Journal: Frontiers in Cell and Developmental Biology

Article Title: HIIT-induced lactate/GPR81 signaling with dual branches converging on ERK1/2 contributes to hippocampal synaptic remodeling and memory improvement

doi: 10.3389/fcell.2026.1699042

Figure Lengend Snippet: GPR81 mediates the regulation of HIIT on the AC-RAP1 and PLC-PKC pathways and ERK1/2 activation in the hippocampus of mice, as well as the expression of synaptic plasticity-related proteins. (A,D,H,M) Representative Western blotting images. (B,C,E,F) Quantitative analysis of AC, RAP1, PLC, and PKC protein expression levels in the hippocampus of different groups. (I–L) Quantitative analysis of protein expression levels of phosphorylated/total c-Raf and ERK1/2 in the hippocampus of different groups. (G) Quantitative analysis of gene expression levels of ERK1/2 in the hippocampus of each group. * p < 0.05, ** p < 0.01 vs . the SC group. ns, no significant difference. (N–S) Quantitative analysis of protein expression levels of NMDAR, PSD95, SYN, BDNF, c-FOS, and Zif268 in the hippocampus of mice from different groups. Protein expression levels were normalized to Tubulin. Phosphorylated proteins were further normalized to their corresponding total protein levels. Relative gene expression was quantified and normalized to Gapdh. For comparisons among multiple groups, one-way ANOVA was applied. The data are presented as mean ± SD. n = 6. * p < 0.05, ** p < 0.01 vs . the SC group. ns, no significant difference. SC, scramble control, sedentary; SCH, scramble control + HIIT; GKD, GPR81 knockdown, sedentary; GKDH, GPR81 knockdown + HIIT.

Article Snippet: GPR81, PA5-114741, Thermo; AC (55067-1-AP, Proteintech), PKA (4782S, CST), RAP1 (2399S, CST), PKC (SC-80 Santa), PLC (14247S, CST), Raf1 (9422S, CST), MSK1 (3489S, CST), P90RSK (9355S, CST), ERK (4370T, CST), CREB (9197S, CST), c-Fos (2250S, CST), Zif268 (4154S, CST), NMDAR (5704S, CST), SYN (4329S, CST), BDNF (28205-1-AP, Proteintech), ARC (16290-1-AP, Proteintech), PSD95 (3450S, CST) p-Raf1 (9421S, CST), p-ERK (4370T, CST), p-MSK (9595S, CST), p-P90RSK (11989S, CST), p-CREB (9198S, CST), Tubulin (10068-1-AP, Proteintech), HRP-conjugated Affinipure Goat Anti-Rabbit IgG (H + L) (SA00001-2, Proteintech), HRP-conjugated Affinipure Goat Anti-Mouse IgG (H + L) (SA00001-1, Proteintech).

Techniques: Activation Assay, Expressing, Western Blot, Gene Expression, Control, Knockdown

Journal: Frontiers in Cell and Developmental Biology

Article Title: HIIT-induced lactate/GPR81 signaling with dual branches converging on ERK1/2 contributes to hippocampal synaptic remodeling and memory improvement

doi: 10.3389/fcell.2026.1699042

Figure Lengend Snippet: GPR81-induced modulation of ERK1/2 via AC-RAP1 and PLC-PKC pathways regulates synaptic plasticity-related protein expression in N2a cells. (A,I) Representative Western blotting images. (B–H,J–P) Quantitative analysis of NMDAR, PSD95, SYN, BDNF, Zif268, c-Fos, and ARC protein expression levels. Protein expression levels were normalized to Tubulin. Phosphorylated proteins were further normalized to their corresponding total protein levels. For comparisons among multiple groups, one-way ANOVA was applied. The data are presented as mean ± SD. * p < 0.05 vs . the DMSO group. n = 3. # p < 0.05, ## p < 0.01, ### p < 0.001 vs . the Ga group. ns, no significant difference. Ga, GPR81 agonist; Ei, ERK1/2 inhibitor; Aa, AC agonist; Pi, PLC inhibitor.

