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a549 wt cells (ATCC)

Name: a549 wt cells
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ATCC a549 wt cells

Micro-PET studies for 68 Ga- 1 in mice models (n = 3). (A) Static PET images of <t>A549-EGFR</t> T790M mice models at different time points; (B) Time-activity curves generated from A549-EGFR T790M mice PET images; (C) Representative static PET images for H1975, H3255, A549 WT and A549-EGFR T790M (blocked with Rociletinib) mice models at 60 min post-injection; (D) Selected organ uptake value for different tumor models at 60 min post-injection. Red arrows denote the tumor.

A549 Wt Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 35523 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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a549 wt cells - by Bioz Stars, 2026-02

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1) Product Images from "Synthesis, radiolabeling, and evaluation of a 68 Ga-labeled tyrosine kinase inhibitor for detecting EGFR T790M mutations in vivo"

Article Title: Synthesis, radiolabeling, and evaluation of a 68 Ga-labeled tyrosine kinase inhibitor for detecting EGFR T790M mutations in vivo

Journal: Frontiers in Bioengineering and Biotechnology

doi: 10.3389/fbioe.2026.1741512

Micro-PET studies for 68 Ga- 1 in mice models (n = 3). (A) Static PET images of A549-EGFR T790M mice models at different time points; (B) Time-activity curves generated from A549-EGFR T790M mice PET images; (C) Representative static PET images for H1975, H3255, A549 WT and A549-EGFR T790M (blocked with Rociletinib) mice models at 60 min post-injection; (D) Selected organ uptake value for different tumor models at 60 min post-injection. Red arrows denote the tumor.

Figure Legend Snippet: Micro-PET studies for 68 Ga- 1 in mice models (n = 3). (A) Static PET images of A549-EGFR T790M mice models at different time points; (B) Time-activity curves generated from A549-EGFR T790M mice PET images; (C) Representative static PET images for H1975, H3255, A549 WT and A549-EGFR T790M (blocked with Rociletinib) mice models at 60 min post-injection; (D) Selected organ uptake value for different tumor models at 60 min post-injection. Red arrows denote the tumor.

Techniques Used: Micro-PET, Activity Assay, Generated, Injection

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Journal: Frontiers in Bioengineering and Biotechnology

Article Title: Synthesis, radiolabeling, and evaluation of a 68 Ga-labeled tyrosine kinase inhibitor for detecting EGFR T790M mutations in vivo

doi: 10.3389/fbioe.2026.1741512

Figure Lengend Snippet: Micro-PET studies for 68 Ga- 1 in mice models (n = 3). (A) Static PET images of A549-EGFR T790M mice models at different time points; (B) Time-activity curves generated from A549-EGFR T790M mice PET images; (C) Representative static PET images for H1975, H3255, A549 WT and A549-EGFR T790M (blocked with Rociletinib) mice models at 60 min post-injection; (D) Selected organ uptake value for different tumor models at 60 min post-injection. Red arrows denote the tumor.

Article Snippet: H1975 L858R/T790M , H3255 L858R and A549 WT cells were purchased from American Type Culture Collection and cultured in the correspond medium recommended by American Type Culture Collection (ATCC).

Techniques: Micro-PET, Activity Assay, Generated, Injection

C3 deficiency alters gene expression in human lung epithelial A549 cell line, which is rescued by cytosolic C3. A ) Three variants of A549 cells expressing C3 (WT), entirely lacking C3 (C3 KO) or expressing only cytosolic C3 (C3 ΔATG1) were used in this study. Western blotting analysis of cell lysates showing the presence of pro-C3 along with mature alpha and beta chains in WT cells ( B ). No C3 was detected in C3 KO cells while C3 ΔATG1 clones expressed only pro-C3 ( C ). D ) While WT and C3 ΔATG1 cells showed similar gene expression, C3 KO cells had strongly altered gene expression compared to WT and C3 ΔATG1 (padj < 0.05). E ) Heat map representation of the expression patterns in WT, C3 KO and C3 ΔATG1 clones (4 clones for each genotype) and F ) Principal component (PC) analysis of RNA-seq data for WT, C3 KO and C3 ΔATG1 clones showed that C3 KO clones cluster separately from WT and C3 ΔATG1 clones. G ) Venn diagram of DEGs across different genotypes. Summary of KEGG enrichment analysis showing pathways with >2 differentially expressed genes between WT and C3 KO ( H ) and between C3 KO and C3 ΔATG1 ( I ). For analysis of differentially regulated genes, we used the following criteria: pair-wise analysis with padj≤ 0.05 & |log2(foldchange)| ≥ 1

