Review

human nsclc cell lines (ATCC)

ATCC is a verified supplier

ATCC manufactures this product

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

ATCC human nsclc cell lines

Exosomal HMGB1 promotes <t>NSCLC</t> progression. (A) Western blot analysis of HMGB1 expression in vector control and HMGB1‐overexpressing <t>(OE)</t> <t>A549</t> and <t>PC9</t> cells. (B) Measurement of HMGB1 levels in exosomes derived from vector control and HMGB1 OE A549 and PC9 cells. (C) Cell proliferation assays of vector and HMGB1 OE A549 and PC9 cells. (D) Cell migration assays in vector and HMGB1 OE A549 and PC9 cells. (E) Colony formation assays for vector and HMGB1 OE A549 and PC9 cells. (F) Cell proliferation of A549 and PC9 cells treated with PBS, recombinant HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (G) Cell migration of A549 and PC9 cells under the same treatment conditions as in (F). (H) Colony formation capacity of A549 and PC9 cells under the same treatment conditions as in (F). (I) Tumour volume in A549‐bearing mice treated with PBS, HMGB1 (10 ng or 100 ng per mouse) or exosomes from vector or HMGB1 OE cells (1 × 10 10 exosomes per mouse). (J) A549 and PC9 cells were seeded at densities of 1 × 10 5 , 1 × 10 6 and 5 × 10 6 cells per six‐well plate and cultured for 3 days. Exosome production was then analysed.

Human Nsclc Cell Lines, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 3569 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human nsclc cell lines/product/ATCC
Average 99 stars, based on 3569 article reviews

human nsclc cell lines - by Bioz Stars, 2026-03

99/100 stars

Images

1) Product Images from "Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4 / NF ‐ κB / IL ‐6/ STAT3 Signalling Cascade"

Article Title: Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4 / NF ‐ κB / IL ‐6/ STAT3 Signalling Cascade

Journal: Journal of Cellular and Molecular Medicine

doi: 10.1111/jcmm.71050

Exosomal HMGB1 promotes NSCLC progression. (A) Western blot analysis of HMGB1 expression in vector control and HMGB1‐overexpressing (OE) A549 and PC9 cells. (B) Measurement of HMGB1 levels in exosomes derived from vector control and HMGB1 OE A549 and PC9 cells. (C) Cell proliferation assays of vector and HMGB1 OE A549 and PC9 cells. (D) Cell migration assays in vector and HMGB1 OE A549 and PC9 cells. (E) Colony formation assays for vector and HMGB1 OE A549 and PC9 cells. (F) Cell proliferation of A549 and PC9 cells treated with PBS, recombinant HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (G) Cell migration of A549 and PC9 cells under the same treatment conditions as in (F). (H) Colony formation capacity of A549 and PC9 cells under the same treatment conditions as in (F). (I) Tumour volume in A549‐bearing mice treated with PBS, HMGB1 (10 ng or 100 ng per mouse) or exosomes from vector or HMGB1 OE cells (1 × 10 10 exosomes per mouse). (J) A549 and PC9 cells were seeded at densities of 1 × 10 5 , 1 × 10 6 and 5 × 10 6 cells per six‐well plate and cultured for 3 days. Exosome production was then analysed.

Figure Legend Snippet: Exosomal HMGB1 promotes NSCLC progression. (A) Western blot analysis of HMGB1 expression in vector control and HMGB1‐overexpressing (OE) A549 and PC9 cells. (B) Measurement of HMGB1 levels in exosomes derived from vector control and HMGB1 OE A549 and PC9 cells. (C) Cell proliferation assays of vector and HMGB1 OE A549 and PC9 cells. (D) Cell migration assays in vector and HMGB1 OE A549 and PC9 cells. (E) Colony formation assays for vector and HMGB1 OE A549 and PC9 cells. (F) Cell proliferation of A549 and PC9 cells treated with PBS, recombinant HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (G) Cell migration of A549 and PC9 cells under the same treatment conditions as in (F). (H) Colony formation capacity of A549 and PC9 cells under the same treatment conditions as in (F). (I) Tumour volume in A549‐bearing mice treated with PBS, HMGB1 (10 ng or 100 ng per mouse) or exosomes from vector or HMGB1 OE cells (1 × 10 10 exosomes per mouse). (J) A549 and PC9 cells were seeded at densities of 1 × 10 5 , 1 × 10 6 and 5 × 10 6 cells per six‐well plate and cultured for 3 days. Exosome production was then analysed.