Article Snippet: GPR81, PA5-114741, Thermo; AC (55067-1-AP, Proteintech), PKA (4782S, CST), RAP1 (2399S, CST), PKC (SC-80 Santa), PLC (14247S, CST), Raf1 (9422S, CST), MSK1 (3489S, CST), P90RSK (9355S, CST), ERK (4370T, CST), CREB (9197S, CST), c-Fos (2250S, CST), Zif268 (4154S, CST), NMDAR (5704S, CST), SYN (4329S, CST), BDNF (28205-1-AP, Proteintech), ARC (16290-1-AP, Proteintech), PSD95 (3450S, CST) p-Raf1 (9421S, CST), p-ERK (4370T, CST), p-MSK (9595S, CST), p-P90RSK (11989S, CST), p-CREB (9198S, CST), Tubulin (10068-1-AP, Proteintech), HRP-conjugated Affinipure Goat Anti-Rabbit IgG (H + L) (SA00001-2, Proteintech), HRP-conjugated Affinipure Goat Anti-Mouse IgG (H + L) (SA00001-1, Proteintech).

Techniques: Expressing, Western Blot

Journal: Cell reports

Article Title: Neuronal hyperactivity becomes mTORC1 independent due to transcriptional changes in tuberous sclerosis complex disease models

doi: 10.1016/j.celrep.2025.116664

Figure Lengend Snippet: (A) Violin plots of expression of top-ranked transcription factors with enriched motifs in differentially expressed genes from cluster 9. This plot shows log 2 -transformed expression in cluster 9 in Tsc2 fl/fl SynCre − and Tsc2 del/fl SynCre + animals. (B) qPCR of dissected lower-layer regions of the cortex comparing Tsc2 del/fl SynCre + to Tsc2 fl/fl SynCre − animals. Bar plot shows mean ± SEM. * p < 0.05 ( n = 3 animals per genotype; t test). (C) Immunohistochemistry of EGR1 in the lower layer of the cortex from Tsc2 fl/fl SynCre − (left) and Tsc2 del/fl SynCre + (right) animals. These sections are also stained for BCL11B, a marker of layer 5 pyramidal neurons. Scale bar = 20 μm. (D) Quantification of EGR1 signal intensity within BCL11B + neurons of the cortex across genotypes. Each dot represents a different animal, which is the mean of 2–3 images per slice and 3–4 slices per animal. Bar plot shows mean ± SEM. * p < 0.05 ( n = 4; t test). (E) Immunoblotting of EGR1 across all genotypes of neurons on day 30 of differentiation and quantification of EGR1 level compared to total protein across all genotypes. * p < 0.05 ( n = 4 separate differentiations; ANOVA with Dunnett’s test).

Article Snippet: Antibodies used included: EGR1, Cell Signaling Technology, 4153S, 1:1000; TAP1, Proteintech, 11114–1-AP, 1:1000; PSMB8, Proteintech, 14859–1-AP, 1:1000; PSME1, Proteintech, 10543–1-AP, 1:1000; DNMT1, Proteintech, 24206–1-AP, 1:200; Phospho-CREB Ser133, Cell Signaling Technology, 9198S, 1:1000; CREB, EMD Millipore, 06–863, 1:1000; Phospho-S6 Ser235/236, Cell Signaling Technology, 2211, 1:1000; S6, Cell Signaling Technology, 2317, 1:1000.

Techniques: Expressing, Transformation Assay, Immunohistochemistry, Staining, Marker, Western Blot

Journal: Cell reports

Article Title: Neuronal hyperactivity becomes mTORC1 independent due to transcriptional changes in tuberous sclerosis complex disease models

doi: 10.1016/j.celrep.2025.116664

Figure Lengend Snippet: (A) Luciferase expression driven by the human EGR1 promoter compared to Renilla expression driven by a constitutive promoter. Experiments were performed in hiPSC-derived neurons of the indicated genotype on day 25 of differentiation. Each dot represents an independent well of neurons across three separate differentiations. Bar plot shows mean ± SEM. * p < 0.05 ( n = 16–32, ANOVA with Dunnett’s test). (B) Representative trace of luciferase expression induced by 50 mM KCl across all three genotypes of hiPSC-derived neurons and quantification of the maximum induction of luciferase due to 50 mM KCl treatment. Experiments were performed in hiPSC-derived neurons of the indicated genotype on day 25 of differentiation. Each dot represents an independent well of neurons across four separate differentiations. Bar plot shows mean ± SEM. * p < 0.05 ( n = 30, ANOVA with Dunnett’s test). (C) Immunoblots of proteasome subunits and proteasome-associated proteins in hiPSC-derived neurons of the indicated genotypes on day 30 of differentiation. Quantification of these immunoblots compared to total protein shows a significant increase in TSC2 −/− neurons of all three proteins compared to TSC2 +/+ neurons. Bar plot shows mean ± SEM. N = 3 separate differentiations, ANOVA with Dunnett’s test. (D) qPCR of proteasome subunits and associated proteins in TSC2 −/− compared to TSC2 +/+ neurons on day 30 of differentiation. * p < 0.05 ( n = 3–4 separate differentiations, t test). (E) Proteasome activity assessed by cleavage of succinate-LLVY-AMC in lysates from hiPSC-derived neurons of the indicated genotypes on day 25 of differentiation5. Each dot represents an independent well from four separate differentiations. Bar plot shows mean ± SEM. * p < 0.05 ( n = 15, ANOVA with Dunnett’s test).

