Structured Review

LGC Standards GmbH a549 cells
Differential responses to carboplatin treatment in PC9 and <t>A549</t> cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.
A549 Cells, supplied by LGC Standards GmbH, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/a549 cells/product/LGC Standards GmbH
Average 92 stars, based on 3 article reviews
Price from $9.99 to $1999.99
a549 cells - by Bioz Stars, 2020-09
92/100 stars

Images

1) Product Images from "Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography"

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography

Journal: PLoS ONE

doi: 10.1371/journal.pone.0091694

Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.
Figure Legend Snippet: Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.

Techniques Used: Inhibition, Sulforhodamine B Assay, Western Blot, Flow Cytometry, Fluorescence, Staining

Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.
Figure Legend Snippet: Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.

Techniques Used: Activity Assay, Western Blot

Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P
Figure Legend Snippet: Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P

Techniques Used: Positron Emission Tomography, Imaging, Software

18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P
Figure Legend Snippet: 18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P

Techniques Used: Positron Emission Tomography, Mouse Assay

2) Product Images from "CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells"

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1402008

CXCL9 inhibits TGF-β1 mediated EMT in A549 cells
Figure Legend Snippet: CXCL9 inhibits TGF-β1 mediated EMT in A549 cells

Techniques Used:

3) Product Images from "Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography"

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography

Journal: PLoS ONE

doi: 10.1371/journal.pone.0091694

Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.
Figure Legend Snippet: Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.

Techniques Used: Inhibition, Sulforhodamine B Assay, Western Blot, Flow Cytometry, Fluorescence, Staining

Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.
Figure Legend Snippet: Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.

Techniques Used: Activity Assay, Western Blot

Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P
Figure Legend Snippet: Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P

Techniques Used: Positron Emission Tomography, Imaging, Software

18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P
Figure Legend Snippet: 18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P

Techniques Used: Positron Emission Tomography, Mouse Assay

4) Product Images from "CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells"

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1402008

CXCL9 inhibits TGF-β1 mediated EMT in A549 cells
Figure Legend Snippet: CXCL9 inhibits TGF-β1 mediated EMT in A549 cells

Techniques Used:

5) Product Images from "CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells"

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1402008

CXCL9 inhibits TGF-β1 mediated EMT in A549 cells
Figure Legend Snippet: CXCL9 inhibits TGF-β1 mediated EMT in A549 cells

Techniques Used:

6) Product Images from "Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography"

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography

Journal: PLoS ONE

doi: 10.1371/journal.pone.0091694

Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.
Figure Legend Snippet: Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.

Techniques Used: Inhibition, Sulforhodamine B Assay, Western Blot, Flow Cytometry, Fluorescence, Staining

Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.
Figure Legend Snippet: Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.

Techniques Used: Activity Assay, Western Blot

Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P
Figure Legend Snippet: Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P

Techniques Used: Positron Emission Tomography, Imaging, Software

18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P
Figure Legend Snippet: 18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P

Techniques Used: Positron Emission Tomography, Mouse Assay

7) Product Images from "Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography"

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography

Journal: PLoS ONE

doi: 10.1371/journal.pone.0091694

Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.
Figure Legend Snippet: Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.

Techniques Used: Inhibition, Sulforhodamine B Assay, Western Blot, Flow Cytometry, Fluorescence, Staining

Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.
Figure Legend Snippet: Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.

Techniques Used: Activity Assay, Western Blot

Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P
Figure Legend Snippet: Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P

Techniques Used: Positron Emission Tomography, Imaging, Software

18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P
Figure Legend Snippet: 18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P

Techniques Used: Positron Emission Tomography, Mouse Assay

8) Product Images from "Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography"

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography

Journal: PLoS ONE

doi: 10.1371/journal.pone.0091694

Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.
Figure Legend Snippet: Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.

Techniques Used: Inhibition, Sulforhodamine B Assay, Western Blot, Flow Cytometry, Fluorescence, Staining

Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.
Figure Legend Snippet: Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.