Techniques Used: Western Blot, Expressing, Plasmid Preparation, Control, Derivative Assay, Migration, Recombinant, Cell Culture

Exosomal HMGB1 activates JAK/STAT3 signalling to promote NSCLC progression. (A) Protein–protein interaction (PPI) network analysis of HMGB1 using the STRING database. (B) Western blot analysis of NF‐κB in A549 and PC9 cells treated with PBS, recombinant HMGB1 (100 ng), exosomes from vector cells or exosomes from HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (C) ELISA quantification of IL‐6 in the supernatant of A549 and PC9 cells under the same treatment conditions as in (B). (D) Immunofluorescence staining of p‐STAT3 of A549 and PC9 cells under the same treatments, including an additional group co‐treated with exosomes from HMGB1 OE cells and NF‐κB inhibitor (50 μM). (E) Cell proliferation of A549 and PC9 cells treated with HMGB1 OE‐derived exosomes alone or in combination with NF‐κB inhibitor (50 μM) or STAT3 inhibitor (20 μM). (F) Cell migration under the same treatment conditions as in (E). (G) Colony formation assays of A549 and PC9 cells under the same treatment conditions as in (E).

Figure Legend Snippet: Exosomal HMGB1 activates JAK/STAT3 signalling to promote NSCLC progression. (A) Protein–protein interaction (PPI) network analysis of HMGB1 using the STRING database. (B) Western blot analysis of NF‐κB in A549 and PC9 cells treated with PBS, recombinant HMGB1 (100 ng), exosomes from vector cells or exosomes from HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (C) ELISA quantification of IL‐6 in the supernatant of A549 and PC9 cells under the same treatment conditions as in (B). (D) Immunofluorescence staining of p‐STAT3 of A549 and PC9 cells under the same treatments, including an additional group co‐treated with exosomes from HMGB1 OE cells and NF‐κB inhibitor (50 μM). (E) Cell proliferation of A549 and PC9 cells treated with HMGB1 OE‐derived exosomes alone or in combination with NF‐κB inhibitor (50 μM) or STAT3 inhibitor (20 μM). (F) Cell migration under the same treatment conditions as in (E). (G) Colony formation assays of A549 and PC9 cells under the same treatment conditions as in (E).

Techniques Used: Western Blot, Recombinant, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Derivative Assay, Migration

Targeting HMGB1 signalling improves therapeutic outcomes in NSCLC. (A) Correlation analysis between immune infiltration scores and HMGB1 expression in 491 LUAD and 500 LUSC patients from the TCGA database. (B) Correlation between HMGB1 expression and the distribution of various immune cell subsets in LUAD and LUSC patients. (C, D) THP‐1–derived M0 macrophages were treated with PBS, HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). M1 macrophage markers (CD86, CD80, iNOS) and M2 markers (CD206, IL‐10, Arg1) were quantified by PCR. (E) Lewis tumour‐bearing mice were treated with PBS, HMGB1 OE‐derived exosomes (1 × 10 10 exosomes per mouse, twice per week), anti‐PD‐1 antibody (RMP1‐14, 200 μg per mouse, twice per week) or combination therapy ( n = 5 per group). Tumour volumes and apoptosis levels in tumour tissues (day 25) were assessed. (F) PC9 cells were treated with PBS or exosomes from HMGB1 OE cells (cell‐to‐exosome ratio = 1:10), followed by Osimertinib (50 nM, 48 h), and apoptosis was measured. (G) A549 and PC9 cells were similarly treated with PBS or HMGB1 OE‐derived exosomes, followed by Cisplatin (5 μM, 48 h), and apoptosis was analysed. (H) A549 and PC9 cells were similarly treated with paclitaxel (10 μM, 48 h) under the same conditions, and cell apoptosis was determined. (I) A549‐bearing mice were treated with HMGB1 OE‐derived exosomes (1 × 10 10 exosomes per mouse), followed by PBS, paclitaxel (PTX, 10 mg/kg, twice per week), STAT3 inhibitor (5 mg/kg, twice per week) or combination therapy. (J) Schematic diagram illustrating the proposed mechanism: HMGB1 upregulates TLR4, thereby activating the NF‐κB–IL‐6 axis and stimulating JAK2/STAT3 signalling to promote tumour progression. Concurrently, HMGB1 facilitates M2 macrophage polarisation.