Article Snippet: Antibodies used included: EGR1, Cell Signaling Technology, 4153S, 1:1000; TAP1, Proteintech, 11114–1-AP, 1:1000; PSMB8, Proteintech, 14859–1-AP, 1:1000; PSME1, Proteintech, 10543–1-AP, 1:1000; DNMT1, Proteintech, 24206–1-AP, 1:200; Phospho-CREB Ser133, Cell Signaling Technology, 9198S, 1:1000; CREB, EMD Millipore, 06–863, 1:1000; Phospho-S6 Ser235/236, Cell Signaling Technology, 2211, 1:1000; S6, Cell Signaling Technology, 2317, 1:1000.

Techniques: Luciferase, Expressing, Derivative Assay, Western Blot, Activity Assay

Journal: Cell reports

Article Title: Neuronal hyperactivity becomes mTORC1 independent due to transcriptional changes in tuberous sclerosis complex disease models

doi: 10.1016/j.celrep.2025.116664

Figure Lengend Snippet: (A) Methylation of the EGR1 promoter in TSC2 +/+ (blue) and TSC2 −/− (red) neurons throughout differentiation. The y axis represents the log 10 p value of change in methylation of individual CpG sites, which is given a sign based on the direction of the change (negative corresponds to demethylation in neurons compared to stem cells; positive corresponds to hypermethylation in neurons compared to stem cells). The x axis shows the genomic coordinates of the EGR1 locus, and the features of this region are shown below. (B) Volcano plot of hypomethylated regions in TSC2 +/+ neurons, comparing methylation levels of these regions in TSC2 +/+ neurons compared to TSC2 +/+ hiPSCs. (C) Volcano plot of hypomethylated regions in TSC2 +/+ neurons, comparing methylation levels of these regions in TSC2 −/− neurons compared to TSC2 −/− hiPSCs. (D) Quantile-quantile plot of log 10 -transformed p values of demethylated genes in TSC2 +/+ vs. TSC2 −/− neurons, where the red line indicates the identity. The deviation of the quantiles demonstrates more significant demethylation of regions in the TSC2 +/+ neurons compared to the TSC2 −/− neurons. (E) Highest-ranked motif across regions that showed impaired demethylation in TSC2 −/− neurons. (F) Bar plot of observed/expected genomic features overlapping with regions that showed impaired demethylation in TSC2 −/− neurons. * p < 0.05 (chi-squared test).

Article Snippet: Antibodies used included: EGR1, Cell Signaling Technology, 4153S, 1:1000; TAP1, Proteintech, 11114–1-AP, 1:1000; PSMB8, Proteintech, 14859–1-AP, 1:1000; PSME1, Proteintech, 10543–1-AP, 1:1000; DNMT1, Proteintech, 24206–1-AP, 1:200; Phospho-CREB Ser133, Cell Signaling Technology, 9198S, 1:1000; CREB, EMD Millipore, 06–863, 1:1000; Phospho-S6 Ser235/236, Cell Signaling Technology, 2211, 1:1000; S6, Cell Signaling Technology, 2317, 1:1000.

Techniques: Methylation, Transformation Assay

Journal: Cell reports

Article Title: Neuronal hyperactivity becomes mTORC1 independent due to transcriptional changes in tuberous sclerosis complex disease models

