Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: DDX11-AS1 competitively binds miR-1183 through competing endogenous RNA (ceRNA) mechanism. ( A ) In silico analysis of the binding site of miR-1183 within DDX11-AS1 sequence. ( B ) Correlation between DDX11-AS1 and miR-1183 expression in clinical glioma samples ( n = 32). ( C , D ) The expression level of miR-1183 in glioma cells with DDX11-AS1 ( C ) knockdown or ( D ) overexpression ( n = 6). ( E ) The relative luciferase activity was examined in U87 glioma cells co-transfected with DDX11-AS1 wild-type (WT) or DDX11-AS1 mutant (MUT) and miR-1183 mimics or the miR-NC. ( F , G ) RIP assay in ( F ) U87 and ( G ) U251 glioma cells. ( H ) Binding of miR-1183 and miR-NC to DDX11-AS1 in the RNA pull-down assay (GAPDH as control). ( I ) RNA FISH for DDX11-AS1 and miR-1183 in human glioma sample. Data are expressed as the mean ± SEM, with statistical significance (* p < 0.05) determined by Student’s t test

Article Snippet: All cell cultures underwent validation via short tandem repeat profiling and confirmed absence of mycoplasma contamination. miR-1183 mimics (catalog #HY-R00073; MCE, Monmouth Junction, NJ, USA), miRNA negative controls (miR-NC; catalog #HY-R04602; MCE) and miR-1183 inhibitor (catalog #HY-RI00073; MCE) were acquired from MCE.

Techniques: In Silico, Binding Assay, Sequencing, Expressing, Knockdown, Over Expression, Luciferase, Activity Assay, Transfection, Mutagenesis, Pull Down Assay, Control

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: DDX11-AS1 promotes glioma cell proliferation and migration by targeting miR-1183. Glioma cells transfected with sh-NC, sh-DDX11-AS1 or sh-DDX11-AS1 followed by miR-1183 inhibitor treatment were used. ( A , B ) CCK-8 assays of ( A ) U87 and ( B ) U251 glioma cells ( n = 6). ( C , D ) Colony formation assays of ( C ) U87 and ( D ) U251 glioma cells ( n = 6). ( E ) Scratch wound healing assay of U87 and U251 glioma cells. ( F ) Transwell assay of U87 and U251 glioma cells. The right panel is the quantified data depicting migrated cell number ( n = 6). All data are represented as the mean ± SEM, * p < 0.05, sh-DDX11-AS1 vs. sh-NC; # p < 0.05, sh-DDX11-AS1 vs. sh-DDX11-AS1 + miR-1183 inhibitor (One-way ANOVA)

Article Snippet: All cell cultures underwent validation via short tandem repeat profiling and confirmed absence of mycoplasma contamination. miR-1183 mimics (catalog #HY-R00073; MCE, Monmouth Junction, NJ, USA), miRNA negative controls (miR-NC; catalog #HY-R04602; MCE) and miR-1183 inhibitor (catalog #HY-RI00073; MCE) were acquired from MCE.

Techniques: Migration, Transfection, CCK-8 Assay, Wound Healing Assay, Transwell Assay

Journal: Oncology Research

Article Title: Competitive Sequestration of miR-1183 by lncRNA DDX11-AS1 Drives Gliomagenesis through E2F7 Activation