Figure Legend Snippet: Targeting HMGB1 signalling improves therapeutic outcomes in NSCLC. (A) Correlation analysis between immune infiltration scores and HMGB1 expression in 491 LUAD and 500 LUSC patients from the TCGA database. (B) Correlation between HMGB1 expression and the distribution of various immune cell subsets in LUAD and LUSC patients. (C, D) THP‐1–derived M0 macrophages were treated with PBS, HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). M1 macrophage markers (CD86, CD80, iNOS) and M2 markers (CD206, IL‐10, Arg1) were quantified by PCR. (E) Lewis tumour‐bearing mice were treated with PBS, HMGB1 OE‐derived exosomes (1 × 10 10 exosomes per mouse, twice per week), anti‐PD‐1 antibody (RMP1‐14, 200 μg per mouse, twice per week) or combination therapy ( n = 5 per group). Tumour volumes and apoptosis levels in tumour tissues (day 25) were assessed. (F) PC9 cells were treated with PBS or exosomes from HMGB1 OE cells (cell‐to‐exosome ratio = 1:10), followed by Osimertinib (50 nM, 48 h), and apoptosis was measured. (G) A549 and PC9 cells were similarly treated with PBS or HMGB1 OE‐derived exosomes, followed by Cisplatin (5 μM, 48 h), and apoptosis was analysed. (H) A549 and PC9 cells were similarly treated with paclitaxel (10 μM, 48 h) under the same conditions, and cell apoptosis was determined. (I) A549‐bearing mice were treated with HMGB1 OE‐derived exosomes (1 × 10 10 exosomes per mouse), followed by PBS, paclitaxel (PTX, 10 mg/kg, twice per week), STAT3 inhibitor (5 mg/kg, twice per week) or combination therapy. (J) Schematic diagram illustrating the proposed mechanism: HMGB1 upregulates TLR4, thereby activating the NF‐κB–IL‐6 axis and stimulating JAK2/STAT3 signalling to promote tumour progression. Concurrently, HMGB1 facilitates M2 macrophage polarisation.

Techniques Used: Expressing, Derivative Assay, Plasmid Preparation

Image Search Results

Journal: Journal of Cellular and Molecular Medicine

Article Title: Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4 / NF ‐ κB / IL ‐6/ STAT3 Signalling Cascade

doi: 10.1111/jcmm.71050

Figure Lengend Snippet: Exosomal HMGB1 promotes NSCLC progression. (A) Western blot analysis of HMGB1 expression in vector control and HMGB1‐overexpressing (OE) A549 and PC9 cells. (B) Measurement of HMGB1 levels in exosomes derived from vector control and HMGB1 OE A549 and PC9 cells. (C) Cell proliferation assays of vector and HMGB1 OE A549 and PC9 cells. (D) Cell migration assays in vector and HMGB1 OE A549 and PC9 cells. (E) Colony formation assays for vector and HMGB1 OE A549 and PC9 cells. (F) Cell proliferation of A549 and PC9 cells treated with PBS, recombinant HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (G) Cell migration of A549 and PC9 cells under the same treatment conditions as in (F). (H) Colony formation capacity of A549 and PC9 cells under the same treatment conditions as in (F). (I) Tumour volume in A549‐bearing mice treated with PBS, HMGB1 (10 ng or 100 ng per mouse) or exosomes from vector or HMGB1 OE cells (1 × 10 10 exosomes per mouse). (J) A549 and PC9 cells were seeded at densities of 1 × 10 5 , 1 × 10 6 and 5 × 10 6 cells per six‐well plate and cultured for 3 days. Exosome production was then analysed.