Techniques Used: Activity Assay, Western Blot

Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P
Figure Legend Snippet: Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P

Techniques Used: Positron Emission Tomography, Imaging, Software

18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P
Figure Legend Snippet: 18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P

Techniques Used: Positron Emission Tomography, Mouse Assay

9) Product Images from "CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells"

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1402008

CXCL9 inhibits TGF-β1 mediated EMT in A549 cells
Figure Legend Snippet: CXCL9 inhibits TGF-β1 mediated EMT in A549 cells

Techniques Used:

10) Product Images from "CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells"

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1402008

CXCL9 inhibits TGF-β1 mediated EMT in A549 cells
Figure Legend Snippet: CXCL9 inhibits TGF-β1 mediated EMT in A549 cells

Techniques Used:

11) Product Images from "CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells"

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1402008

CXCL9 inhibits TGF-β1 mediated EMT in A549 cells
Figure Legend Snippet: CXCL9 inhibits TGF-β1 mediated EMT in A549 cells

Techniques Used:

12) Product Images from "Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography"

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography

Journal: PLoS ONE

doi: 10.1371/journal.pone.0091694

Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.
Figure Legend Snippet: Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.

Techniques Used: Inhibition, Sulforhodamine B Assay, Western Blot, Flow Cytometry, Fluorescence, Staining

Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.
Figure Legend Snippet: Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.

Techniques Used: Activity Assay, Western Blot

Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P
Figure Legend Snippet: Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P

Techniques Used: Positron Emission Tomography, Imaging, Software

18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P
Figure Legend Snippet: 18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P

Techniques Used: Positron Emission Tomography, Mouse Assay

13) Product Images from "CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells"

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1402008

CXCL9 inhibits TGF-β1 mediated EMT in A549 cells
Figure Legend Snippet: CXCL9 inhibits TGF-β1 mediated EMT in A549 cells

Techniques Used:

14) Product Images from "CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells"

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells

Journal: Journal of immunology (Baltimore, Md. : 1950)

doi: 10.4049/jimmunol.1402008

CXCL9 inhibits TGF-β1 mediated EMT in A549 cells
Figure Legend Snippet: CXCL9 inhibits TGF-β1 mediated EMT in A549 cells

Techniques Used:

Related Articles

Selection:

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells
Article Snippet: .. TGF-β1 treatment of A549 cells significantly induced some, but not all mesenchymal markers and suppressed the expression of a selection of epithelial markers, though not a full panel. ..

Cell Culture:

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography
Article Snippet: .. Cell Culture PC9 and A549 cells were from LGC Standards (Teddington, Middlesex, UK). ..

Concentration Assay:

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells
Article Snippet: .. To prepare samples for analysis, A549 cells were serum starved for 24 h then incubated in medium alone or supplemented with TGF-β1, CXCL9 or both at a concentration of 10 ng/mL for the time periods indicated. .. Following the indicated treatment, cells were fixed, permeabilized and blocked by incubation in 5% BSA (Sigma-Aldrich).

Incubation:

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells
Article Snippet: .. To prepare samples for analysis, A549 cells were serum starved for 24 h then incubated in medium alone or supplemented with TGF-β1, CXCL9 or both at a concentration of 10 ng/mL for the time periods indicated. .. Following the indicated treatment, cells were fixed, permeabilized and blocked by incubation in 5% BSA (Sigma-Aldrich).

other:

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography
Article Snippet: No significant change in 18 F-ICMT-11 uptake was detected with A549 cells following addition of carboplatin ( ).

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography
Article Snippet: In A549 cells, cell death was induced via the necrotic pathway, concurrent with minimal 18 F-ICMT-11 uptake, indicating great specificity of 18 F-ICMT-11 to trace apoptotic, but not necrotic mechanisms of cell death.

Activity Assay:

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography
Article Snippet: .. Despite the detection of faint bands corresponding to cleaved caspase-3 and PARP with A549 cells treated either 48 h or 72 h ( (ii)), there was no increase in detectable caspase-3/7 activity ( ). ..

