Review

tead1 (OriGene)

OriGene is a verified supplier

OriGene manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

OriGene tead1
Tead1, supplied by OriGene, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+tead1/TEF1+(TEAD1)+(NM_021961)+Human+Tagged+ORF+Clone/10__1161_slash_circulationaha__125__076218-120-5-6
Average 94 stars, based on 2 article reviews

tead1 - by Bioz Stars, 2026-10

94/100 stars

Images

Expressing:

Article Title: Targeting TEAD/YAP-transcription-dependent necrosis, TRIAD, ameliorates Huntington's disease pathology.
Article Snippet: Luciferase assay 2 × 10 4 293T cells were transiently transfected with 125ng of 8xGTIIC-luciferase (Addgene, MA, USA) or pGL3-Bax-Luc (80) with 85 ng of pGL4.74[hRluc/TK] at SU N Y H ealth Science C enter at B rooklyn on Septem ber 14, 2016 http://hm g.oxfordjournals.org/ D ow nloaded from 63 (Promega, WI, USA), and 85ng of expression vectors or 5 pmol of siRNAs using Lipofectamine 2000 (Invitrogen, MA, USA). .. The expression vectors were pCI-FL-YAP, pCI-YAP∆C (5), human TEAD1 (Origene, MD, USA, Cat. #SC112830), TEAD2 (Origene, MD, USA, Cat. #SC320274), TEAD3 (Origene, MD, USA, Cat. #SC313452), TEAD4 (Origene, MD, USA, Cat. #SC111037) cDNA, pcDNA-HA-p73alpha (81). .. Pre-designated Gene Solution siRNA for human YAP (Santa Cruz, TX, USA, Cat. #sc-38637), TEAD1 (Hs_TEAD1_5-8) or AllStars negative control were purchased from Qiagen (Limburg, Netherland, Cat. #SI03650318) The sense sequences of humanTEAD1 (_5-8), and non-sense control siRNA were 5’-CACATTGGGCATGCCAACCAT-3’, 5’-CGCCGCTTCATTGCACATTCA-3’, 5’-ATGGCCGATTTGTATACCGAA-3’, 5’-CCCGTAAGCAGTGCCTTAGTA-3’, and 5’-CGUUAAUCGCGUAUAAUACGCGUAT-3’respectively.

Image Search Results

(A) UMAP showing expression profiles of HSP90AA1 , EPCAM , YAP1 , and BIRC5 genes in all PC cells from single cell RNA-seq (scRNA-seq) data. (B) Violin plot showing YAP1 and BIRC5 expressions according to long-term and short-term survivors of GAC patients from scRNA-seq data. (C) YAP1 and BIRC5 gene expressions according to tumor, adjacent normal, and normal tissue in GAC patients’ samples from TCGA-STAD and GTEX cohort. Jonckheere–Terpstra test was used for trend analysis. (D) Gene set enrichment analysis (GSEA) of hallmark geneset from Reverse-phase protein arrays (RPPA) results of AUY922-treated GA0518 cells (25 nM for 48 h, N = 3) compared to vehicle control. (E) Heatmap of phosphorylated protein expressions from RPPA results. (F) Barplots of TEAD1-4 and phospho-YAP1 (Ser127) expression changes from RPPA results. (G) Immunoblotting showing protein expression changes after vehicle control or AUY922 treatments with corresponding concentration for 48 h in AGS and GA0518 cells. (H) Representative image of immunofluorescence staining of YAP1 (red) in AGS and GA0518 cells after AUY922 treatment (25 nM for 48 h, N = 3). Nuclei were counterstained with DAPI (blue). Scale bars indicate 5um. (I) Quantification of YAP1/DAPI ratio in nuclei of AGS and GA0518 cells after vehicle control or AUY922 treatment. Three replicates were analyzed. (J) Immunoblotting showing Hippo pathway protein expressions after vehicle control or AUY922 treatments with corresponding concentration for 48 h in AGS and GA0518 cells. Data are presented as mean ± SD. Statistical significance compared to control was calculated using two-sided Student’s t-tests or one-way ANOVA, followed by post-hoc Tukey’s HSD tests according to sample style. P -values were indicated in the graph. N represents the number of biological replicates.