Article Snippet: Human NSCLC cell lines (A549, PC9), human embryonic kidney cells (HEK293T) and the human monocytic leukaemia cell line THP‐1 were obtained from the American Type Culture Collection (ATCC, USA).

Techniques: Western Blot, Expressing, Plasmid Preparation, Control, Derivative Assay, Migration, Recombinant, Cell Culture

Journal: Journal of Cellular and Molecular Medicine

Article Title: Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4 / NF ‐ κB / IL ‐6/ STAT3 Signalling Cascade

doi: 10.1111/jcmm.71050

Figure Lengend Snippet: Exosomal HMGB1 activates JAK/STAT3 signalling to promote NSCLC progression. (A) Protein–protein interaction (PPI) network analysis of HMGB1 using the STRING database. (B) Western blot analysis of NF‐κB in A549 and PC9 cells treated with PBS, recombinant HMGB1 (100 ng), exosomes from vector cells or exosomes from HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). (C) ELISA quantification of IL‐6 in the supernatant of A549 and PC9 cells under the same treatment conditions as in (B). (D) Immunofluorescence staining of p‐STAT3 of A549 and PC9 cells under the same treatments, including an additional group co‐treated with exosomes from HMGB1 OE cells and NF‐κB inhibitor (50 μM). (E) Cell proliferation of A549 and PC9 cells treated with HMGB1 OE‐derived exosomes alone or in combination with NF‐κB inhibitor (50 μM) or STAT3 inhibitor (20 μM). (F) Cell migration under the same treatment conditions as in (E). (G) Colony formation assays of A549 and PC9 cells under the same treatment conditions as in (E).

Techniques: Western Blot, Recombinant, Plasmid Preparation, Enzyme-linked Immunosorbent Assay, Immunofluorescence, Staining, Derivative Assay, Migration

Journal: Journal of Cellular and Molecular Medicine

Article Title: Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4 / NF ‐ κB / IL ‐6/ STAT3 Signalling Cascade

doi: 10.1111/jcmm.71050

Figure Lengend Snippet: Targeting HMGB1 signalling improves therapeutic outcomes in NSCLC. (A) Correlation analysis between immune infiltration scores and HMGB1 expression in 491 LUAD and 500 LUSC patients from the TCGA database. (B) Correlation between HMGB1 expression and the distribution of various immune cell subsets in LUAD and LUSC patients. (C, D) THP‐1–derived M0 macrophages were treated with PBS, HMGB1 (10 or 100 ng) or exosomes derived from vector or HMGB1 OE cells (cell‐to‐exosome ratio = 1:10). M1 macrophage markers (CD86, CD80, iNOS) and M2 markers (CD206, IL‐10, Arg1) were quantified by PCR. (E) Lewis tumour‐bearing mice were treated with PBS, HMGB1 OE‐derived exosomes (1 × 10 10 exosomes per mouse, twice per week), anti‐PD‐1 antibody (RMP1‐14, 200 μg per mouse, twice per week) or combination therapy ( n = 5 per group). Tumour volumes and apoptosis levels in tumour tissues (day 25) were assessed. (F) PC9 cells were treated with PBS or exosomes from HMGB1 OE cells (cell‐to‐exosome ratio = 1:10), followed by Osimertinib (50 nM, 48 h), and apoptosis was measured. (G) A549 and PC9 cells were similarly treated with PBS or HMGB1 OE‐derived exosomes, followed by Cisplatin (5 μM, 48 h), and apoptosis was analysed. (H) A549 and PC9 cells were similarly treated with paclitaxel (10 μM, 48 h) under the same conditions, and cell apoptosis was determined. (I) A549‐bearing mice were treated with HMGB1 OE‐derived exosomes (1 × 10 10 exosomes per mouse), followed by PBS, paclitaxel (PTX, 10 mg/kg, twice per week), STAT3 inhibitor (5 mg/kg, twice per week) or combination therapy. (J) Schematic diagram illustrating the proposed mechanism: HMGB1 upregulates TLR4, thereby activating the NF‐κB–IL‐6 axis and stimulating JAK2/STAT3 signalling to promote tumour progression. Concurrently, HMGB1 facilitates M2 macrophage polarisation.