doi: 10.1016/j.celrep.2025.116664

Figure Lengend Snippet: (A) Heatmap of correlation of gene expression between hiPSC-derived neurons of all three genotypes that were treated with rapamycin or vehicle starting on day of differentiation ( n = 6–8 per genotype per treatment). TSC2 −/− vehicle-treated neurons form a distinct cluster, while TSC2 −/− rapamycin-treated neurons are similar to other genotypes of neurons treated with rapamycin. (B) Heatmap of correlation of gene expression between hiPSC-derived neurons of all three genotypes that were treated with rapamycin or vehicle starting on day 30 of differentiation. TSC2 −/− rapamycin-treated neurons remain distinct from other genotypes and are more closely related to TSC2 −/− vehicle-treated neurons. (C) Gene expression from the co-expression module (ME9) that is most strongly associated with persistent gene expression changes after late rapamycin treatment. (D) Gene Ontology analysis of genes from ME9 that shows persistent changes in genes related to synapses and DNA binding. (E) GSEA of genes near five or more distal enhancers that do not show demethylation during differentiation of TSC2 −/− neurons across ME9. The green line shows the weighted cumulative sum of enrichment of EGR1 target genes, denoted by black lines across the x axis. The color at the bottom of the graph denotes the correlation of all genes with ME9 (red, positive correlation; blue, negative correlation). (F) Cumulative distribution function for k ME in ME9 of EGR1 target genes (red) compared to all other genes (gray).

Article Snippet: Antibodies used included: EGR1, Cell Signaling Technology, 4153S, 1:1000; TAP1, Proteintech, 11114–1-AP, 1:1000; PSMB8, Proteintech, 14859–1-AP, 1:1000; PSME1, Proteintech, 10543–1-AP, 1:1000; DNMT1, Proteintech, 24206–1-AP, 1:200; Phospho-CREB Ser133, Cell Signaling Technology, 9198S, 1:1000; CREB, EMD Millipore, 06–863, 1:1000; Phospho-S6 Ser235/236, Cell Signaling Technology, 2211, 1:1000; S6, Cell Signaling Technology, 2317, 1:1000.

Techniques: Gene Expression, Derivative Assay, Expressing, Binding Assay

Journal: Molecular carcinogenesis

Article Title: CtBP2 Regulates Wnt Signal Through EGR1 to Influence the Proliferation and Apoptosis of DLBCL Cells.

doi: 10.1002/mc.23901

Figure Lengend Snippet: FIGURE 5 | Interfering with EGR1 inhibited the proliferation and cycle acceleration of DLBCL cells and promotes apoptosis. The EGR1 gene in cells was silenced through siRNA transfection. (A) The interference level of EGR1 was measured by western blot analysis. (B) Cell proliferation was detected by CCK8 assay. (C) EdU staining was performed to evaluate the level of cell proliferation; Flow cytometry was conducted to analyze the cell cycle (D) and the level of apoptosis (E). (F) The expressions of CtBP2 and apoptosis‐related proteins were detected by western blot. ***p < 0.001. [Color figure can be viewed at wileyonlinelibrary.com]

Article Snippet: The antibodies utilized in this study included CtBP2 (10346‐1‐AP; Proteintech), EGR‐1 (22008‐1‐AP; Proteintech), Bcl‐2 (12789‐1‐AP; Proteintech), Bax (ab32503; Abcam), Caspase 3 (9961, CST), cleaved‐Caspase 3 (9962, CST), DKK1 (ab307367; Abcam), β‐catenin (ab32572; Abcam) and c‐Myc (ab185656; Abcam).

Techniques: Transfection, Western Blot, CCK-8 Assay, Staining, Flow Cytometry

Journal: Molecular carcinogenesis

Article Title: CtBP2 Regulates Wnt Signal Through EGR1 to Influence the Proliferation and Apoptosis of DLBCL Cells.

doi: 10.1002/mc.23901

Figure Lengend Snippet: FIGURE 6 | Interfere with CtBP2 inhibited the proliferation and cycle acceleration of DLBCL cells and promoted apoptosis through EGR1. The cells were transfected with an Ov‐EGR1 overexpression plasmid. (A) The overexpression level of EGR1 was assessed using Western blot analysis. (B) Cell proliferation was evaluated by CCK‐8 assay. (C) Cell proliferation was measured through EdU staining; Flow cytometry was performed to analyze the cell cycle (D) and the level of apoptosis (E). (F) The expression of apoptosis‐related proteins was detected by western blot assay. ***p < 0.001. [Color figure can be viewed at wileyonlinelibrary.com]

Article Snippet: The antibodies utilized in this study included CtBP2 (10346‐1‐AP; Proteintech), EGR‐1 (22008‐1‐AP; Proteintech), Bcl‐2 (12789‐1‐AP; Proteintech), Bax (ab32503; Abcam), Caspase 3 (9961, CST), cleaved‐Caspase 3 (9962, CST), DKK1 (ab307367; Abcam), β‐catenin (ab32572; Abcam) and c‐Myc (ab185656; Abcam).