Journal: Cancer letters

Article Title: HSP90 inhibitor AUY922 suppresses tumor growth and modulates immune response through YAP1-TEAD pathway inhibition in gastric cancer

doi: 10.1016/j.canlet.2024.217354

Figure Lengend Snippet: (A) UMAP showing expression profiles of HSP90AA1 , EPCAM , YAP1 , and BIRC5 genes in all PC cells from single cell RNA-seq (scRNA-seq) data. (B) Violin plot showing YAP1 and BIRC5 expressions according to long-term and short-term survivors of GAC patients from scRNA-seq data. (C) YAP1 and BIRC5 gene expressions according to tumor, adjacent normal, and normal tissue in GAC patients’ samples from TCGA-STAD and GTEX cohort. Jonckheere–Terpstra test was used for trend analysis. (D) Gene set enrichment analysis (GSEA) of hallmark geneset from Reverse-phase protein arrays (RPPA) results of AUY922-treated GA0518 cells (25 nM for 48 h, N = 3) compared to vehicle control. (E) Heatmap of phosphorylated protein expressions from RPPA results. (F) Barplots of TEAD1-4 and phospho-YAP1 (Ser127) expression changes from RPPA results. (G) Immunoblotting showing protein expression changes after vehicle control or AUY922 treatments with corresponding concentration for 48 h in AGS and GA0518 cells. (H) Representative image of immunofluorescence staining of YAP1 (red) in AGS and GA0518 cells after AUY922 treatment (25 nM for 48 h, N = 3). Nuclei were counterstained with DAPI (blue). Scale bars indicate 5um. (I) Quantification of YAP1/DAPI ratio in nuclei of AGS and GA0518 cells after vehicle control or AUY922 treatment. Three replicates were analyzed. (J) Immunoblotting showing Hippo pathway protein expressions after vehicle control or AUY922 treatments with corresponding concentration for 48 h in AGS and GA0518 cells. Data are presented as mean ± SD. Statistical significance compared to control was calculated using two-sided Student’s t-tests or one-way ANOVA, followed by post-hoc Tukey’s HSD tests according to sample style. P -values were indicated in the graph. N represents the number of biological replicates.

Article Snippet: The following primary antibodies were utilized at specified dilutions: human YAP1 (Santa Cruz Biotechnology, Cat#sc101199, 1:50), human BIRC5 (Survivin) (Cell Signaling Technology (CST), Cat#2803, 1:500), human CTGF (Santa Cruz Biotechnology, Cat#sc365970, 1:50), human Ki67 (Fisher Scientific, Cat# RM-9106-S1, 1:150), human TEAD1 (CST, Cat#12292, 1:100), human TEAD4 (Abcam, Cat#58310, 1:100), human HLA class-I ABC (Proteintech, Cat#15240-1-AP, 1:100), mouse CD8α (CST, Cat#98941, 1:100), mouse CD206 (Abcam, Cat#64693, 1:100), mouse F4/80 (CST, Cat#70076, 1:100).

Techniques: Expressing, RNA Sequencing, Control, Western Blot, Concentration Assay, Immunofluorescence, Staining