Techniques: Expressing, Derivative Assay, Plasmid Preparation

Bi-CD47-IT bound and inhibited two non-small cell lung cancer (NSCLC) cells. (A and D) In vitro binding affinity analysis of the Alexa Fluor 488-labeled bi-CD47-IT to human NSCLC A549 cells (A) and human NSCLC H1299 cells (D) by flow cytometry analysis. FITC-anti-human CD47 mAb (B6H12) was used as a positive control, and Alexa Fluor 488-labeled isotype mouse IgG1 served as a negative control. The data are representative of three individual experiments. (B and E) K D determination of bi-CD47-IT to human NSCLC A549 cells (B) and human NSCLC H1299 cells (E) using flow cytometry and nonlinear least-squares fitting. The mean fluorescence intensity (MFI) was plotted over a wide range of Alexa Fluor 488-labeled bi-CD47-IT concentrations. Nonlinear regression was based on the equation Y = Bmax × X/ (K D + X), where Y = MFI at the given Alexa Fluor 488-labeled bi-CD47-IT after subtracting the background, X = Alexa Fluor 488-labeled bi-CD47-IT concentration, and Bmax = the maximum specific binding in the same units as Y. (C and F) In vitro efficacy of bi-CD47-IT to human NSCLC A549 cells (C) and human NSCLC H1299 cells (F) determined by the CellTiter-Glo ® Luminescent Cell Viability Assay (purple line: bi-CD47-IT group; black line: pCD3-IT group as negative control). Y-axis: percent inhibition of cell viability determined by the number of viable cells based on the quantification of ATP. X-axis: immunotoxin concentration. Cycloheximide (1.25 mg/mL) was used as a positive control. The negative control wells contained cells without immunotoxin. Data is from three individual experiments. Error bars indicate SD.

Journal: bioRxiv

Article Title: Bivalent CD47 Immunotoxin for Targeted Therapy of Lung Cancer

doi: 10.64898/2025.12.24.696420

Figure Lengend Snippet: Bi-CD47-IT bound and inhibited two non-small cell lung cancer (NSCLC) cells. (A and D) In vitro binding affinity analysis of the Alexa Fluor 488-labeled bi-CD47-IT to human NSCLC A549 cells (A) and human NSCLC H1299 cells (D) by flow cytometry analysis. FITC-anti-human CD47 mAb (B6H12) was used as a positive control, and Alexa Fluor 488-labeled isotype mouse IgG1 served as a negative control. The data are representative of three individual experiments. (B and E) K D determination of bi-CD47-IT to human NSCLC A549 cells (B) and human NSCLC H1299 cells (E) using flow cytometry and nonlinear least-squares fitting. The mean fluorescence intensity (MFI) was plotted over a wide range of Alexa Fluor 488-labeled bi-CD47-IT concentrations. Nonlinear regression was based on the equation Y = Bmax × X/ (K D + X), where Y = MFI at the given Alexa Fluor 488-labeled bi-CD47-IT after subtracting the background, X = Alexa Fluor 488-labeled bi-CD47-IT concentration, and Bmax = the maximum specific binding in the same units as Y. (C and F) In vitro efficacy of bi-CD47-IT to human NSCLC A549 cells (C) and human NSCLC H1299 cells (F) determined by the CellTiter-Glo ® Luminescent Cell Viability Assay (purple line: bi-CD47-IT group; black line: pCD3-IT group as negative control). Y-axis: percent inhibition of cell viability determined by the number of viable cells based on the quantification of ATP. X-axis: immunotoxin concentration. Cycloheximide (1.25 mg/mL) was used as a positive control. The negative control wells contained cells without immunotoxin. Data is from three individual experiments. Error bars indicate SD.