Techniques: Transfection, Over Expression, Plasmid Preparation, Western Blot, CCK-8 Assay, Staining, Flow Cytometry, Expressing

Journal: Molecular carcinogenesis

Article Title: CtBP2 Regulates Wnt Signal Through EGR1 to Influence the Proliferation and Apoptosis of DLBCL Cells.

doi: 10.1002/mc.23901

Figure Lengend Snippet: FIGURE 7 | EGR1 may be involved in the regulation of the Wnt/β‐catenin signaling pathway by CtBP2. The expressions of Wnt/β‐catenin signaling‐related proteins DKK1, β‐catenin and c‐MyC were detected by western blot. ***p < 0.001. [Color figure can be viewed at wileyonlinelibrary.com]

Article Snippet: The antibodies utilized in this study included CtBP2 (10346‐1‐AP; Proteintech), EGR‐1 (22008‐1‐AP; Proteintech), Bcl‐2 (12789‐1‐AP; Proteintech), Bax (ab32503; Abcam), Caspase 3 (9961, CST), cleaved‐Caspase 3 (9962, CST), DKK1 (ab307367; Abcam), β‐catenin (ab32572; Abcam) and c‐Myc (ab185656; Abcam).

Techniques: Western Blot

Journal: Oncology Reports

Article Title: Lentinan induces apoptosis of mouse hepatocellular carcinoma cells through the EGR1/PTEN/AKT signaling axis

doi: 10.3892/or.2023.8579

Figure Lengend Snippet: Effects of LNT on the EGR1/PTEN/AKT axis in Hepa1-6 cells. (A) Protein expression levels of EGR1, PTEN, p-Akt and phosphorylation of Akt after treatment with a gradient of LNT concentrations as detected by WB. All data for protein expression were normalized using β-actin as a loading reference. (B) Immunofluorescence co-staining was used to assess the localization and expression of EGR1 and PTEN in Hepa1-6 cells treated with a gradient of LNT concentrations. Images were observed at ×630 magnification. Scale bars, 50 µm (white). (C) WB was used to detect the expression of EGR1 in the nuclear and cytoplasmic fractions following treatment with a gradient of LNT concentrations. (D) WB was used to detect the expression of EGR1, PTEN, p-Akt, and phosphorylation of Akt after EGR1 overexpression. *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. LNT, Lentinan; EGR1, early growth response 1; p-, phosphorylated; PARP1, poly-(ADP ribose) polymerase 1; Hsp60, heat shock protein 60; OE, overexpression; WB, western blotting.

Article Snippet: Subsequently, they were incubated with a mixture of different primary antibodies, including mouse EGR1 (1:100; cat. no. H00001958-M03; Novus Biologicals, LLC) and rabbit PTEN (1:100; cat. no. AF6351; Affinity Biosciences), overnight at 4°C.

Techniques: Expressing, Phospho-proteomics, Immunofluorescence, Staining, Over Expression, Western Blot

Journal: Oncology Reports

Article Title: Lentinan induces apoptosis of mouse hepatocellular carcinoma cells through the EGR1/PTEN/AKT signaling axis

doi: 10.3892/or.2023.8579

Figure Lengend Snippet: Inhibitory effect of LNT on DEN-induced primary liver cancer in mice. (A) The expression levels of EGR1, PTEN and other proteins in the liver tissues of the normal group and the model group, as analyzed by WB. (B) Expression of EGR1, PTEN and other proteins in liver tissues of the model and LNT-treated groups, as analyzed by WB. (C) Immunohistochemical analysis of EGR1, PTEN and Ki-67 in the tissue sections. Magnification, ×400. Scale bars, 200 µm (black). *P<0.05, **P<0.01, ***P<0.001 and ****P<0.0001. LNT, Lentinan; DEN, diethylnitrosamine; EGR1, early growth response 1; WB, western blotting; p-, phosphorylated; PCNA, proliferating cell nuclear antigen.

Article Snippet: Subsequently, they were incubated with a mixture of different primary antibodies, including mouse EGR1 (1:100; cat. no. H00001958-M03; Novus Biologicals, LLC) and rabbit PTEN (1:100; cat. no. AF6351; Affinity Biosciences), overnight at 4°C.

Techniques: Expressing, Immunohistochemical staining, Western Blot

Journal: Oncology Reports

Article Title: Lentinan induces apoptosis of mouse hepatocellular carcinoma cells through the EGR1/PTEN/AKT signaling axis

doi: 10.3892/or.2023.8579

Figure Lengend Snippet: Possible mechanism of LNT against liver cancer through the EGR1/PTEN/AKT axis. Blunt arrows indicate that the signaling pathways are inhibited, whilst pointed arrows indicate that the signaling pathways are activated. LNT, Lentinan; EGR1, early growth response 1.