(A) RT-qPCR analysis of down-stream target genes YAP1/TEAD signaling in AGS cells after vehicle control or AUY922 treatment with corresponding concentrations for 48 h (N = 3). Only significant statistical results are shown. (B) Representative image of co-immunofluorescent staining of BIRC5 (green), and CTGF (red) in the vehicle- or AUY922-treated AGS cells. Nuclei were counterstained with DAPI (blue). The scale bars indicate 25um. (C – D) Luciferase reporter assay measuring YAP1/TEAD transcriptional activity in AGS (C) and GA0518 (D) cells. The cells were treated with vehicle control or AUY922 (25 nM for 40 h after transfection; N = 3). (E – F) Immunoblots represent immunoprecipitated AGS (E) and GA0518 (F) cells after treatment of vehicle control or 25 nM AUY922 for 48 h. GAC cell lysates were immunoprecipitated (IP) with anti-YAP1 and anti-HSP90α or normal IgG antibody, and immunoblotted (IB) for YAP1, HSP90α, and TEAD1. (G – H) Quantitative ChIP-qPCR analysis of the CTGF (G) and YAP1 (H) promoter spanning the TEAD1 binding site after pulling down with YAP1, HSP90α, or IgG antibody in AGS and GA0518 cells treated with vehicle control or AUY922 (25 nM for 48 h; N = 3 per group). (I) Protein expression of YAP1 and TAZ in YAP1-KO GA0518 cells (clone#C and clone#D) compared to control. (J) Cell proliferation rates of YAP1-KO and corresponding parental control GA0518 cells under vehicle control or 10 nM AUY922 (N = 4 per group). †† indicates statistical significance (P < 0.0001) between control and AUY922 groups in YAP1-KO GA0518 cells. (K) Cell confluency ratio of 1 YAP1-KO and corresponding parental control GA0518 cells under vehicle control or 10 nM AUY922 (N = 4 per group). Overall, data are presented as mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001, **** P < 0.0001 unless otherwise indicated in the graph. Statistical significance compared to control was calculated using one-way ANOVA, and post-hoc Tukey’s HSD tests. P -values were indicated in the graph, and N represents the number of biological replicates.

Journal: Cancer letters

Article Title: HSP90 inhibitor AUY922 suppresses tumor growth and modulates immune response through YAP1-TEAD pathway inhibition in gastric cancer

doi: 10.1016/j.canlet.2024.217354

Figure Lengend Snippet: (A) RT-qPCR analysis of down-stream target genes YAP1/TEAD signaling in AGS cells after vehicle control or AUY922 treatment with corresponding concentrations for 48 h (N = 3). Only significant statistical results are shown. (B) Representative image of co-immunofluorescent staining of BIRC5 (green), and CTGF (red) in the vehicle- or AUY922-treated AGS cells. Nuclei were counterstained with DAPI (blue). The scale bars indicate 25um. (C – D) Luciferase reporter assay measuring YAP1/TEAD transcriptional activity in AGS (C) and GA0518 (D) cells. The cells were treated with vehicle control or AUY922 (25 nM for 40 h after transfection; N = 3). (E – F) Immunoblots represent immunoprecipitated AGS (E) and GA0518 (F) cells after treatment of vehicle control or 25 nM AUY922 for 48 h. GAC cell lysates were immunoprecipitated (IP) with anti-YAP1 and anti-HSP90α or normal IgG antibody, and immunoblotted (IB) for YAP1, HSP90α, and TEAD1. (G – H) Quantitative ChIP-qPCR analysis of the CTGF (G) and YAP1 (H) promoter spanning the TEAD1 binding site after pulling down with YAP1, HSP90α, or IgG antibody in AGS and GA0518 cells treated with vehicle control or AUY922 (25 nM for 48 h; N = 3 per group). (I) Protein expression of YAP1 and TAZ in YAP1-KO GA0518 cells (clone#C and clone#D) compared to control. (J) Cell proliferation rates of YAP1-KO and corresponding parental control GA0518 cells under vehicle control or 10 nM AUY922 (N = 4 per group). †† indicates statistical significance (P < 0.0001) between control and AUY922 groups in YAP1-KO GA0518 cells. (K) Cell confluency ratio of 1 YAP1-KO and corresponding parental control GA0518 cells under vehicle control or 10 nM AUY922 (N = 4 per group). Overall, data are presented as mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001, **** P < 0.0001 unless otherwise indicated in the graph. Statistical significance compared to control was calculated using one-way ANOVA, and post-hoc Tukey’s HSD tests. P -values were indicated in the graph, and N represents the number of biological replicates.