Article Snippet: Human NSCLC A549 and H1299 cell lines were obtained from ATCC (Cat# CCL-185 and CRL-5803, Manassas, VA).

Techniques: In Vitro, Binding Assay, Labeling, Flow Cytometry, Positive Control, Negative Control, Fluorescence, Concentration Assay, Cell Viability Assay, Inhibition

Bi-CD47-IT effectively inhibited tumor growth in two NSCLC CDX mouse models. (A-D) Human NSCLC A549 CDX mouse model ( NSG mice). (A) A549 tumor volume curves. (B) A549 tumor volume on day 4 (pre-treatment), 14 (post-treatment), 35 and 40 (study endpoint). (C) A549 tumor volume on day 35 and tumor size on day 40. (D) A549 tumor-weight on day 40. No visible tumors were found on day 40 in 50% (3 of 6) of the tumor-bearing mice. (E-H) Human NSCLC H1299 CDX mouse model ( NSG mice). (E) H1299 tumor volume curves. (F) H1299 tumor volume on day 4 (pre-treatment), 14 (post-treatment), and 28 (study endpoint). (G) H1299 tumor size on day 28. (H) H1299 tumor weight on day 28. The p values in panel (A) and (E) were calculated using Two-Way ANOVA (GraphPad Prism 10). The p values in panel (B), (D), (F) and (H) were calculated using two-tailed Student t-test (GraphPad Prism 10).

Journal: bioRxiv

Article Title: Bivalent CD47 Immunotoxin for Targeted Therapy of Lung Cancer

doi: 10.64898/2025.12.24.696420

Figure Lengend Snippet: Bi-CD47-IT effectively inhibited tumor growth in two NSCLC CDX mouse models. (A-D) Human NSCLC A549 CDX mouse model ( NSG mice). (A) A549 tumor volume curves. (B) A549 tumor volume on day 4 (pre-treatment), 14 (post-treatment), 35 and 40 (study endpoint). (C) A549 tumor volume on day 35 and tumor size on day 40. (D) A549 tumor-weight on day 40. No visible tumors were found on day 40 in 50% (3 of 6) of the tumor-bearing mice. (E-H) Human NSCLC H1299 CDX mouse model ( NSG mice). (E) H1299 tumor volume curves. (F) H1299 tumor volume on day 4 (pre-treatment), 14 (post-treatment), and 28 (study endpoint). (G) H1299 tumor size on day 28. (H) H1299 tumor weight on day 28. The p values in panel (A) and (E) were calculated using Two-Way ANOVA (GraphPad Prism 10). The p values in panel (B), (D), (F) and (H) were calculated using two-tailed Student t-test (GraphPad Prism 10).

Article Snippet: Human NSCLC A549 and H1299 cell lines were obtained from ATCC (Cat# CCL-185 and CRL-5803, Manassas, VA).

Techniques: Two Tailed Test

Bi-CD47-IT effectively inhibited tumor growth in a humanized NSCLC A549 CDX mouse model. Hu-CD34 + NSG-SGM3 mice were used for this study. (A) Tumor volume curves. (B) Tumor volume on day 5 (pre-treatment), 15 (post-treatment), and 33 (study endpoint). (C) Tumor size on day 33. (D) Tumor weight on day 33. The p value in panel (A) was calculated using Two-Way ANOVA (GraphPad Prism 10). The p values in panel (B) and (D) were calculated using two-tailed Student t-test (GraphPad Prism 10).