doi: 10.32604/or.2025.065380

Figure Lengend Snippet: E2F7 is a target of miR-1183. ( A ) The bioinformatics analysis tools were used to predict the binding site of miR-1183 in E2F7. ( B ) Correlation between miR-1183 and E2F7 expression. ( C ) Luciferase activity in U87 cells co-transfected with miR-1183 and WT/MUT E2F7 reporter constructs ( n = 6). ( D – G ) U87 and U251 cells transfected with miR-1183, miR-NC or E2F7-overexpression vectors were used; ( D , E ) Relative expression of E2F7 was determined by RT-qPCR ( n = 6); ( F , G ) CCK-8 assay of ( F ) U87 and ( G ) U251 cells ( n = 6); ( H , I ) U87 and U251 cells transfected with sh-NC, sh-DDX11-AS1 or sh-DDX11-AS1 followed with miR-1183 inhibitor treatment were used. ( H ) Relative expression of E2F7 was determined by RT-qPCR ( n = 6). ( I ) Immunoblotting assays detected E2F7 and GAPDH in U87 and U251 cells. The bar chart quantifies relative E2F7 protein abundance normalized to GAPDH ( n = 6). All data are represented as the mean ± SEM, * p < 0.05, sh-DDX11-AS1 vs. sh-NC; # p < 0.05, sh-DDX11-AS1 vs. sh-DDX11-AS1 + miR-1183 inhibitor (One-way ANOVA)

Article Snippet: All cell cultures underwent validation via short tandem repeat profiling and confirmed absence of mycoplasma contamination. miR-1183 mimics (catalog #HY-R00073; MCE, Monmouth Junction, NJ, USA), miRNA negative controls (miR-NC; catalog #HY-R04602; MCE) and miR-1183 inhibitor (catalog #HY-RI00073; MCE) were acquired from MCE.

Techniques: Binding Assay, Expressing, Luciferase, Activity Assay, Transfection, Construct, Over Expression, Quantitative RT-PCR, CCK-8 Assay, Western Blot, Quantitative Proteomics

Journal: Frontiers in Pharmacology

Article Title: Profilin 1 Induces Tumor Metastasis by Promoting Microvesicle Secretion Through the ROCK 1/p-MLC Pathway in Non-Small Cell Lung Cancer

doi: 10.3389/fphar.2022.890891

Figure Lengend Snippet: PFN1 is correlated with NSCLC metastasis and could promote NSCLC cell migration in vitro . (A) Representative IHC images of PFN1 expression on the NSCLC tissues. (B) The staining index of PFN1 on the tissue chip. ** p < 0.01. (C) Representative IHC images of PFN1 expression on the tissue chip. (D) The expression of PFN1 in TCGA LUAD data. ** p < 0.01. (E) The Kaplan–Meier survival analysis of PFN1 in NSCLC patients. (Data source: TCGA LUAD dataset) (F,G) Wound healing assays conducted to evaluate the migration ability of PFN1 -overexpressing (F) and PFN1 knockdown (KD) (G) H1299 cells. ** p < 0.01; scale bar, 500 μm. (H,I) Transwell migration assays conducted to evaluate the migration of PFN1 -overexpressing (H) and PFN1 KD (I) H1299 cells. ** p < 0.01; scale bar, 500 μm. EV, empty vector; OE, PFN1 overexpression; NC, negative control; si-1/ 2, PFN1 siRNA1 1/2.

Article Snippet: PFN1 siRNA and control scramble siRNA were synthesized by Guangzhou RiboBio Co. (Guangzhou, China), and the sequences are listed in .

Techniques: Migration, In Vitro, Expressing, Staining, Knockdown, Plasmid Preparation, Over Expression, Negative Control

Journal: Frontiers in Pharmacology

Article Title: Profilin 1 Induces Tumor Metastasis by Promoting Microvesicle Secretion Through the ROCK 1/p-MLC Pathway in Non-Small Cell Lung Cancer

doi: 10.3389/fphar.2022.890891

Figure Lengend Snippet: PFN1 could promote MVs secretion in NSCLC. (A) Heatmap of differentially expressed proteins between EV and PFN1 OE cells. (B) GO enrichment analysis of differentially expressed proteins. (C) COG/KOG analysis of differentially expressed proteins. (D) MVs extracted from EV-expressing and PFN1 -overexpressing cells, using continuous differential centrifugation, identified using transmission electron microscopy. Scale bar, 100 nm. (E,F) Flow cytometry (E) and western blotting (F) were used to quantify MVs in PFN1 -overexpressing and EV-expressing cells. ARF6 and actin were used as MV markers. (G) Expression of PFN1 and annexin A1 in lung tumor tissues detected using immunofluorescence. (H) The staining index of p-MLC on the tissue chip. ** p < 0.01. (I) Representative IHC images of p-MLC expression. (J) Spearman rank correlation analysis was used to assess the relationship between PFN1 and p-MLC expression on the tissue chip; p and r values are shown in the plot.