Techniques: Activity Assay, Quantitative RT-PCR, Control, Staining, Luciferase, Reporter Assay, Transfection, Western Blot, Immunoprecipitation, ChIP-qPCR, Binding Assay, Expressing

(A) Experimental design of the orthotopic PDX Model. 0.5 × 10 6 GA0518-mCh2 cells were orthotopically inoculated on the stomach wall in NOD/SCID mice. Vehicle control or AUY922 (25 mg/kg, weekly) treatment was initiated 3 days after tumor cell inoculation (N = 10 per group). (B) Representative image of H&E staining of resected inoculated tumor on the stomach wall. The scale bars are indicated in the figure. (C) Representative in-vivo bioluminescence images of the orthotopic PDX models on Day 17. (D) Quantification of the bioluminescence images of tumor burden in orthotopic PDX models on Day 17 (N = 10 per group). (E) Representative macro images of the resected stomach of the orthotopic PDX models at sacrifice. Tumor parts are indicated with a yellow dashed line. (F) Final weight of the extracted orthotopic tumors at the endpoint (N = 10 per group). (G) Immunofluorescent stainings of Ki67, YAP1, TEAD1, TEAD4, and BIRC5 expressions (green) in the tumor tissues according to experimental groups as Indicated. Nuclei were counterstained with DAPI (blue). The scale bars indicate 50um. (H) Quantification of the immunofluorescent Ki67, YAP1, TEAD1, TEAD4, and BIRC5 positivity. The ratios of positively stained cells per DAPI-stained cells were analyzed (N = 4 per group). Data are presented as mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001, **** P < 0.0001 unless otherwise indicated in the graph. Statistical significance compared to the control was calculated using two-sided Student’s t-tests. N represents the number of biological replicates.

Journal: Cancer letters

Article Title: HSP90 inhibitor AUY922 suppresses tumor growth and modulates immune response through YAP1-TEAD pathway inhibition in gastric cancer

doi: 10.1016/j.canlet.2024.217354

Figure Lengend Snippet: (A) Experimental design of the orthotopic PDX Model. 0.5 × 10 6 GA0518-mCh2 cells were orthotopically inoculated on the stomach wall in NOD/SCID mice. Vehicle control or AUY922 (25 mg/kg, weekly) treatment was initiated 3 days after tumor cell inoculation (N = 10 per group). (B) Representative image of H&E staining of resected inoculated tumor on the stomach wall. The scale bars are indicated in the figure. (C) Representative in-vivo bioluminescence images of the orthotopic PDX models on Day 17. (D) Quantification of the bioluminescence images of tumor burden in orthotopic PDX models on Day 17 (N = 10 per group). (E) Representative macro images of the resected stomach of the orthotopic PDX models at sacrifice. Tumor parts are indicated with a yellow dashed line. (F) Final weight of the extracted orthotopic tumors at the endpoint (N = 10 per group). (G) Immunofluorescent stainings of Ki67, YAP1, TEAD1, TEAD4, and BIRC5 expressions (green) in the tumor tissues according to experimental groups as Indicated. Nuclei were counterstained with DAPI (blue). The scale bars indicate 50um. (H) Quantification of the immunofluorescent Ki67, YAP1, TEAD1, TEAD4, and BIRC5 positivity. The ratios of positively stained cells per DAPI-stained cells were analyzed (N = 4 per group). Data are presented as mean ± SD. * P < 0.05; ** P < 0.01; *** P < 0.001, **** P < 0.0001 unless otherwise indicated in the graph. Statistical significance compared to the control was calculated using two-sided Student’s t-tests. N represents the number of biological replicates.

Techniques: In Vivo, Derivative Assay, Control, Staining

Graphical illustration outlines the mechanism of AUY922 in GAC. AUY922 inhibits the aggressive tumor characteristics of GAC by disrupting the YAP1-TEAD axis by inhibiting the interaction among HSP90, YAP1, and TEAD1, as well as subsequent TEAD transcriptional activity. Simultaneously, AUY922 promotes Hippo pathway activity through the phosphorylation of YAP1 (Ser127) and dephosphorylation of LATS1/2 and MST1/2. AUY922 additionally induces changes in the tumor immune microenvironment, shifting it toward an inflamed state, which enhances the responsiveness to immunotherapy.

