Journal: Cancer Biology & Therapy

Article Title: ARHGAP40 suppresses clear cell renal cell carcinoma progression and is associated with altered glutamine-related metabolism and redox balance

doi: 10.1080/15384047.2026.2746137

Figure Lengend Snippet: ARHGAP40 suppresses proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT)-associated changes in ccRCC cells. (A) CCK-8 proliferation curves for 786-O and ACHN cells with ARHGAP40 overexpression and A498 cells transfected with siARHGAP40-1. (B) Representative Annexin V/PI flow-cytometry plots and quantification of Annexin V-positive cells. (C) Representative Transwell migration images and quantification. Scale bar, 50 μm. (D) Representative Transwell invasion images and quantification. Scale bar, 50 μm. (E) Representative western blots and densitometric analyzes of E-cadherin, N -cadherin, and vimentin. n = 3 independent biological replicates; data are presented as mean ± SEM. Time-course CCK-8 data were analyzed by two-way repeated-measures ANOVA with Geisser-Greenhouse correction, followed by Šídák-adjusted multiple comparisons between groups at each time point. For 786-O cells, significant effects were observed for ARHGAP40 status ( P < 0.0001), time ( P < 0.0001), and the ARHGAP40 × time interaction ( P = 0.00011). For ACHN cells, the corresponding P values were < 0.0001, < 0.0001, and 0.0043, respectively; for A498 cells, they were 0.0037, < 0.0001, and 0.0012, respectively. Other two-group comparisons were analyzed using two-tailed Student's t-tests. * P < 0.05, ** P < 0.01, *** P < 0.001.

Article Snippet: Membranes were blocked with 5% non-fat milk in TBST and incubated overnight at 4 °C with primary antibodies: β -actin (CST, 4970, 1:1000), ARHGAP40 (MyBioSource, MBS9215052, 1:1000), AKT (CST, 9272, 1:2000), phospho-AKT Ser473 (CST, 4060, 1:1000), PI3K p85 (CST, 4257, 1:1000), phospho-PI3K p85 Tyr458 (CST, 4228, 1:1000), RhoA (CST, 2117, 1:2000), E-cadherin (CST, 3195, 1:2000), N -cadherin (CST, 4061, 1:2000), and vimentin (CST, 5741, 1:2000).

Techniques: Migration, CCK-8 Assay, Over Expression, Transfection, Flow Cytometry, Western Blot, Two Tailed Test

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: circIdh2 attenuated TGF‐ β 1–induced EndMT changes in rEPCs. rEPCs were treated with or without TGF‐ β 1 (5 ng/mL) for 7 days, and then transfected with PCDH‐NC or PCDH‐circIdh2. (A) qRT‐PCR analysis of circIdh2 expression after transfection for 24 h. (B) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin) after transfection for 48 h. (C) Transwell assay was performed to assess cell migration after transfection for 24 h. (D) Representative scratch wound healing images at 0, 24, and 48 h. Scale bars, 200 μ m. (E) Quantification of relative wound width (% of PCDH‐NC at 0 h). Data are mean ± SD; n = 3 independent biological experiments; one‐way ANOVA; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The primary antibodies used were as follows: VE‐cadherin (1:1000, #27956‐1‐AP, Proteintech, Wuhan, China), vimentin (1:1000, #ap2739b, Abcepta, Jiangsu, China), N‐cadherin (1:5000, #22018‐1‐AP, Proteintech), FLAG (1:2000, #20543‐1‐AP, Proteintech), and GAPDH (1:50000, #60004‐1‐Ig, Proteintech).

Techniques: Transfection, Quantitative RT-PCR, Analysis, Expressing, Western Blot, Transwell Assay, Migration

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: Knockdown of circIdh2 promoted EndMT changes in rEPCs. rEPCs were transfected with si‐NC or siRNAs targeting circIdh2. (A) qRT‐PCR analysis of circIdh2 expression after transfection for 24 h. (B) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin) after transfection for 48 h. (C) Cell migration was assessed using a Transwell assay after transfection for 24 h. (D) Representative scratch wound healing images were obtained at 0, 24, and 48 h. Scale bars, 200 μ m. (E) Quantification of relative wound width (% of si‐NC at 0 h). Data are mean ± SD; n = 3 independent biological experiments; Student′s t ‐test was used for two‐group comparisons and one‐way ANOVA for multiple‐group comparisons; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The primary antibodies used were as follows: VE‐cadherin (1:1000, #27956‐1‐AP, Proteintech, Wuhan, China), vimentin (1:1000, #ap2739b, Abcepta, Jiangsu, China), N‐cadherin (1:5000, #22018‐1‐AP, Proteintech), FLAG (1:2000, #20543‐1‐AP, Proteintech), and GAPDH (1:50000, #60004‐1‐Ig, Proteintech).