Expressing:

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells
Article Snippet: .. Treatment of A549 cells with CXCL9 for 48 h did not lead to any significant change in the expression of mesenchymal or epithelial marker mRNA compared to control cells ( ). .. Expression of collagen 1a1, vimentin and α-SMA mRNA measured by qRT-PCR was significantly reduced in cells treated with TGF-β1 and CXCL9 compared to those treated with TGF-β1 alone ( ).

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells
Article Snippet: .. TGF-β1 treatment of A549 cells significantly induced some, but not all mesenchymal markers and suppressed the expression of a selection of epithelial markers, though not a full panel. ..

Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography
Article Snippet: .. In contrast, A549 cells have high ERCC1 expression (low- and high-expressing for PC9 and A549 respectively; Online Resource 1) and have wt EGFR . .. Cell death was induced in vitro in PC9 and A549 human NSCLC cells following carboplatin treatment (0–200 µM).

Marker:

Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells
Article Snippet: .. Treatment of A549 cells with CXCL9 for 48 h did not lead to any significant change in the expression of mesenchymal or epithelial marker mRNA compared to control cells ( ). .. Expression of collagen 1a1, vimentin and α-SMA mRNA measured by qRT-PCR was significantly reduced in cells treated with TGF-β1 and CXCL9 compared to those treated with TGF-β1 alone ( ).

Similar Products

  • Logo
  • About
  • News
  • Press Release
  • Team
  • Advisors
  • Partners
  • Contact
  • Bioz Stars
  • Bioz vStars
  • 91
    LGC Standards GmbH lung cancer cell lines human lung cancer cell lines a549
    Tumor take Tumor growth kinetics in xenografts. Monolateral xenograft tumors were established s.c. in athymic Balb/c nu-nu mice. ( A ) Timeline reflecting tumor take and growth kinetics between experimental groups. Green indicates time-points when tumors reached 4 mm; Red reflects time-points when tumors reached 7 mm; Black X : reflects tumors retrieved due to ulceration or with diameters ≥10 mm. ( B ) Tumor growth kinetics: (○) <t>A549</t> lung tumor cells (n = 7), (◊) A549 tumor cells with control CAFs (n = 8), (●) A549 tumor cells with irradiated CAFs (iCAFs) (1 × 18 Gy) (n = 7), (▪) A549 tumor cells with fractionated-irradiated CAFs (3 × 6 Gy) (n = 5). ( C ) Tumor volumes at 41 days post-implantation. Group 1 (n = 7); group 2 (n = 8); group 3 (n = 7); group 4 (n = 5). Differences in tumor volumes between group 1 and 2 were statistically significant (*p
    Lung Cancer Cell Lines Human Lung Cancer Cell Lines A549, supplied by LGC Standards GmbH, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/lung cancer cell lines human lung cancer cell lines a549/product/LGC Standards GmbH
    Average 91 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    lung cancer cell lines human lung cancer cell lines a549 - by Bioz Stars, 2020-09
    91/100 stars
      Buy from Supplier

    92
    LGC Standards GmbH a549 cells
    Differential responses to carboplatin treatment in PC9 and <t>A549</t> cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.
    A549 Cells, supplied by LGC Standards GmbH, used in various techniques. Bioz Stars score: 92/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/a549 cells/product/LGC Standards GmbH
    Average 92 stars, based on 3 article reviews
    Price from $9.99 to $1999.99
    a549 cells - by Bioz Stars, 2020-09
    92/100 stars
      Buy from Supplier

    Image Search Results


    Tumor take Tumor growth kinetics in xenografts. Monolateral xenograft tumors were established s.c. in athymic Balb/c nu-nu mice. ( A ) Timeline reflecting tumor take and growth kinetics between experimental groups. Green indicates time-points when tumors reached 4 mm; Red reflects time-points when tumors reached 7 mm; Black X : reflects tumors retrieved due to ulceration or with diameters ≥10 mm. ( B ) Tumor growth kinetics: (○) A549 lung tumor cells (n = 7), (◊) A549 tumor cells with control CAFs (n = 8), (●) A549 tumor cells with irradiated CAFs (iCAFs) (1 × 18 Gy) (n = 7), (▪) A549 tumor cells with fractionated-irradiated CAFs (3 × 6 Gy) (n = 5). ( C ) Tumor volumes at 41 days post-implantation. Group 1 (n = 7); group 2 (n = 8); group 3 (n = 7); group 4 (n = 5). Differences in tumor volumes between group 1 and 2 were statistically significant (*p

