Objective:Gastric cancer(GC)is a globally common cancer characterized by high incidence and mortality worldwide.Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy.Long...Objective:Gastric cancer(GC)is a globally common cancer characterized by high incidence and mortality worldwide.Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy.Long non-coding RNAs(lncRNAs)and their downstream regulators are regarded to be implicated in the progression of multiple types of malignancies.Studies have shown that the lncRNA small nucleolar RNA host gene 4(SNHG4)serves as a tumor promoter in various malignancies,while its function in GC has yet to be characterized.Therefore,our study aimed to explore the role and underlying mechanism of SNHG4 in GC.Methods:We used qRT-PCR to analyze SNHG4 expression in GC tissues and cells.Kaplan-Meier analysis was used to assess the correlation between SNHG4 expression and the survival rate of GC patients.Cellular function experiments such as CCK-8,BrdU,colony formation,flow cytometry analysis,and transwell were performed to explore the effects of SNHG4 on GC cell proliferation,apoptosis,cell cycle,migration,and invasion.We also established xenograft mouse models to explore the effect of SNHG4 on GC tumor growth.Mechanically,dual luciferase reporter assay was used to verify the interaction between SNHG4 and miR-409-3p and between miR-409-3p and cAMP responsive element binding protein 1(CREB1).Results:The results indicated that SNHG4 was overexpressed in GC tissues and cell lines,and was linked with poor survival rate of GC patients.SNHG4 promoted GC cell proliferation,migration,and invasion while inhibiting cell apoptosis and cell cycle arrest in vitro.The in vivo experiment indicated that SNHG4 facilitated GC tumor growth.Furthermore,SNHG4 was demonstrated to bind to miR-409-3p.Moreover,CREB1 was directly targeted by miR-409-3p.Rescue assays demonstrated that miR-409-3p deficiency reversed the suppressive impact of SNHG4 knockdown on GC cell malignancy.Additionally,miR-409-3p was also revealed to inhibit GC cell proliferation,migration,and invasion by targeting CREB1.Conclusion:In conclusion,we verified that the SNHG4 promoted GC growth and metastasis by binding to miR-409-3p to upregulate CREB1,which may deepen the understanding of the underlying mechanism in GC development.展开更多
Objective: TO study the mechanism of cancer, theDNA for BAC was cloned from an ascites hepatoma cellline Hca-F25lCL-16A3 using PCR. Methods: The nucleotide sequences were determined using ABI PRISMTM377 DNA sequencer....Objective: TO study the mechanism of cancer, theDNA for BAC was cloned from an ascites hepatoma cellline Hca-F25lCL-16A3 using PCR. Methods: The nucleotide sequences were determined using ABI PRISMTM377 DNA sequencer. The expression of hcf-2 and CDK4gene were determined using im munohis tochemis try.Results: The sequences of BAC segment on Hca-F25lCL-16A3 have nearly identical sequences withhuman BAC. The hcl-2 and CDK4 are highly expressionon this cell line. Conclusion: The highly expression ofhcf-2 and CDK4 may the one of mechanisms for tumorgrowth.展开更多
The effect of repressors on ion channel gene expression was studied. The hKv4. 3 promoter and the sequence （ ＋ 2-- ＋ 160, S160） of 5＇-UTR of the hKv4. 3 gene was cloned into the pβ-gal-Basic vector. The transien...The effect of repressors on ion channel gene expression was studied. The hKv4. 3 promoter and the sequence （ ＋ 2-- ＋ 160, S160） of 5＇-UTR of the hKv4. 3 gene was cloned into the pβ-gal-Basic vector. The transient expression of the pβ-gal vector and the analysis of the relative activity of β-galactosidase were carried out. The analysis of the mRNA level was carried out with the RT-PCR method. S160 could intensively repress the expression of the hKv4. 3 gene with position-specificity. The level of mRNA did not alter obviously. A repressor（ S160）, in 5＇-UTR of the hKv4. 3 gene was found and its repression to gene expression may play a role in the post-transcription process.展开更多
Objective:Congenital heart disease(CHD)is caused by abnormal cardiac development,which is the most common congenital malformation at home and abroad.NKX2-5,GATA4 and ZIC3 have been shown to be associated with CHD.This...Objective:Congenital heart disease(CHD)is caused by abnormal cardiac development,which is the most common congenital malformation at home and abroad.NKX2-5,GATA4 and ZIC3 have been shown to be associated with CHD.This experiment explored the relationship between NKX2-5,GATA4 and ZIC3 gene mutations and sporadic CHD in Hainan Province.Methods:To collect 210 sporadic CHD patients in Hainan,the DNA of patients was extracted from blood,and the target gene fragments were amplified.Using high-resolution melting(HRM)and DNA sequencing technology,and we analyzed the sequences of NKX2-5,GATA4 and ZIC3 genes.Results:NKX2-5,GATA4 and ZIC3 genes were sequenced in 210 CHD patients,and seven gene mutations were found,including NKX2-5 heterozygous missense mutation(c.178G>T)and three heterozygous mutations in GATA4(c.677C>T,c.928A>G,c.1123G>A),three heterozygous mutations in ZIC3(c.19G>C,c.1255C>G,c.1348C>T),in which NKX2-5(c.178G>T),GATA4(c.1123G>A),and ZIC3(c.1255C>G,c.1348C>T)are new mutation sites.These gene mutations were predicted to be pathogenic mutations by bioinformatics software.Conclusion:Conclusion:Seven gene mutations were found in 210 patients,and it was the first report that the gene mutations of NKX2-5,GATA4 and ZIC3 in Hainan Province associated with the pathogenesis of CHD.展开更多