Techniques: Knockdown, Transfection, Quantitative RT-PCR, Analysis, Expressing, Western Blot, Migration, Transwell Assay

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: The FLAG‐tagged circIdh2 construct affected EndMT‐related markers and cell migration in rEPCs. rEPCs were transfected with PCDH‐NC or PCDH‐flag‐circIdh2. (A) qRT‐PCR analysis of circIdh2 expression after transfection for 24 h. (B) Western blot analysis of FLAG expression after transfection for 48 h. (C) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin) after transfection for 48 h. (D) Cell migration was examined by Transwell assay after transfection for 24 h. (E) Representative images from the scratch wound healing assay at 0, 24, and 48 h. Scale bar, 200 μ m. (F) Quantification of relative wound width (% of PCDH‐NC at 0 h). Data are mean ± SD; n = 3 independent biological experiments; unpaired Student′s t ‐test; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The primary antibodies used were as follows: VE‐cadherin (1:1000, #27956‐1‐AP, Proteintech, Wuhan, China), vimentin (1:1000, #ap2739b, Abcepta, Jiangsu, China), N‐cadherin (1:5000, #22018‐1‐AP, Proteintech), FLAG (1:2000, #20543‐1‐AP, Proteintech), and GAPDH (1:50000, #60004‐1‐Ig, Proteintech).

Techniques: Construct, Migration, Transfection, Quantitative RT-PCR, Analysis, Expressing, Western Blot, Transwell Assay, Wound Healing Assay

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: The circIdh2 mutant did not reproduce the effects of wild‐type circIdh2 on EndMT‐related markers and cell migration. rEPCs were transfected with PCDH‐NC, PCDH‐circIdh2, or PCDH‐circIdh2‐mut. (A) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin) after transfection for 48 h. (B) Cell migration was assessed using a Transwell assay after transfection for 24 h. (C) Representative scratch wound healing images at 0, 24, and 48 h, with quantification of relative wound width (% of PCDH‐NC at 0 h). Scale bar, 200 μ m. Data are mean ± SD; n = 3 independent biological experiments; one‐way ANOVA; ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The primary antibodies used were as follows: VE‐cadherin (1:1000, #27956‐1‐AP, Proteintech, Wuhan, China), vimentin (1:1000, #ap2739b, Abcepta, Jiangsu, China), N‐cadherin (1:5000, #22018‐1‐AP, Proteintech), FLAG (1:2000, #20543‐1‐AP, Proteintech), and GAPDH (1:50000, #60004‐1‐Ig, Proteintech).

Techniques: Mutagenesis, Migration, Transfection, Western Blot, Analysis, Transwell Assay

Journal: Cardiovascular Therapeutics

Article Title: CircIdh2 Attenuates Endothelial‐to‐Mesenchymal Transition and Myocardial Fibrosis and Exhibits Translational Potential

doi: 10.1155/cdr/2005876

Figure Lengend Snippet: AAV‐mediated delivery of circIdh2 or circIdh2‐aa attenuated myocardial fibrosis and EndMT‐related marker changes in vivo. (A) HE staining of myocardial infarction tissues from the sham, model, circIdh2‐AAV, and circIdh2‐aa‐AAV groups. (B) Masson staining of MI tissues. (C) IF detection and quantification of fibrotic markers (Collagen I and TGF‐ β ) in myocardial tissues. Scale bars, 100 μ m. (D) Western blot analysis of EndMT‐related proteins (VE‐cadherin, vimentin, and N‐cadherin). Data are mean ± SD; n = 3 rats per group; one‐way ANOVA; ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001.

Article Snippet: The primary antibodies used were as follows: VE‐cadherin (1:1000, #27956‐1‐AP, Proteintech, Wuhan, China), vimentin (1:1000, #ap2739b, Abcepta, Jiangsu, China), N‐cadherin (1:5000, #22018‐1‐AP, Proteintech), FLAG (1:2000, #20543‐1‐AP, Proteintech), and GAPDH (1:50000, #60004‐1‐Ig, Proteintech).

Techniques: Marker, In Vivo, H&E Stain, Staining, Western Blot, Analysis