Full-length RNA4 of beet necrotic yellow vein virus (BNYVV) and its mutants, including a frame-shift and deletions within the coding region, were inserted into a transcription plasmid. Transcripts derived from these p...Full-length RNA4 of beet necrotic yellow vein virus (BNYVV) and its mutants, including a frame-shift and deletions within the coding region, were inserted into a transcription plasmid. Transcripts derived from these plasmids and RNAs extracted from a BNYVV isolate containing only RNAs 1, 2 and 3 were coinoculated to Tetragona expansa. Then these recombinant isolates were inoculated to sugar beet plants grown in a sand culture system containing Po-lymyxa betae that had been freed of virus particles to test efficiency of BNYVV transmission. The result showed that the efficiency of BNYVV transmission among the plants by Polymyxa betae was highly decreased by different deletions in the coding region of RNA4, but not affected by the frame-shift mutant with four nucleotides insertion. The observations suggest that at least some of the RNA4 sequence encompassing the deleted region of 580 nucleotide acids (525 -1105 nt) are necessary for high efficient transmission of the virus by the fungus.展开更多
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
基金This work was partially supported by the National Natural Science Foundation of China (Grant No. 39670035)the State "863" High-Tech Program Specifical Fund for Young Scientists.
文摘Full-length RNA4 of beet necrotic yellow vein virus (BNYVV) and its mutants, including a frame-shift and deletions within the coding region, were inserted into a transcription plasmid. Transcripts derived from these plasmids and RNAs extracted from a BNYVV isolate containing only RNAs 1, 2 and 3 were coinoculated to Tetragona expansa. Then these recombinant isolates were inoculated to sugar beet plants grown in a sand culture system containing Po-lymyxa betae that had been freed of virus particles to test efficiency of BNYVV transmission. The result showed that the efficiency of BNYVV transmission among the plants by Polymyxa betae was highly decreased by different deletions in the coding region of RNA4, but not affected by the frame-shift mutant with four nucleotides insertion. The observations suggest that at least some of the RNA4 sequence encompassing the deleted region of 580 nucleotide acids (525 -1105 nt) are necessary for high efficient transmission of the virus by the fungus.
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.
