Journal: Clinical and Experimental Pharmacology & Physiology

Article Title: Mechanisms of IL‐17A Neutralisation in Alleviating Renal Fibrosis and Inflammation in Spontaneously Hypertensive Rats

doi: 10.1111/1440-1681.70116

Figure Lengend Snippet: IL‐17A NAb inhibited EMT in SHR renal tissues. (A) Representative IHC images showing the expression of E‐cadherin, α‐SMA, and Collagen III, with quantitative analysis of their positive areas. (B) Representative immunoblots and relative expression levels of E‐cadherin, α‐SMA, and Collagen III proteins. (C) mRNA expression levels of E‐cadherin, α‐SMA, and Collagen III. Data are expressed as mean ± SD ( n = 6).

Article Snippet: Sections were then incubated overnight at 4°C with primary antibodies against: E‐cadherin (Boster, China), Collagen III (Boster, China), inducible nitric oxide synthase (iNOS) (Boster, China), CD86 (Boster, China), arginase‐1 (Arg‐1) (Boster, China), CD163 (Boster, China), α‐smooth muscle actin (α‐SMA) (Cell Signalling Technology, USA).

Techniques: Expressing, Western Blot

Journal: Frontiers in oncology

Article Title: The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.

doi: 10.3389/fonc.2021.663671

Figure Lengend Snippet: FIGURE 1 | High ACE2 expression was linked to increased VM and better prognosis in NSCLC. (A) Typical image of ACE2, VE-cadherin, EphA2 protein expression and CD34/PAS double staining in TMA tissues. Case B1 had massive CD34−/PAS+ VM (yellow arrows) lined by ACE2, VE-cadherin and EphA2 high expressing tumor cells. Case G1 had abundant CD34+/PAS−MVs (black arrows) with ACE2, VE-cadherin and EphA2 low expressing tumor cells. (B) Kaplan-Meier analysis of OS in NSCLC patients with ACE2 low or high expression. P = 0.044.

Article Snippet: The sections were dewaxed, rehydrated, treated with antigen retrieval, hatched with primary antibodies of ACE2 (1:200), VE-cadherin (1:200), EphA2 (1:100), and CD34 (1:200, ab81289, Abcam) overnight at 4°C, individually exposed to secondary antibody (SA1020, BOSTER, USA) 1 h at RT, and colored with DAB peroxidase substrate.

Techniques: Expressing, Double Staining

Journal: Frontiers in oncology

Article Title: The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.

doi: 10.3389/fonc.2021.663671

Figure Lengend Snippet: FIGURE 5 | VM formation was increased, and vasculature was lessened due to inhibition of RAS in vivo. (A) Growth curve of allograft tumors of A549-ACE2-OE cells, A549-NC cells with or without ACEI treatment, Mean ± SD, n = 3, *p < 0.05. ns, no significance. (B) Weight of resected tumors, Mean ± SD, n = 3, **p < 0.01, *p < 0.05. (C) Continuous sections of allograft tumor tissues stained with PAS, CD34, VE-cadherin, or EphA2 immunohistochemical stain. Black arrow points out a typical MV (CD34+/PAS−); yellow arrows point out typical VM (CD34−/PAS+). (D) Quantification of MV and VM in different groups, Mean ± SD, n = 3, per field, ***p < 0.001, **p < 0.01. (E) Quantification of VE-cadherin and EphA2 mean optical density in three groups, Mean ± SD, n = 3, ***p < 0.001, **p < 0.01.

Article Snippet: The sections were dewaxed, rehydrated, treated with antigen retrieval, hatched with primary antibodies of ACE2 (1:200), VE-cadherin (1:200), EphA2 (1:100), and CD34 (1:200, ab81289, Abcam) overnight at 4°C, individually exposed to secondary antibody (SA1020, BOSTER, USA) 1 h at RT, and colored with DAB peroxidase substrate.