Journal: bioRxiv

Article Title: Bivalent CD47 Immunotoxin for Targeted Therapy of Lung Cancer

doi: 10.64898/2025.12.24.696420

Figure Lengend Snippet: Bi-CD47-IT effectively inhibited tumor growth in a humanized NSCLC A549 CDX mouse model. Hu-CD34 + NSG-SGM3 mice were used for this study. (A) Tumor volume curves. (B) Tumor volume on day 5 (pre-treatment), 15 (post-treatment), and 33 (study endpoint). (C) Tumor size on day 33. (D) Tumor weight on day 33. The p value in panel (A) was calculated using Two-Way ANOVA (GraphPad Prism 10). The p values in panel (B) and (D) were calculated using two-tailed Student t-test (GraphPad Prism 10).

Article Snippet: Human NSCLC A549 and H1299 cell lines were obtained from ATCC (Cat# CCL-185 and CRL-5803, Manassas, VA).

Techniques: Two Tailed Test

Bi-CD47-IT effectively inhibited tumor growth in orthotopic NSCLC CDX mouse models. (A-F) Orthotopic NSCLC A549 CDX mouse model ( NSG mice). (A) Representative lungs by micro-CT scan analysis. (B) Tumor volumes by micro-CT scan analysis on day 10 and 24. ( C) Tumor volume curves by micro-CT scan analysis. (D) Survival curves. E) Gross examination of the representative lungs on day 25. (F) Histology analysis (H&E staining) of the representative lungs on day 25. (G-L) Humanized orthotopic NSCLC A549 CDX mouse model (Hu-CD34 + NSG-SGM3 mice). (G) Representative lungs by micro-CT scan analysis on day 28. (H) Tumor volumes by micro-CT scan analysis on day 7 (pre-treatment) and 28. (I) Tumor volume curves by micro-CT scan analysis. (J) Survival curves. (K) Gross examination of the representative lungs on day 29. (L) Histology analysis (H&E staining) of the representative lungs on day 29. The p values in panel (B) and (H) were calculated using two-tailed Student t-test (GraphPad Prism 10). The p values in panel (C) and (I) were calculated using Two-way ANNOVA (GraphPad Prism 10). The p values in panel (D) and (J) were calculated using the Mantel-Cox log-rank test (GraphPad Prism 10).

Journal: bioRxiv

Article Title: Bivalent CD47 Immunotoxin for Targeted Therapy of Lung Cancer

doi: 10.64898/2025.12.24.696420

Figure Lengend Snippet: Bi-CD47-IT effectively inhibited tumor growth in orthotopic NSCLC CDX mouse models. (A-F) Orthotopic NSCLC A549 CDX mouse model ( NSG mice). (A) Representative lungs by micro-CT scan analysis. (B) Tumor volumes by micro-CT scan analysis on day 10 and 24. ( C) Tumor volume curves by micro-CT scan analysis. (D) Survival curves. E) Gross examination of the representative lungs on day 25. (F) Histology analysis (H&E staining) of the representative lungs on day 25. (G-L) Humanized orthotopic NSCLC A549 CDX mouse model (Hu-CD34 + NSG-SGM3 mice). (G) Representative lungs by micro-CT scan analysis on day 28. (H) Tumor volumes by micro-CT scan analysis on day 7 (pre-treatment) and 28. (I) Tumor volume curves by micro-CT scan analysis. (J) Survival curves. (K) Gross examination of the representative lungs on day 29. (L) Histology analysis (H&E staining) of the representative lungs on day 29. The p values in panel (B) and (H) were calculated using two-tailed Student t-test (GraphPad Prism 10). The p values in panel (C) and (I) were calculated using Two-way ANNOVA (GraphPad Prism 10). The p values in panel (D) and (J) were calculated using the Mantel-Cox log-rank test (GraphPad Prism 10).