Article Snippet: PFN1 siRNA and control scramble siRNA were synthesized by Guangzhou RiboBio Co. (Guangzhou, China), and the sequences are listed in .

Techniques: Expressing, Centrifugation, Transmission Assay, Electron Microscopy, Flow Cytometry, Western Blot, Immunofluorescence, Staining

Journal: Frontiers in Pharmacology

Article Title: Profilin 1 Induces Tumor Metastasis by Promoting Microvesicle Secretion Through the ROCK 1/p-MLC Pathway in Non-Small Cell Lung Cancer

doi: 10.3389/fphar.2022.890891

Figure Lengend Snippet: MVs derived from PFN1 OE cells promote migration in NSCLC cells. (A) MVs collected from sera of patients with NSCLC quantified using flow cytometry. ** p < 0.01. (B) Protein expression of ARF6 and β-actin in MVs collected from sera of patients with NSCLC detected using western blotting. (C) Effect of PFN1 -overexpressing cell supernatants on cell migration evaluated through wound healing assays. ** p < 0.01; scale bar, 500 μm. (D) PKH67-labeled MVs taken up by H1299 cells. DAPI was used to stain the nuclei of H1299 cells. Scale bar, 500 μm. (E,F) Wound healing (E) and Transwell migration (F) assays conducted to evaluate the migration of H1299 cells after treatment with MVs derived from EV-expressing and PFN1 -overexpressing cells; ** p < 0.01; scale bar, 500 μm.

Article Snippet: PFN1 siRNA and control scramble siRNA were synthesized by Guangzhou RiboBio Co. (Guangzhou, China), and the sequences are listed in .

Techniques: Derivative Assay, Migration, Flow Cytometry, Expressing, Western Blot, Labeling, Staining

Journal: Frontiers in Pharmacology

Article Title: Profilin 1 Induces Tumor Metastasis by Promoting Microvesicle Secretion Through the ROCK 1/p-MLC Pathway in Non-Small Cell Lung Cancer

doi: 10.3389/fphar.2022.890891

Figure Lengend Snippet: PFN1 promotes in vivo NSCLC metastasis by elevating MV secretion. (A) Schematic illustration of the mouse model of metastatic tumor established to determine the role of PFN1 in tumor metastasis. (B) Body weight changes in mice after intracardiac injection of PFN1 -overexpressing and EV-expressing cell lines. (C,D) Representative images of lung (C) and liver (D) metastases of the mouse model. The number of metastases is displayed in the right-hand side graph. * p < 0.05, ** p < 0.01. (E) Representative images of HE-stained lung tissues of the mouse model. (F) Representative IHC images of PFN1 and p-MLC expression in lung tissues. The staining index is shown in the right-hand side graph. ** p < 0.01. (G) Representative images of HE-stained liver tissues of the mouse model. (H) Representative IHC images of PFN1 and p-MLC expression in liver tissues. The staining index is shown in the right-hand side graph. ** p < 0.01. (I) Body weight changes in mice after intracardiac injection of H1299 cells and MVs. (J) Representative images of lung metastases of the mouse model. The number of metastases is shown in the bottom graph. * p < 0.05. (K) Representative images of HE-stained lung tissues of the mouse model. (L) Representative IHC images of PFN1 and p-MLC expression in lung tissues. The staining index is shown in the right-hand side graph; * p < 0.05.