Techniques: Inhibition, In Vivo, Staining, Immunohistochemical staining

Journal: Frontiers in oncology

Article Title: The Angiotensin-Converting Enzyme Inhibitory State Promotes the Transformation of Non-Small Cell Lung Cancer Blood Supply Pattern Toward Vasculogenic Mimicry Formation.

doi: 10.3389/fonc.2021.663671

Figure Lengend Snippet: FIGURE 6 | VE-cadherin and EphA2 expression was upregulated in A549 cells and NSCLC tissues with impaired local RAS status. (A, B) RT-PCR experiment of VE-cadherin and EphA2 mRNA level in A549-ACE2-OE cells and control cells, Mean ± SD, n = 3, ***p < 0.001. (C–E) Western blot analysis and quantification of VE- cadherin and EphA2 expression level in A549-ACE2-OE cells and control cells, Mean ± SD, n = 3, ***p < 0.001. (F, G) Linear regressions of VM number and VE- cadherin (P < 0.0001) or EphA2 (P = 0.0108) score in TMA. (H) Typical tissue images of both groups stained with VE-cadherin, ACE2 or CD34/PAS. Case F13 with ACE2 low status was provided with rambling VM covered by tumor cells which only expressed VE-cadherin in nuclei; case D6 with ACE2 high status had ordered VM lined by tumor cells expressing VE-cadherin in both nuclei and cytomembranes. Red arrow: VE-cadherin membrane expression.

Article Snippet: The sections were dewaxed, rehydrated, treated with antigen retrieval, hatched with primary antibodies of ACE2 (1:200), VE-cadherin (1:200), EphA2 (1:100), and CD34 (1:200, ab81289, Abcam) overnight at 4°C, individually exposed to secondary antibody (SA1020, BOSTER, USA) 1 h at RT, and colored with DAB peroxidase substrate.

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction, Control, Western Blot, Staining, Membrane

Journal: Molecular Medicine Reports

Article Title: O-GlcNAcylation promotes migration and invasion in human ovarian cancer cells via the RhoA/ROCK/MLC pathway

doi: 10.3892/mmr.2017.6244

Figure Lengend Snippet: O-GlcNAcylation in ovarian cancer cells is upregulated in response to ThiaG treatment and downregulated in response to OGT silencing. Protein expression levels were measured by western blotting in SKOV3 (A) and 59M (B) cells. GAPDH was used as an internal reference. ThiaG, Thiamet-G; OGT, O-GlcNAc transferase; Ctrl, control; siOGT, O-GlcNAc transferase small interfering RNA; O-GlcNAc, O-linked β-N-acetylglucosamine; GADPH, glyceraldehyde 3-phosphate dehydrogenase.

Article Snippet: Human ovarian epithelial adenocarcinoma SKOV3 cells were purchased from the Cell Bank of the Chinese Academy of Sciences (Shanghai, China) and endometrioid-type ovarian epithelial carcinoma 59M cells were purchased from the European Collection of Authenticated Cell Cultures; Public Health England (Salisbury, UK).

Techniques: Expressing, Western Blot, Control, Small Interfering RNA

Journal: Molecular Medicine Reports

Article Title: O-GlcNAcylation promotes migration and invasion in human ovarian cancer cells via the RhoA/ROCK/MLC pathway

doi: 10.3892/mmr.2017.6244

Figure Lengend Snippet: O-GlcNAcylation regulates (A) migration and (B) invasion in SKOV3 and 59M ovarian cancer cells in in vitro Transwell assays. OGT was silenced with siOGT, and upregulated with ThiaG treatment. **P<0.01 vs. ctrl. O-GlcNAc, O-Linked β-N-acetylglucosamine; OGT, O-GlcNActransferase; siOGT, O-linked β-N-acetylglucosamine transferase small interfering RNA; Ctrl, control; ThiaG, Thiamet-G.

Article Snippet: Human ovarian epithelial adenocarcinoma SKOV3 cells were purchased from the Cell Bank of the Chinese Academy of Sciences (Shanghai, China) and endometrioid-type ovarian epithelial carcinoma 59M cells were purchased from the European Collection of Authenticated Cell Cultures; Public Health England (Salisbury, UK).