    Journal: Scientific Reports

    Article Title: Ionizing radiation abrogates the pro-tumorigenic capacity of cancer-associated fibroblasts co-implanted in xenografts

    doi: 10.1038/srep46714

    Figure Lengend Snippet: Tumor take Tumor growth kinetics in xenografts. Monolateral xenograft tumors were established s.c. in athymic Balb/c nu-nu mice. ( A ) Timeline reflecting tumor take and growth kinetics between experimental groups. Green indicates time-points when tumors reached 4 mm; Red reflects time-points when tumors reached 7 mm; Black X : reflects tumors retrieved due to ulceration or with diameters ≥10 mm. ( B ) Tumor growth kinetics: (○) A549 lung tumor cells (n = 7), (◊) A549 tumor cells with control CAFs (n = 8), (●) A549 tumor cells with irradiated CAFs (iCAFs) (1 × 18 Gy) (n = 7), (▪) A549 tumor cells with fractionated-irradiated CAFs (3 × 6 Gy) (n = 5). ( C ) Tumor volumes at 41 days post-implantation. Group 1 (n = 7); group 2 (n = 8); group 3 (n = 7); group 4 (n = 5). Differences in tumor volumes between group 1 and 2 were statistically significant (*p

    Article Snippet: Lung cancer cell lines Human lung cancer cell lines A549 (lung adenocarcinoma) and NCl-H520 (squamous cell carcinoma) were purchased from LGC Standards AB (Borås, Sweden).

    Techniques: Mouse Assay, Irradiation

    Fate of human CAFs co-transplanted in A549 xenografts. ( A ) Time-course experiment showing presence/absence of implanted human CAFs in tumors harvested at 1, 2 and 4 weeks post-implantation. ( B ) Detection of irradiated CAFs (1 × 18 Gy) in tumors 1 week post-implantation; Exogenously administered CAFs are visualized by green CMFDA fluorescence (left panels) and by immune-staining against human-specific anti-PDGFRα antibody (right panels). ( C ) Blinded quantitative scorings of PDGFRα-positive fibroblasts in early tumor tissues with admixed CAFs.

    Journal: Scientific Reports

    Article Title: Ionizing radiation abrogates the pro-tumorigenic capacity of cancer-associated fibroblasts co-implanted in xenografts

    doi: 10.1038/srep46714

    Figure Lengend Snippet: Fate of human CAFs co-transplanted in A549 xenografts. ( A ) Time-course experiment showing presence/absence of implanted human CAFs in tumors harvested at 1, 2 and 4 weeks post-implantation. ( B ) Detection of irradiated CAFs (1 × 18 Gy) in tumors 1 week post-implantation; Exogenously administered CAFs are visualized by green CMFDA fluorescence (left panels) and by immune-staining against human-specific anti-PDGFRα antibody (right panels). ( C ) Blinded quantitative scorings of PDGFRα-positive fibroblasts in early tumor tissues with admixed CAFs.

    Article Snippet: Lung cancer cell lines Human lung cancer cell lines A549 (lung adenocarcinoma) and NCl-H520 (squamous cell carcinoma) were purchased from LGC Standards AB (Borås, Sweden).