Article Snippet: PFN1 siRNA and control scramble siRNA were synthesized by Guangzhou RiboBio Co. (Guangzhou, China), and the sequences are listed in .

Techniques: In Vivo, Injection, Expressing, Staining

Journal: Frontiers in Pharmacology

Article Title: Profilin 1 Induces Tumor Metastasis by Promoting Microvesicle Secretion Through the ROCK 1/p-MLC Pathway in Non-Small Cell Lung Cancer

doi: 10.3389/fphar.2022.890891

Figure Lengend Snippet: Mechanisms underlying the promotion of MLC phosphorylation by PFN1. (A,B) Protein expression after PFN1 overexpression (A) and knockdown (B) measured using western blotting. (C) Protein expression in PFN1 mutants measured using western blotting. (D) PFN1 interactions with ROCK1/2 confirmed using co-IP. (E) Protein expression after treatment with Y27632 (10 µM) measured using western blotting. (F) Effect of PFN1 on ROCK1 activity. ** p < 0.01. (G) Effect of PFN1 on ROCK2 activity. (H) Flow cytometry measuring changes in the amount of MVs after treatment with Y27632; * p < 0.05.

Article Snippet: PFN1 siRNA and control scramble siRNA were synthesized by Guangzhou RiboBio Co. (Guangzhou, China), and the sequences are listed in .

Techniques: Phospho-proteomics, Expressing, Over Expression, Knockdown, Western Blot, Co-Immunoprecipitation Assay, Activity Assay, Flow Cytometry

Journal: Frontiers in Pharmacology

Article Title: Profilin 1 Induces Tumor Metastasis by Promoting Microvesicle Secretion Through the ROCK 1/p-MLC Pathway in Non-Small Cell Lung Cancer

doi: 10.3389/fphar.2022.890891

Figure Lengend Snippet: ROCK1 inhibitor Y27632 partially reversed the promotion of lung cancer metastasis by PFN1 in vitro and in vivo . (A,B) Wound healing assays conducted to evaluate the effect of Y27632 (A) and Y27632 combined with MVs (B) on cell migration. ** p < 0.01; scale bar, 500 μm. (C) Transwell migration assays conducted to evaluate the effect of Y27632 and Y27632 combined with MVs on cell migration. ** p < 0.01; scale bar, 500 μm. (D) Schematic diagram of the mouse model of metastatic tumor established to determine the effect of Y27632 on PFN1-induced lung cancer metastasis. (E) Body weight changes in mice after intracardiac injection of PFN1 -overexpressing H1299 cells and intraperitoneal injection of Y27632 (10 mg/kg). (F) Representative images of lung and liver metastatic tissue in mice. The number of metastatic nodules is shown in the right-hand side graph. * p < 0.05. (G,H) Representative images of HE-stained lung (G) and liver (H) metastases. (I) Representative IHC images of PFN1 and p-MLC expression in lung tissues. The staining index is shown in the right-hand side graph. ** p < 0.01. (J) Representative IHC images of PFN1 and p-MLC expression in liver tissues. The staining index is shown in the right-hand side graph; ** p < 0.01.

Article Snippet: PFN1 siRNA and control scramble siRNA were synthesized by Guangzhou RiboBio Co. (Guangzhou, China), and the sequences are listed in .

Techniques: In Vitro, In Vivo, Migration, Injection, Staining, Expressing

Journal: Frontiers in Pharmacology

Article Title: Profilin 1 Induces Tumor Metastasis by Promoting Microvesicle Secretion Through the ROCK 1/p-MLC Pathway in Non-Small Cell Lung Cancer

doi: 10.3389/fphar.2022.890891

Figure Lengend Snippet: Schematic diagram of the role of PFN1 in NSCLC metastasis. In the initiation stage of NSCLC, cells with upregulated PFN1 secret more MVs through PFN1 interactions with the ROCK/p-MLC pathway. These MVs contain numerous oncogenenic moleculars, which could enhance migration abilities of PFN1 normal expressed NSCLC cells, and untimately promote progression and metastasis of NSCLC.