Journal: Cancer letters

Article Title: HSP90 inhibitor AUY922 suppresses tumor growth and modulates immune response through YAP1-TEAD pathway inhibition in gastric cancer

doi: 10.1016/j.canlet.2024.217354

Figure Lengend Snippet: Graphical illustration outlines the mechanism of AUY922 in GAC. AUY922 inhibits the aggressive tumor characteristics of GAC by disrupting the YAP1-TEAD axis by inhibiting the interaction among HSP90, YAP1, and TEAD1, as well as subsequent TEAD transcriptional activity. Simultaneously, AUY922 promotes Hippo pathway activity through the phosphorylation of YAP1 (Ser127) and dephosphorylation of LATS1/2 and MST1/2. AUY922 additionally induces changes in the tumor immune microenvironment, shifting it toward an inflamed state, which enhances the responsiveness to immunotherapy.

Techniques: Inhibition, Activity Assay, Phospho-proteomics, De-Phosphorylation Assay

Fig. 4 | DNA binding thermodynamics of OC2 base-speciﬁc mutants. a–c ITC binding analysis of OC2SQ, OC2N and OC2RR, to PEG10 DNA. The raw heats (differential power, DP) for each injection are shown on top and binding isotherms are shown in the bottom. The data shown is representative of three independent experiments (n = 3; technical replicates). Source data are provided as a Source Data ﬁle.

Journal: Nature communications

Article Title: The homeodomain regulates stable DNA binding of prostate cancer target ONECUT2.

doi: 10.1038/s41467-024-53159-8

Figure Lengend Snippet: Fig. 4 | DNA binding thermodynamics of OC2 base-speciﬁc mutants. a–c ITC binding analysis of OC2SQ, OC2N and OC2RR, to PEG10 DNA. The raw heats (differential power, DP) for each injection are shown on top and binding isotherms are shown in the bottom. The data shown is representative of three independent experiments (n = 3; technical replicates). Source data are provided as a Source Data ﬁle.

Article Snippet: Protein expression and purification The human OC2 DNA binding region spanning residues 330–485 (OC2) was cloned into pET-His6-TEV-LIC expression plasmid (Addgene Plasmid #29653).

Techniques: Binding Assay, Injection

Figure 5. AP000695.2 promotes TEAD1-mediated transcription of GLUT1 (A) Spearman correlation analysis in The Cancer Genome Atlas (TCGA) database showed that there is a positive correlation between AP000695.2 expression and TEAD1 mRNA expression (r = 0.2829). A significant positive correlation between the expression of TEAD1 mRNA and the mRNA expression of various glycolysis-related factors was observed. (B) Cellular experiments showed that the protein expression level of TEAD1 was increased after overexpression of AP000695.2, but decreased after the downregulation of AP000695.2. (C) In the GLUT1 Promoter, wt group, the expression of luciferase was significantly increased after overexpression of TEAD1. In the GLUT1 Promoter, mt group, the expression of luciferase was significantly increased after overexpression of TEAD1, and the expression level of luciferase in GLUT1 Promoter, wt group was significantly higher than that of GLUT1 Promoter, mt group after overexpression of TEAD1. MCS indicates negative control while TEAD1 indicates TEAD1 overexpression plasmid. (D) The expression of TEAD1 in TEAD1 overexpression (TEAD1) group was significantly higher than that in the NC group. (E) qPCR analysis showed that the mRNA expression level of GLUT1 in A549 and H1299 cell lines was increased after upregulating the expression of TEAD1. (F) Western blot analysis showed that the protein expression levels of GLUT1, HK2, PKM2 and LDHA in A549 and H1299 cell lines were increased after upregulating the expression of TEAD1. (G) Western blot analysis showed that the protein expression level of HIF-1α in A549 and H1299 cell lines was increased after upregulating the expression of TEAD1. *P<0.05, **P<0.01, ***P<0.001.