Article Snippet: Subsequently, they were incubated with a mixture of different primary antibodies, including mouse EGR1 (1:100; cat. no. H00001958-M03; Novus Biologicals, LLC) and rabbit PTEN (1:100; cat. no. AF6351; Affinity Biosciences), overnight at 4°C.

Techniques: Protein-Protein interactions

Journal: iScience

Article Title: A mechanism of cooling hot tumors: Lactate attenuates inflammation in dendritic cells

doi: 10.1016/j.isci.2021.103067

Figure Lengend Snippet:

Article Snippet: Plasmid: Egr1 , OriGene Technologies , MC217560.

Techniques: Control, Recombinant, Isolation, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Cell Isolation, Reporter Assay, Mutagenesis, Chromatin Immunoprecipitation, DNA Purification, Staining, Lactate Assay, Microarray, Negative Control, Plasmid Preparation, Software, Transfection

Journal: Autophagy

Article Title: Downregulation of ATG14 by EGR1-MIR152 sensitizes ovarian cancer cells to cisplatin-induced apoptosis by inhibiting cyto-protective autophagy.

doi: 10.1080/15548627.2015.1009781

Figure Lengend Snippet: Figure 6. Downregulation of EGR1 mediates cisplatin-resistance through MIR152 at the transcriptional level. (A) EGR1 protein levels were determined by western blotting in cells. (B) Upper: sequence alignment of the MIR152 gene promoter containing EGR1 consensus DNA-binding sites. Lower: The biotin end-labeled MIR152 promoter DNA fragment was incubated with or without A2780 nuclear extraction and an excess (100-fold) unlabeled DNA fragment. The EMSA assay was performed as described in Materials and Methods. (C) A2780 cells were transiently transfected with a siEGR1 Smartpool or a nega- tive siRNA control for 72 h. MIR152 expression was determined by Taqman RT-PCR. (D) A2780/CP70 cells were transiently transfected with an EGR1 plas- mid for 72 h. MIR152 expression was determined by Taqman RT-PCR. Data are presented as mean § SD. * Indicates significant difference compared with control (P < 0.05). (E) A2780 cells were transiently transfected with a siEGR1 Smartpool or a negative siRNA control for 72 h. EGR1 and ATG14 expression levels were determined by western blotting. (F) A2780/CP70 cells were transfected with the EGR1 plasmid for 48 h, and reseeded into 96- well plates followed by cisplatin treatments at various concentrations for 72 h. Cell viability was measured by MTT assay. *Indicates significant difference compared with control at the same time point (P < 0.05).

Article Snippet: Quantitative realtime PCR primers for EGR1 and ATG14 were purchased from (Origene, HP205725, HP211256).

Techniques: Western Blot, Sequencing, Binding Assay, Labeling, Incubation, Extraction, Transfection, Control, Expressing, Reverse Transcription Polymerase Chain Reaction, Plasmid Preparation, MTT Assay

Journal: Autophagy

Article Title: Downregulation of ATG14 by EGR1-MIR152 sensitizes ovarian cancer cells to cisplatin-induced apoptosis by inhibiting cyto-protective autophagy.

doi: 10.1080/15548627.2015.1009781

Figure Lengend Snippet: Figure 7. Lower levels of EGR1 and MIR152 in ovarian tumors are associated with cisplatin-resistance. (A) EGR1 expression levels in normal ovarian tissues vs. ovarian cancer tissues in 2 individual microarrays were shown using the Oncomine gene expression tool. (B) EGR1 mRNA levels were determined by SYBR-Green RT-PCR in 14 high ERCC1 ovarian tumors (ERCC1 score 1) and 21 low ERCC1 ovarian tumors (ERCC score < 1). Bars are indicated as median of the group. (C) MIR152 expression levels were determined by Taqman RT-PCR in 14 high ERCC1 ovarian cancer tissues and 21 low ERCC1 ovarian cancer tissues. Bars are indicated as the median of the group. *Indicates significant difference (P < 0.05). (D) ATG14 mRNA levels were determined by SYBR- Green RT-PCR in 30 ovarian tumors. Correlation analysis between MIR152 and ATG14 levels in human ovarian cancer tissues was performed.

Article Snippet: Quantitative realtime PCR primers for EGR1 and ATG14 were purchased from (Origene, HP205725, HP211256).

Techniques: Expressing, Gene Expression, SYBR Green Assay, Reverse Transcription Polymerase Chain Reaction