Article Snippet: PFN1 siRNA and control scramble siRNA were synthesized by Guangzhou RiboBio Co. (Guangzhou, China), and the sequences are listed in .

Techniques: Migration

Journal: Molecular Cancer

Article Title: Circular RNA circNHSL1 promotes gastric cancer progression through the miR-1306-3p/SIX1/vimentin axis

doi: 10.1186/s12943-019-1054-7

Figure Lengend Snippet: CircNHSL1 promotes gastric cancer progression by serving as a miRNA sponge of miR-1306-3p. a Pearson correlation analysis determined the significantly negative correlation between the levels of circNHSL1 and miR-1306-3p in 61 paired gastric cancer tissues (p < 0.01). b The effects of circNHSL1 on the expression of SIX1 was detected by qRT-PCR. c The effects of mimics, inhibitor and negative control on the luciferase activities were detected in gastric cancer cells after transfecting luciferase reporter plasmids with wild type of WT, Mutant or negative control. d Schematic illustration of the sequence of wild type of SIX1 3′-UTR (WT) and mutant sequences on the complementary sites of SIX1 3′-UTR with miR-1306-3p (Mutant). e and f Anti-AGO2 RIP assay was performed in MKN-28 cells after transfection with mimics or negative control, followed by agarose gel electrophoresis ( e ) and qRT-PCR ( f ) to detect the expression of circNHSL1 and miR-1306-3p. g The effects of circNHSL1 and miR-1306-3p on the luciferase activities of wild type of SIX1 mRNA 3′-UTR in gastric cancer cells were detected. h and i The effects of circNHSL1 and miR-1306-3p on the mRNA and protein expressions of SIX1 and Vimentin were detected by qRT-PCR and western blotting. j and k The effects of circNHSL1 and miR-1306-3p on the mobility, migration and invasion were confirmed by wound healing and transwell assays. All data are presented as the mean ± SEM of three experiments. ** p < 0.01

Article Snippet: The mimics, inhibitor and negative controls for hsa-miR-1306-3p were purchased from RiBoBio (Guangzhou, China).

Techniques: Expressing, Quantitative RT-PCR, Negative Control, Luciferase, Mutagenesis, Sequencing, Transfection, Agarose Gel Electrophoresis, Western Blot, Migration

Journal: Molecular Cancer

Article Title: Circular RNA circNHSL1 promotes gastric cancer progression through the miR-1306-3p/SIX1/vimentin axis

doi: 10.1186/s12943-019-1054-7

Figure Lengend Snippet: MiR-1306-3p is down-regulated in gastric cancer tissues and correlated with the progression and poor prognosis. The expression of miR-1306-3p was detected by ISH with TMA including 54 paired gastric cancer tissues and paired normal tissues. a Represent images of miR-1306-3p expression in normal gastric mucosa and gastric cancer tissues with Stage II, Stage III, M0, M1, G1, G2, G3, pT2, pT3 and pT4. b The level of miR-1306-3p in gastric cancer tissues was significantly lower than in normal gastric tissues. c-f The level of miR-1306-3p in gastric cancer tissues with Stage II ( c ), M0 ( d ), well differentiation ( e ) and pT2 and pT3 ( f ) was significantly higher than these with Stage III, M1, moderate and poor differentiation and pT4. g - h Kaplan-Meier survival analysis (log-rank test) showed that gastric cancer patients with low miR-1306-3p expression have a lower OS and DFS than these with high miR-1306-3p expression ( p < 0.01). All data are presented as the mean ± SEM. ** p < 0.01

Article Snippet: The mimics, inhibitor and negative controls for hsa-miR-1306-3p were purchased from RiBoBio (Guangzhou, China).