Journal: Acta biochimica et biophysica Sinica

Article Title: LncRNA AP000695.2 promotes glycolysis of lung adenocarcinoma via the miR-335-3p/TEAD1 axis.

doi: 10.3724/abbs.2023227

Figure Lengend Snippet: Figure 5. AP000695.2 promotes TEAD1-mediated transcription of GLUT1 (A) Spearman correlation analysis in The Cancer Genome Atlas (TCGA) database showed that there is a positive correlation between AP000695.2 expression and TEAD1 mRNA expression (r = 0.2829). A significant positive correlation between the expression of TEAD1 mRNA and the mRNA expression of various glycolysis-related factors was observed. (B) Cellular experiments showed that the protein expression level of TEAD1 was increased after overexpression of AP000695.2, but decreased after the downregulation of AP000695.2. (C) In the GLUT1 Promoter, wt group, the expression of luciferase was significantly increased after overexpression of TEAD1. In the GLUT1 Promoter, mt group, the expression of luciferase was significantly increased after overexpression of TEAD1, and the expression level of luciferase in GLUT1 Promoter, wt group was significantly higher than that of GLUT1 Promoter, mt group after overexpression of TEAD1. MCS indicates negative control while TEAD1 indicates TEAD1 overexpression plasmid. (D) The expression of TEAD1 in TEAD1 overexpression (TEAD1) group was significantly higher than that in the NC group. (E) qPCR analysis showed that the mRNA expression level of GLUT1 in A549 and H1299 cell lines was increased after upregulating the expression of TEAD1. (F) Western blot analysis showed that the protein expression levels of GLUT1, HK2, PKM2 and LDHA in A549 and H1299 cell lines were increased after upregulating the expression of TEAD1. (G) Western blot analysis showed that the protein expression level of HIF-1α in A549 and H1299 cell lines was increased after upregulating the expression of TEAD1. *P<0.05, **P<0.01, ***P<0.001.

Article Snippet: TEAD1 overexpression plasmid (Origene, Rockville, USA) and si-TEAD1 (target sequence: 5′- Xu et al. Acta Biochim Biophys Sin 2023 GGATCCTCACAAGACGTCA-3′; RiboBio, Guangzhou, China) were used to regulate TEAD1 expression. miR-335-3p mimics, negative control (NC), miR-335-3p inhibitor and inhibitor NC (Synbio-tech) were used for the overexpression and knockdown of miR-335-3p.

Techniques: Expressing, Over Expression, Luciferase, Negative Control, Plasmid Preparation, Western Blot

Figure 6. AP000695.2 promotes LUAD glycolysis, proliferation and migration via TEAD1 (A) The relative amount of FDG uptake of the L+sT group (transfected with AP000695.2 overexpression plasmid and TEAD1 siRNA) was lower than that of the L+s-NC (transfected with AP000695.2 overexpression plasmid and TEAD1 siRNA NC) group. The amount of FDG uptake in the s+T (transfected with AP000695.2 siRNA and TEAD1 overexpression plasmid) group was higher than that of the s+T-NC group (transfected with AP000695.2 siRNA and NC of TEAD1 overexpression plasmid). (B) The amount of lactic acid production in the L+sT group was lower than that in the L+s-NC group. The amount of lactic acid produced in the s+T group was higher than that in the s+T-NC group. (C) The level of glycolysis, glycolytic capacity and glycolytic reverse in the L+sT group were lower than those in the L+s-NC group. The level of glycolysis, glycolytic capacity and glycolytic reverse in the s+T group were higher than those of the s+T-NC group. (D) The cell proliferation ability of the L+sT group was lower than that of the L+s-NC group, and that of the s+T group was higher than that of the s+T-NC group on the 2nd and 3rd day after transfection. (E) The cell migration ability of the L+sT group was lower than that of the L+s-NC group, and that of the s+T group was higher than that of the s+T-NC group (magnification×200, scale bar: 100 μm). (F) The cell migration ability of the L+sT group was lower than that of the L+s-NC group, and that of the s+T group was higher than that of the s+T- NC group (magnification×100). **P<0.01, ***P<0.001.

