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Image Search Results
Journal: BMC Cancer
Article Title: Interaction between DNMT3B and MYH11 via hypermethylation regulates gastric cancer progression
doi: 10.1186/s12885-021-08653-3
Figure Lengend Snippet: Primer used for RT-qPCR
Article Snippet: The overexpressed (oe) DNA plasmids oe-MYH11, oe-TNFRSF14,
Techniques:
Journal: BMC Cancer
Article Title: Interaction between DNMT3B and MYH11 via hypermethylation regulates gastric cancer progression
doi: 10.1186/s12885-021-08653-3
Figure Lengend Snippet: DNMT3B upregulation is responsible for the hypermethylation of the MYH11 promoter. A , the expression of DNMT3A and DNMT3B in GC was queried in StarBase Pan-cancer platform; B , the enrichment ability of DNMT3A and DNMT3B on MYH11 promoter examined by ChIP-qPCR; C , DNMT3B mRNA expression in GC tumor tissues and their adjacent tissues by RT-qPCR; D , correlation of DNMT3B expression with MYH11 promoter methylation levels in tumor tissues analyzed by Pearson’s correlation analysis (r = 0.623, p < 0.001); E , correlation of DNMT3B expression with MYH11 expression in tumor tissues (r = − 0.609, p < 0.001); F , transfection efficiency of oe-DNMT3B in GC cells by RT-qPCR; G , the effects of DNMT3B overexpression on the methylation level of MYH11 promoter examined by qMSP; H , effects of DNMT3B overexpression on MYH11 expression by RT-qPCR. Each assay was performed at least three times. Statistical significance was analyzed by paired t test (panel C) or two-way ANOVA (panels B, F, G and H) and Tukey’s multiple range tests
Article Snippet: The overexpressed (oe) DNA plasmids oe-MYH11, oe-TNFRSF14,
Techniques: Expressing, Quantitative RT-PCR, Methylation, Transfection, Over Expression
Journal: BMC Cancer
Article Title: Interaction between DNMT3B and MYH11 via hypermethylation regulates gastric cancer progression
doi: 10.1186/s12885-021-08653-3
Figure Lengend Snippet: Mechanism diagram. Overexpression of DNMT3B in GC inhibited MYH11 expression by promoting methylation of the MYH11 promoter, thereby attenuating the repressive effect of MYH11 on TNFRSF14 transcriptional activity and promoting GC progression
Article Snippet: The overexpressed (oe) DNA plasmids oe-MYH11, oe-TNFRSF14,
Techniques: Over Expression, Expressing, Methylation, Activity Assay
Journal: Frontiers in Genetics
Article Title: Long Non-coding RNA FGD5-AS1 Regulates Cancer Cell Proliferation and Chemoresistance in Gastric Cancer Through miR-153-3p/CITED2 Axis
doi: 10.3389/fgene.2020.00715
Figure Lengend Snippet: Effects of FGD5-AS1 inhibition on gastric cancer cell proliferation and 5-FU chemoresistance. (A) Two gastric cancer cell lines, SGC-7901 and MKN-28 were transduced with a lentivirus containing human lncRNA FGD5-AS1 sh_RNA (sh_FGD5AS1), or a lentivirus containing negative control shRNA (sh-NC). After transduction was stabilized, qRT-PCR was applied to compare FGD5-AS1 expression levels (* P < 0.05). (B) A 5-day MTT assay was used to assess in vitro proliferation rates between SGC-7901 and MKN-28 cells transduced with sh-NC and those transduced with sh-FGD5AS1 (** P < 0.05). (C) Lentiviral-transduced SGC-7901 and MKN-28 cells were treated with 0, 5, 10, 20, 50, or 100 μg/mL 5-FU for 24 h, followed by an MTT assay to compare 5-FU chemoresistance between those transduced with sh-NC and those transduced with sh-FGD5AS1 (** P < 0.05). (D) Lentiviral-transduced SGC-7901 cells were subcutaneously inoculated (1 × 10 6 /injection) into the flanks of 2-month-old female athymic mice for 5 weeks. The in vivo tumor volumes (mm 3 ) were compared between those transduced with sh-NC and those transduced with sh-FGD5AS1 (** P < 0.05). (E) After the in vivo tumorigenicity assay, SGC-7901 tumors were retrieved and compared directly.
Article Snippet: A
Techniques: Inhibition, Transduction, Negative Control, shRNA, Quantitative RT-PCR, Expressing, MTT Assay, In Vitro, Injection, In Vivo, Tumorigenicity Assay