Techniques: Migration, In Vitro, Small Interfering RNA, Control

Journal: Molecular Medicine Reports

Article Title: O-GlcNAcylation promotes migration and invasion in human ovarian cancer cells via the RhoA/ROCK/MLC pathway

doi: 10.3892/mmr.2017.6244

Figure Lengend Snippet: O-GlcNAcylation affects RhoA activity and MLC phosphorylation in SKOV3 and 59M human ovarian cancer cells. (A) RhoA activity was evaluated by pull-down assay and western blotting. (B) MLC phosphorylation levels were assessed by western blotting. Transfection with siOGT and treatment with ThiaG were used to downregulate and upregulate O-GlcNAcylation, respectively. O-GlcNAc, O-linked β-N-acetylglucosamine; RhoA, Ras homolog family member A; ThiaG, Thiamet-G; siOGT, O-Linked β-N-acetylglucosamine transferase small interfering RNA; Ctrl, control; MLC, myosin light chain; p-, phosphorylated.

Article Snippet: Human ovarian epithelial adenocarcinoma SKOV3 cells were purchased from the Cell Bank of the Chinese Academy of Sciences (Shanghai, China) and endometrioid-type ovarian epithelial carcinoma 59M cells were purchased from the European Collection of Authenticated Cell Cultures; Public Health England (Salisbury, UK).

Techniques: Activity Assay, Phospho-proteomics, Pull Down Assay, Western Blot, Transfection, Small Interfering RNA, Control

Journal: Molecular Medicine Reports

Article Title: O-GlcNAcylation promotes migration and invasion in human ovarian cancer cells via the RhoA/ROCK/MLC pathway

doi: 10.3892/mmr.2017.6244

Figure Lengend Snippet: siRhoA attenuates O-GlcNAcylation-induced cell migration and invasion in SKOV3 and 59M human ovarian cancer cells. The effect of siRhoA transfection on RhoA (A) mRNA and (B) protein expression levels, assessed by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. (C) Migration and (D) invasion in RhoA silenced and non-silenced cells following ThiaG treatment, assessed by Transwell assay. **P<0.01, with comparisons indicated by lines. O-GlcNAc, O-linked β-N-acetylglucosamine; siRhoA, Ras homolog family member A small interfering RNA; RhoA, Ras homolog family member A; Ctrl, control; GADPH, glyceraldehyde 3-phosphate dehydrogenase; ThiaG, Thiamet-G; N.S., not significant.

Article Snippet: Human ovarian epithelial adenocarcinoma SKOV3 cells were purchased from the Cell Bank of the Chinese Academy of Sciences (Shanghai, China) and endometrioid-type ovarian epithelial carcinoma 59M cells were purchased from the European Collection of Authenticated Cell Cultures; Public Health England (Salisbury, UK).

Techniques: Migration, Transfection, Expressing, Reverse Transcription, Real-time Polymerase Chain Reaction, Western Blot, Transwell Assay, Small Interfering RNA, Control

Journal: Molecular Medicine Reports

Article Title: O-GlcNAcylation promotes migration and invasion in human ovarian cancer cells via the RhoA/ROCK/MLC pathway

doi: 10.3892/mmr.2017.6244

Figure Lengend Snippet: O-GlcNAcylation-induced cell migration and invasion, measured by Transwell assays, is inhibited by Y-27632 treatment in SKOV3 and 59M human ovarian cancer cells. **P<0.01, with comparisons indicated by lines. O-GlcNAc, O-linked β-N-acetylglucosamine; Ctrl, control, ThiaG, Thiamet-G; N.S., not significant.

Article Snippet: Human ovarian epithelial adenocarcinoma SKOV3 cells were purchased from the Cell Bank of the Chinese Academy of Sciences (Shanghai, China) and endometrioid-type ovarian epithelial carcinoma 59M cells were purchased from the European Collection of Authenticated Cell Cultures; Public Health England (Salisbury, UK).

Techniques: Migration, Control