Journal: Acta biochimica et biophysica Sinica

Article Title: LncRNA AP000695.2 promotes glycolysis of lung adenocarcinoma via the miR-335-3p/TEAD1 axis.

doi: 10.3724/abbs.2023227

Figure Lengend Snippet: Figure 6. AP000695.2 promotes LUAD glycolysis, proliferation and migration via TEAD1 (A) The relative amount of FDG uptake of the L+sT group (transfected with AP000695.2 overexpression plasmid and TEAD1 siRNA) was lower than that of the L+s-NC (transfected with AP000695.2 overexpression plasmid and TEAD1 siRNA NC) group. The amount of FDG uptake in the s+T (transfected with AP000695.2 siRNA and TEAD1 overexpression plasmid) group was higher than that of the s+T-NC group (transfected with AP000695.2 siRNA and NC of TEAD1 overexpression plasmid). (B) The amount of lactic acid production in the L+sT group was lower than that in the L+s-NC group. The amount of lactic acid produced in the s+T group was higher than that in the s+T-NC group. (C) The level of glycolysis, glycolytic capacity and glycolytic reverse in the L+sT group were lower than those in the L+s-NC group. The level of glycolysis, glycolytic capacity and glycolytic reverse in the s+T group were higher than those of the s+T-NC group. (D) The cell proliferation ability of the L+sT group was lower than that of the L+s-NC group, and that of the s+T group was higher than that of the s+T-NC group on the 2nd and 3rd day after transfection. (E) The cell migration ability of the L+sT group was lower than that of the L+s-NC group, and that of the s+T group was higher than that of the s+T-NC group (magnification×200, scale bar: 100 μm). (F) The cell migration ability of the L+sT group was lower than that of the L+s-NC group, and that of the s+T group was higher than that of the s+T- NC group (magnification×100). **P<0.01, ***P<0.001.

Techniques: Migration, Transfection, Over Expression, Plasmid Preparation, Produced

Figure 7. miR-335-3p acts as a competing endogenous RNA participating in the regulation of TEAD1 and AP000695.2 (A) The binding site of TEAD1 and miR-335-3p and the binding site of miR-335-3p and AP000695.2. (B) qPCR experiment showed that the expression of miR-335-3p in A549 cells was decreased after upregulating AP000695.2 expression. The expression of miR-335-3p in H1299 cells was increased after AP000695.2 was downregulated. (C) The expression of miR-335-3p in A549 and H299 cells was increased after the transfection of miR-335-3p mimics. (D) Western blot analysis showed that the protein expression of TEAD1 was decreased after the transfection with miR-335-3p mimics, and increased after the transfection with miR-335-3p inhibitor, compared with the negative control group. (E) Dual-luciferase reporter assay indicated that miR- 335-3p has binding sites with TEAD1 and AP000695.2. **P<0.01, ***P<0.001. NS, no significance.

Journal: Acta biochimica et biophysica Sinica

Article Title: LncRNA AP000695.2 promotes glycolysis of lung adenocarcinoma via the miR-335-3p/TEAD1 axis.

doi: 10.3724/abbs.2023227

Figure Lengend Snippet: Figure 7. miR-335-3p acts as a competing endogenous RNA participating in the regulation of TEAD1 and AP000695.2 (A) The binding site of TEAD1 and miR-335-3p and the binding site of miR-335-3p and AP000695.2. (B) qPCR experiment showed that the expression of miR-335-3p in A549 cells was decreased after upregulating AP000695.2 expression. The expression of miR-335-3p in H1299 cells was increased after AP000695.2 was downregulated. (C) The expression of miR-335-3p in A549 and H299 cells was increased after the transfection of miR-335-3p mimics. (D) Western blot analysis showed that the protein expression of TEAD1 was decreased after the transfection with miR-335-3p mimics, and increased after the transfection with miR-335-3p inhibitor, compared with the negative control group. (E) Dual-luciferase reporter assay indicated that miR- 335-3p has binding sites with TEAD1 and AP000695.2. **P<0.01, ***P<0.001. NS, no significance.