    Techniques: Irradiation, Fluorescence, Staining

    Viability of irradiated CAFs Tumor growth characteristics. Viability ( A ) and plating efficiency ( B ) of cultured irradiated CAFs, prior to implantation. In ( A ), viability was measured 24 hours after last radiation dose. In ( B ), plating efficiency of CAFs also 24 hours post-IR. Columns in A and B show values from one CAF donor and are representative outcomes from three different donors. In ( C , D ) fluorescent micrographs of cultured human lung CAFs stained with anti-human PDGFRα antibody (red) and nuclear DNA (DAPI, blue). Panel ( D ) shows PDGFRα-staining of CAFs that were irradiated (1 × 18 Gy) and fixed 5 days post-IR. Panels ( E – G ) demonstrate tumor growth curves for xenografts established s.c. in athymic nude mice in pilot experiments. In ( E ), tumor take and growth from two different human lung tumor cell lines, A549 and H520, was compared. In ( F ), tumor growth characteristics of bilateral tumors established with tumor cells vs. tumor cells/CAFs. Left flank was inoculated with only A549 cells (1 × 10 6 ), whereas right flank received a mix of A549 cells (1 × 10 6 ) and CAFs (1 × 10 6 ). In ( G ), comparative tumor growth kinetics in animals inoculated with admixed control CAFs or irradiated (1 × 18 Gy) CAFs. CAFs were irradiated 24 hours prior to implantation. Tumor area: A = π·l·b .

    Journal: Scientific Reports

    Article Title: Ionizing radiation abrogates the pro-tumorigenic capacity of cancer-associated fibroblasts co-implanted in xenografts

    doi: 10.1038/srep46714

    Figure Lengend Snippet: Viability of irradiated CAFs Tumor growth characteristics. Viability ( A ) and plating efficiency ( B ) of cultured irradiated CAFs, prior to implantation. In ( A ), viability was measured 24 hours after last radiation dose. In ( B ), plating efficiency of CAFs also 24 hours post-IR. Columns in A and B show values from one CAF donor and are representative outcomes from three different donors. In ( C , D ) fluorescent micrographs of cultured human lung CAFs stained with anti-human PDGFRα antibody (red) and nuclear DNA (DAPI, blue). Panel ( D ) shows PDGFRα-staining of CAFs that were irradiated (1 × 18 Gy) and fixed 5 days post-IR. Panels ( E – G ) demonstrate tumor growth curves for xenografts established s.c. in athymic nude mice in pilot experiments. In ( E ), tumor take and growth from two different human lung tumor cell lines, A549 and H520, was compared. In ( F ), tumor growth characteristics of bilateral tumors established with tumor cells vs. tumor cells/CAFs. Left flank was inoculated with only A549 cells (1 × 10 6 ), whereas right flank received a mix of A549 cells (1 × 10 6 ) and CAFs (1 × 10 6 ). In ( G ), comparative tumor growth kinetics in animals inoculated with admixed control CAFs or irradiated (1 × 18 Gy) CAFs. CAFs were irradiated 24 hours prior to implantation. Tumor area: A = π·l·b .

    Article Snippet: Lung cancer cell lines Human lung cancer cell lines A549 (lung adenocarcinoma) and NCl-H520 (squamous cell carcinoma) were purchased from LGC Standards AB (Borås, Sweden).

    Techniques: Irradiation, Cell Culture, Staining, Mouse Assay

    Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.

    Journal: PLoS ONE

    Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography

    doi: 10.1371/journal.pone.0091694

    Figure Lengend Snippet: Differential responses to carboplatin treatment in PC9 and A549 cells. A: Carboplatin-induced growth inhibition in PC9 and A549 cells using a sulforhodamine B assay 72 h post treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 72 h post carboplatin treatment (0–200 µM) in PC9 and A549 cells. Actin was used as a loading control. C, D: Flow cytometric analysis of PC9 (C) and A549 cells (D) treated with carboplatin (100 µM) or vehicle. Apoptotic cells were identified by Annexin V-Alexafluor488 (λ Ex/Em = 495/519 nm) and necrotic cells by 7-AAD (λ Ex/Em = 546/647 nm). Population Q4 represents viable cells, whereas population Q3 represents apoptotic cells that have low 7-AAD fluorescence and stain with Annexin V. Population Q2 represents secondary apoptotic/necrotic cells.