BACKGROUND Congenital lymphangiectasia is a rare disease characterized by dilated interstitial lymphatic vessels and cystic expansion of the lymphatic vessels.Congenital lymphangiectasia can affect various organ syste...BACKGROUND Congenital lymphangiectasia is a rare disease characterized by dilated interstitial lymphatic vessels and cystic expansion of the lymphatic vessels.Congenital lymphangiectasia can affect various organ systems;however,it frequently occurs in the lungs accompanied with unexplained pleural effusion.Further,it might not be diagnosed during prenatal examination owing to the absence of pronounced abnormalities.However,after birth the newborn rapidly develops respiratory distress that quickly deteriorates.Genetic variations in proteins controlling the development of lymphatic vessels contribute to the pathophysiology of this disease.We report a rare case of heterozygous mutation of ADAMTS3 and FLT4 genes,which have not been reported previously.CASE SUMMARY We analysed the case of a neonate who had presented with only pleural effusion at a late gestational age and eventually died due to its inability to establish spontaneous breathing after birth.An autopsy revealed lymphangiectasia of the organ systems.Further,whole exome sequencing revealed heterozygous mutations of the lymphangiogenesis-controlling genes,ADAMTS3 and FLT4,and Sanger verification revealed similar lesions in the mother with no symptoms.CONCLUSION Considering the presented case,obstetricians should observe unexplained foetal pleural effusion,and perform pathology analysis and whole exome sequencing for a conclusive diagnosis and prompt treatment.展开更多
应用Long and Accurate—PCR(LA-PCR)技术,扩增克隆了鸡传染性法氏囊病病毒上海超强毒(wIB-DV)的VP2—4—3基因。应用粘性末端连接策略,将VP2-4-3基因克隆人真核表达载体pALTER-MAX。经酶切鉴定,表明VP2-4-3基因为正向插入,位于CMV启动...应用Long and Accurate—PCR(LA-PCR)技术,扩增克隆了鸡传染性法氏囊病病毒上海超强毒(wIB-DV)的VP2—4—3基因。应用粘性末端连接策略,将VP2-4-3基因克隆人真核表达载体pALTER-MAX。经酶切鉴定,表明VP2-4-3基因为正向插入,位于CMV启动子下游。该真核表达质粒在脂质体的介导下转染Vero细胞,经特异性抗IBDV抗体的免疫荧光检测,发现在细胞内有特异蛋白表达。展开更多
文摘Objective:Gastric cancer(GC)is a globally common cancer characterized by high incidence and mortality worldwide.Advances in the molecular understanding of GC provide promising targets for GC diagnosis and therapy.Long non-coding RNAs(lncRNAs)and their downstream regulators are regarded to be implicated in the progression of multiple types of malignancies.Studies have shown that the lncRNA small nucleolar RNA host gene 4(SNHG4)serves as a tumor promoter in various malignancies,while its function in GC has yet to be characterized.Therefore,our study aimed to explore the role and underlying mechanism of SNHG4 in GC.Methods:We used qRT-PCR to analyze SNHG4 expression in GC tissues and cells.Kaplan-Meier analysis was used to assess the correlation between SNHG4 expression and the survival rate of GC patients.Cellular function experiments such as CCK-8,BrdU,colony formation,flow cytometry analysis,and transwell were performed to explore the effects of SNHG4 on GC cell proliferation,apoptosis,cell cycle,migration,and invasion.We also established xenograft mouse models to explore the effect of SNHG4 on GC tumor growth.Mechanically,dual luciferase reporter assay was used to verify the interaction between SNHG4 and miR-409-3p and between miR-409-3p and cAMP responsive element binding protein 1(CREB1).Results:The results indicated that SNHG4 was overexpressed in GC tissues and cell lines,and was linked with poor survival rate of GC patients.SNHG4 promoted GC cell proliferation,migration,and invasion while inhibiting cell apoptosis and cell cycle arrest in vitro.The in vivo experiment indicated that SNHG4 facilitated GC tumor growth.Furthermore,SNHG4 was demonstrated to bind to miR-409-3p.Moreover,CREB1 was directly targeted by miR-409-3p.Rescue assays demonstrated that miR-409-3p deficiency reversed the suppressive impact of SNHG4 knockdown on GC cell malignancy.Additionally,miR-409-3p was also revealed to inhibit GC cell proliferation,migration,and invasion by targeting CREB1.Conclusion:In conclusion,we verified that the SNHG4 promoted GC growth and metastasis by binding to miR-409-3p to upregulate CREB1,which may deepen the understanding of the underlying mechanism in GC development.
文摘Objective: TO study the mechanism of cancer, theDNA for BAC was cloned from an ascites hepatoma cellline Hca-F25lCL-16A3 using PCR. Methods: The nucleotide sequences were determined using ABI PRISMTM377 DNA sequencer. The expression of hcf-2 and CDK4gene were determined using im munohis tochemis try.Results: The sequences of BAC segment on Hca-F25lCL-16A3 have nearly identical sequences withhuman BAC. The hcl-2 and CDK4 are highly expressionon this cell line. Conclusion: The highly expression ofhcf-2 and CDK4 may the one of mechanisms for tumorgrowth.
文摘The effect of repressors on ion channel gene expression was studied. The hKv4. 3 promoter and the sequence （ ＋ 2-- ＋ 160, S160） of 5＇-UTR of the hKv4. 3 gene was cloned into the pβ-gal-Basic vector. The transient expression of the pβ-gal vector and the analysis of the relative activity of β-galactosidase were carried out. The analysis of the mRNA level was carried out with the RT-PCR method. S160 could intensively repress the expression of the hKv4. 3 gene with position-specificity. The level of mRNA did not alter obviously. A repressor（ S160）, in 5＇-UTR of the hKv4. 3 gene was found and its repression to gene expression may play a role in the post-transcription process.
基金Natural Science Foundation of Hainan Province(No.821RC562)Re-research Project of Hainan Province(No.ZDYF2022SHF2081)+1 种基金National Natural Science Foundation of China(No.81660224)Graduate Innovation Project of Hainan Province(No.Qhys2021-353)。
文摘Objective:Congenital heart disease(CHD)is caused by abnormal cardiac development,which is the most common congenital malformation at home and abroad.NKX2-5,GATA4 and ZIC3 have been shown to be associated with CHD.This experiment explored the relationship between NKX2-5,GATA4 and ZIC3 gene mutations and sporadic CHD in Hainan Province.Methods:To collect 210 sporadic CHD patients in Hainan,the DNA of patients was extracted from blood,and the target gene fragments were amplified.Using high-resolution melting(HRM)and DNA sequencing technology,and we analyzed the sequences of NKX2-5,GATA4 and ZIC3 genes.Results:NKX2-5,GATA4 and ZIC3 genes were sequenced in 210 CHD patients,and seven gene mutations were found,including NKX2-5 heterozygous missense mutation(c.178G>T)and three heterozygous mutations in GATA4(c.677C>T,c.928A>G,c.1123G>A),three heterozygous mutations in ZIC3(c.19G>C,c.1255C>G,c.1348C>T),in which NKX2-5(c.178G>T),GATA4(c.1123G>A),and ZIC3(c.1255C>G,c.1348C>T)are new mutation sites.These gene mutations were predicted to be pathogenic mutations by bioinformatics software.Conclusion:Conclusion:Seven gene mutations were found in 210 patients,and it was the first report that the gene mutations of NKX2-5,GATA4 and ZIC3 in Hainan Province associated with the pathogenesis of CHD.
基金The Wu Jieping Medical Foundation Clinical Research Special Grant Fund in China,No.320.6750.2022-15-9.
文摘BACKGROUND Congenital lymphangiectasia is a rare disease characterized by dilated interstitial lymphatic vessels and cystic expansion of the lymphatic vessels.Congenital lymphangiectasia can affect various organ systems;however,it frequently occurs in the lungs accompanied with unexplained pleural effusion.Further,it might not be diagnosed during prenatal examination owing to the absence of pronounced abnormalities.However,after birth the newborn rapidly develops respiratory distress that quickly deteriorates.Genetic variations in proteins controlling the development of lymphatic vessels contribute to the pathophysiology of this disease.We report a rare case of heterozygous mutation of ADAMTS3 and FLT4 genes,which have not been reported previously.CASE SUMMARY We analysed the case of a neonate who had presented with only pleural effusion at a late gestational age and eventually died due to its inability to establish spontaneous breathing after birth.An autopsy revealed lymphangiectasia of the organ systems.Further,whole exome sequencing revealed heterozygous mutations of the lymphangiogenesis-controlling genes,ADAMTS3 and FLT4,and Sanger verification revealed similar lesions in the mother with no symptoms.CONCLUSION Considering the presented case,obstetricians should observe unexplained foetal pleural effusion,and perform pathology analysis and whole exome sequencing for a conclusive diagnosis and prompt treatment.
文摘应用Long and Accurate—PCR(LA-PCR)技术,扩增克隆了鸡传染性法氏囊病病毒上海超强毒(wIB-DV)的VP2—4—3基因。应用粘性末端连接策略,将VP2-4-3基因克隆人真核表达载体pALTER-MAX。经酶切鉴定,表明VP2-4-3基因为正向插入,位于CMV启动子下游。该真核表达质粒在脂质体的介导下转染Vero细胞,经特异性抗IBDV抗体的免疫荧光检测,发现在细胞内有特异蛋白表达。