Techniques: Binding Assay, Expressing, Transfection, Western Blot, Negative Control, Luciferase, Reporter Assay

Figure 9. Silencing of AP000695.2 inhibits tumor growth and aerobic glycolysis in vivo (A) The qPCR experiment showed that the expression of si-AP000695.2 group is significantly lower than that of negative control group. (B) The tumor volumes at different time points showed that from the 6th day after injection, compared with the si-NC group, the si-AP000695.2 significantly inhibited the growth of transplanted tumor. (C) The uptake of 18F-FDG by tumor was decreased after the expression of AP000695.2 was decreased. The picture on the left showed the micro-PET images. The right picture showed the quantitative analysis results of SUVmax. (D) Immunohistochemistry (IHC) staining showed that the expression levels of GLUT1, HK2, PKM2, LDHA and TEAD1 in si-AP000695.2 group were lower than those in si-NC group. (magnification × 400, scale bar: 100 μm). **P<0.01, ***P<0.001.

Journal: Acta biochimica et biophysica Sinica

Article Title: LncRNA AP000695.2 promotes glycolysis of lung adenocarcinoma via the miR-335-3p/TEAD1 axis.

doi: 10.3724/abbs.2023227

Figure Lengend Snippet: Figure 9. Silencing of AP000695.2 inhibits tumor growth and aerobic glycolysis in vivo (A) The qPCR experiment showed that the expression of si-AP000695.2 group is significantly lower than that of negative control group. (B) The tumor volumes at different time points showed that from the 6th day after injection, compared with the si-NC group, the si-AP000695.2 significantly inhibited the growth of transplanted tumor. (C) The uptake of 18F-FDG by tumor was decreased after the expression of AP000695.2 was decreased. The picture on the left showed the micro-PET images. The right picture showed the quantitative analysis results of SUVmax. (D) Immunohistochemistry (IHC) staining showed that the expression levels of GLUT1, HK2, PKM2, LDHA and TEAD1 in si-AP000695.2 group were lower than those in si-NC group. (magnification × 400, scale bar: 100 μm). **P<0.01, ***P<0.001.

Techniques: In Vivo, Expressing, Negative Control, Injection, Micro-PET, Immunohistochemistry

Figure 10. Schematic diagram of the mechanisms of AP000695.2/miR-335-3p/TEAD1/GLUT1 axis in the glycolysis of LUAD AP000695.2 is involved in the mechanism of LUAD through functioning as a ceRNA to competitively sponge miR-335-3p, thereby regulating the expression of TEAD1. Then TEAD1 promotes glycolysis of lung adenocarcinoma by promoting GLUT1 transcription.

Journal: Acta biochimica et biophysica Sinica

Article Title: LncRNA AP000695.2 promotes glycolysis of lung adenocarcinoma via the miR-335-3p/TEAD1 axis.

doi: 10.3724/abbs.2023227

Figure Lengend Snippet: Figure 10. Schematic diagram of the mechanisms of AP000695.2/miR-335-3p/TEAD1/GLUT1 axis in the glycolysis of LUAD AP000695.2 is involved in the mechanism of LUAD through functioning as a ceRNA to competitively sponge miR-335-3p, thereby regulating the expression of TEAD1. Then TEAD1 promotes glycolysis of lung adenocarcinoma by promoting GLUT1 transcription.

Techniques: Expressing

Journal: RSC Chemical Biology

Article Title: A covalent inhibitor of the YAP–TEAD transcriptional complex identified by high-throughput screening †

doi: 10.1039/d3cb00044c

Figure Lengend Snippet:

Article Snippet: pCMV6-FLAG-TEAD1 , TEAD1 , N-Terminal FLAG , Origene RC215492.

Techniques: Plasmid Preparation, Luciferase

Journal: RSC Chemical Biology

Article Title: A covalent inhibitor of the YAP–TEAD transcriptional complex identified by high-throughput screening †

doi: 10.1039/d3cb00044c

Figure Lengend Snippet:

Article Snippet: pCMV6-FLAG-TEAD1 , TEAD1 , N-Terminal FLAG , Origene RC215492.

Techniques: Plasmid Preparation, Luciferase

Review

tead1 (OriGene)

Structured Review

Images

Related Articles

Expressing:

Similar Products

Image Search Results