    Article Snippet: In A549 cells, cell death was induced via the necrotic pathway, concurrent with minimal 18 F-ICMT-11 uptake, indicating great specificity of 18 F-ICMT-11 to trace apoptotic, but not necrotic mechanisms of cell death.

    Techniques: Inhibition, Sulforhodamine B Assay, Western Blot, Flow Cytometry, Fluorescence, Staining

    Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.

    Journal: PLoS ONE

    Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography

    doi: 10.1371/journal.pone.0091694

    Figure Lengend Snippet: Temporal changes in cell death markers and 18 F-ICMT-11 uptake after carboplatin treatment. A: Time course of changes in caspase 3/7 activity following carboplatin treatment. B: Western blot analysis of the levels of uncleaved PARP, cleaved PARP and cleaved (active) caspase 3 post 50 µM carboplatin treatment (0–96 h) in PC9 (i) and A549 cells (ii). C: Temporal changes in 18 F-ICMT-11 uptake in cells following carboplatin treatment. D: Correlation between caspase 3 activity and 18 F-ICMT-11 uptake in PC9 cells.

    Article Snippet: In A549 cells, cell death was induced via the necrotic pathway, concurrent with minimal 18 F-ICMT-11 uptake, indicating great specificity of 18 F-ICMT-11 to trace apoptotic, but not necrotic mechanisms of cell death.

    Techniques: Activity Assay, Western Blot

    Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P

    Journal: PLoS ONE

    Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography

    doi: 10.1371/journal.pone.0091694

    Figure Lengend Snippet: Voxel-wise analysis of 18 F-ICMT-11 PET imaging data by PVIS. The intensities of all voxels within the tumour ROIs were computed and expressed as histogram plots of normalized voxel intensity versus the number of voxels. A, B: Typical data from three representative animals (vehicle, 24 h or 48 h carboplatin-treated) for PC9 (A) and A549 (B) are shown. C, D: The statistical comparison of 95 th percentile voxel intensities for PC9 (C) and A549 (D) was performed using Prism v5.0 software (GraphPad). Mean ± SD ( n = 4–6 animals per group).*, P

    Article Snippet: In A549 cells, cell death was induced via the necrotic pathway, concurrent with minimal 18 F-ICMT-11 uptake, indicating great specificity of 18 F-ICMT-11 to trace apoptotic, but not necrotic mechanisms of cell death.

    Techniques: Positron Emission Tomography, Imaging, Software

    18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P

    Journal: PLoS ONE

    Article Title: Preclinical Assessment of Carboplatin Treatment Efficacy in Lung Cancer by 18F-ICMT-11-Positron Emission Tomography

    doi: 10.1371/journal.pone.0091694

    Figure Lengend Snippet: 18 F-ICMT-11 PET image analysis of PC9 and A549 xenografts in vehicle and carboplatin-treated mice. A, B: Tumour volumes recorded by calliper measurements of PC9 (A) and A549 tumours (B) pre- and post-carboplatin treatment as indicated. Data shown are mean ± SD of % volume compared to baseline ( n = 4). *, P

    Article Snippet: In A549 cells, cell death was induced via the necrotic pathway, concurrent with minimal 18 F-ICMT-11 uptake, indicating great specificity of 18 F-ICMT-11 to trace apoptotic, but not necrotic mechanisms of cell death.

    Techniques: Positron Emission Tomography, Mouse Assay

    CXCL9 inhibits TGF-β1 mediated EMT in A549 cells

    Journal: Journal of immunology (Baltimore, Md. : 1950)

    Article Title: CXCL9 Regulates TGF-β1 induced Epithelial to Mesenchymal Transition in Human Alveolar Epithelial Cells

    doi: 10.4049/jimmunol.1402008

    Figure Lengend Snippet: CXCL9 inhibits TGF-β1 mediated EMT in A549 cells

    Article Snippet: TGF-β1 treatment of A549 cells significantly induced some, but not all mesenchymal markers and suppressed the expression of a selection of epithelial markers, though not a full panel.

    Techniques: