tumor,1.007±0.215 vs.75.213±18.403,t=18.401,P<0.001)while miR-485-5p was down-regulated(normal vs.tumor,4.894±0.684 vs.1.586±0.398,t=16.191,P<0.001).Inhibition of miR-485-5p promoted cell proliferation(73.33%±5.13%vs.41.33%±3.51%,t=8.913,P<0.001),migration(102±8 cells vs.46±8 cells,t=8.681,P<0.001),invasion(59±7 cells vs.28±2 cells,t=8.034,P<0.01),and suppressed apoptosis(22.64%±6.97%vs.36.33%±3.96%,t=2.958,P<0.05)of HepG2 cells with which MUC1 is knocked down.Mechanically,miR-485-5p binds to MUC1,while circHECTD1 binds to miR-485-5p,resulting in the indirect up-regulation of the MUC1 level.Conclusions::Our findings reveal that circHECTD1 facilitates HCC progression by sponging miR-485-5p to up-regulate MUC1.