Article Snippet: Human NSCLC A549 and H1299 cell lines were obtained from ATCC (Cat# CCL-185 and CRL-5803, Manassas, VA).

Techniques: Micro-CT, Staining, Two Tailed Test

Bi-CD47-IT was even more effective in an experimental metastasis NSCLC A549 CDX mouse model. (A) Survival curves. (B) Gross examination of the representative lungs on day 38. (C) Histology analysis (H&E staining) of the representative lungs on day 38. (D) Gross examination of the representative spleens on day 38. (E-F) Immunohistochemistry (IHC) analysis of representative spleens using an anti-human CD47 mAb on day 38. The p value in panel (A) was calculated using the Mantel-Cox log-rank test (GraphPad Prism 10). The p value in panel (F) was calculated using two-tailed Student t-test (GraphPad Prism 10).

Journal: bioRxiv

Article Title: Bivalent CD47 Immunotoxin for Targeted Therapy of Lung Cancer

doi: 10.64898/2025.12.24.696420

Figure Lengend Snippet: Bi-CD47-IT was even more effective in an experimental metastasis NSCLC A549 CDX mouse model. (A) Survival curves. (B) Gross examination of the representative lungs on day 38. (C) Histology analysis (H&E staining) of the representative lungs on day 38. (D) Gross examination of the representative spleens on day 38. (E-F) Immunohistochemistry (IHC) analysis of representative spleens using an anti-human CD47 mAb on day 38. The p value in panel (A) was calculated using the Mantel-Cox log-rank test (GraphPad Prism 10). The p value in panel (F) was calculated using two-tailed Student t-test (GraphPad Prism 10).

Article Snippet: Human NSCLC A549 and H1299 cell lines were obtained from ATCC (Cat# CCL-185 and CRL-5803, Manassas, VA).

Techniques: Staining, Immunohistochemistry, Two Tailed Test

Bi-CD47-IT was highly effective in two NSCLC PDX models. (A-C) NSCLC PDX1 (CT257-F4) mouse model. (A) Tumor volume on day 15 (pre-treatment), 25 (post treatment) and 44 (study endpoint). (B) Tumor size on day 44. (C) Tumor weight on day 44. (D-F) NSCLC PDX2 (220900-M3) mouse model. (D) Tumor volume on day 12 (pre-treatment), 22 (post treatment), 30 and 35 (study endpoint). (E) Tumor size on day 35. (F) Tumor weight on day 35. The p values in panel (A), (C), (D) and (F) were calculated using two-tailed Student t-test (GraphPad Prism 10).

Journal: bioRxiv

Article Title: Bivalent CD47 Immunotoxin for Targeted Therapy of Lung Cancer

doi: 10.64898/2025.12.24.696420

Figure Lengend Snippet: Bi-CD47-IT was highly effective in two NSCLC PDX models. (A-C) NSCLC PDX1 (CT257-F4) mouse model. (A) Tumor volume on day 15 (pre-treatment), 25 (post treatment) and 44 (study endpoint). (B) Tumor size on day 44. (C) Tumor weight on day 44. (D-F) NSCLC PDX2 (220900-M3) mouse model. (D) Tumor volume on day 12 (pre-treatment), 22 (post treatment), 30 and 35 (study endpoint). (E) Tumor size on day 35. (F) Tumor weight on day 35. The p values in panel (A), (C), (D) and (F) were calculated using two-tailed Student t-test (GraphPad Prism 10).

Article Snippet: Human NSCLC A549 and H1299 cell lines were obtained from ATCC (Cat# CCL-185 and CRL-5803, Manassas, VA).

Techniques: Two Tailed Test

Review

Structured Review

Images

1) Product Images from "Exosomal HMGB1 Orchestrates NSCLC Progression and Immunosuppressive Macrophage Polarisation Through the TLR4 / NF ‐ κB / IL ‐6/ STAT3 Signalling Cascade"

Similar Products

Image Search Results