Techniques: Expressing

Journal: Experimental and Therapeutic Medicine

Article Title: Natural emodin reduces myocardial ischemia/reperfusion injury by modulating the RUNX1/miR‑142‑3p/DRD2 pathway and attenuating inflammation

doi: 10.3892/etm.2022.11681

Figure Lengend Snippet: miR-142-3p negatively regulates the expression of DRD2. (A) Reverse transcription-quantitative PCR for the identification of the downstream target gene of miR-142-3p by overexpressing miR-142-3p mimic in H9c2 cells. n=4. (B) The DRD2 protein levels were detected by western blotting in cardiac tissues with MIRI or miR-142-3p antagomir (anti-ago) treatment. (C) Summary for the protein expression of DRD2 based on (B), n=3. (D) DRD2 protein levels were detected by western blotting in H9c2 cells with H/R injury or emodin treatment. (E) Summary for the protein expression of DRD2 based on (D), n=3. (F) DRD2 protein levels were measured using western blotting in cardiac tissues with MIRI or emodin treatment. Three bands represent three independent samples. (G) Summary for the protein expression of DRD2 based on (F), n=3. * P<0.05, ** P<0.01. NC, negative control; MIRI, myocardial ischemia/reperfusion injury; anti-ago, antagomir; DRD2, dopamine receptor D2; Ctrl, control; miR, microRNA; H/R, hypoxia/reoxygenation.

Article Snippet: The mmu-miR-142-3p antagomir (miR-142-3p anti-ago; cat. no. miR-311620131514-4-5) and negative control antagomir (NC anti-ago; cat. no. miR3N0000001-4-5) were purchased from Guangzhou RiboBio Co., Ltd., and administered by tail vein injection with 5 nmol three times (once every two days).

Techniques: Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Negative Control, Control

Journal: Experimental and Therapeutic Medicine

Article Title: Natural emodin reduces myocardial ischemia/reperfusion injury by modulating the RUNX1/miR‑142‑3p/DRD2 pathway and attenuating inflammation

doi: 10.3892/etm.2022.11681

Figure Lengend Snippet: Inhibition of miR-142-3p or overexpression of DRD2 suppresses NF-κB-mediated inflammation in MIRI model of mice. The secretions of inflammatory cytokines (A) IL-6 and (B) TNF-α in cardiac tissues with MIRI of mice were measured by ELISA under the conditions of pretreatment with miR-142-3p antagomir (anti-ago) or overexpression of AAV-DRD2. n=4. (C) P65 and p-P65 were detected using western blotting to determine the activity of NF-κB. (D) Bar diagram showing the protein expression of p-P65 based on (C). n=3. (E) The schematic model for the anti-inflammation action of emodin in MIRI model of mice. ** P<0.01. DRD2, dopamine receptor D2; MIRI, myocardial ischemia/reperfusion injury; anti-ago, antagomir; AAV, adeno-associated virus; p-, phosphorylated-; Ctrl, control; miR, microRNA.

Article Snippet: The mmu-miR-142-3p antagomir (miR-142-3p anti-ago; cat. no. miR-311620131514-4-5) and negative control antagomir (NC anti-ago; cat. no. miR3N0000001-4-5) were purchased from Guangzhou RiboBio Co., Ltd., and administered by tail vein injection with 5 nmol three times (once every two days).

Techniques: Inhibition, Over Expression, Enzyme-linked Immunosorbent Assay, Western Blot, Activity Assay, Expressing, Virus, Control

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, oe-DNMT3B and control oe-negative control (NC) used for cell transfection were from VectorBuilder (Guangzhou, Guangdong, China).

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, oe-DNMT3B and control oe-negative control (NC) used for cell transfection were from VectorBuilder (Guangzhou, Guangdong, China).

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, oe-DNMT3B and control oe-negative control (NC) used for cell transfection were from VectorBuilder (Guangzhou, Guangdong, China).

Techniques: Over Expression, Expressing, Methylation, Activity Assay