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Intracellular C3 regulates the immune response to infection via NF-κB signaling

doi: 10.1007/s00018-025-05975-4

Figure Lengend Snippet: C3 deficiency alters gene expression in human lung epithelial A549 cell line, which is rescued by cytosolic C3. A ) Three variants of A549 cells expressing C3 (WT), entirely lacking C3 (C3 KO) or expressing only cytosolic C3 (C3 ΔATG1) were used in this study. Western blotting analysis of cell lysates showing the presence of pro-C3 along with mature alpha and beta chains in WT cells ( B ). No C3 was detected in C3 KO cells while C3 ΔATG1 clones expressed only pro-C3 ( C ). D ) While WT and C3 ΔATG1 cells showed similar gene expression, C3 KO cells had strongly altered gene expression compared to WT and C3 ΔATG1 (padj < 0.05). E ) Heat map representation of the expression patterns in WT, C3 KO and C3 ΔATG1 clones (4 clones for each genotype) and F ) Principal component (PC) analysis of RNA-seq data for WT, C3 KO and C3 ΔATG1 clones showed that C3 KO clones cluster separately from WT and C3 ΔATG1 clones. G ) Venn diagram of DEGs across different genotypes. Summary of KEGG enrichment analysis showing pathways with >2 differentially expressed genes between WT and C3 KO ( H ) and between C3 KO and C3 ΔATG1 ( I ). For analysis of differentially regulated genes, we used the following criteria: pair-wise analysis with padj≤ 0.05 & |log2(foldchange)| ≥ 1

Article Snippet: The wild-type (WT) human lung epithelial A549 cells were from the American Type Culture Collection (ATCC).

Techniques: Gene Expression, Expressing, Western Blot, Clone Assay, RNA Sequencing

Cytokine secretion from A549 cells is modulated by the presence of C3. XL cytokine array analysis of supernatants from WT and C3 KO A549 cells infected with M. catarrhalis shows lower secretion from C3 KO cells. Reference spots and negative controls are indicated by + and –, respectively ( A ) with quantification in ( B ), and black arrows indicating IL-8 and MCP-1, as differentially secreted cytokines. Bio-Plex Pro human cytokine 27-plex assay with supernatants from WT, C3 KO and C3 ΔATG1 cells infected with M. catarrhalis ( C ) or Y. enterocolitica ( D ) shows lower secretion from C3 KO cells that is rescued in C3 ΔATG1. Bars represent the average of three biological repetitions indicated with symbols. Two-way ANOVA with Tukey´s multiple comparison test, matched measures within the experiment, * p < 0.05, **** p < 0.0001

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Intracellular C3 regulates the immune response to infection via NF-κB signaling

doi: 10.1007/s00018-025-05975-4

Figure Lengend Snippet: Cytokine secretion from A549 cells is modulated by the presence of C3. XL cytokine array analysis of supernatants from WT and C3 KO A549 cells infected with M. catarrhalis shows lower secretion from C3 KO cells. Reference spots and negative controls are indicated by + and –, respectively ( A ) with quantification in ( B ), and black arrows indicating IL-8 and MCP-1, as differentially secreted cytokines. Bio-Plex Pro human cytokine 27-plex assay with supernatants from WT, C3 KO and C3 ΔATG1 cells infected with M. catarrhalis ( C ) or Y. enterocolitica ( D ) shows lower secretion from C3 KO cells that is rescued in C3 ΔATG1. Bars represent the average of three biological repetitions indicated with symbols. Two-way ANOVA with Tukey´s multiple comparison test, matched measures within the experiment, * p < 0.05, **** p < 0.0001

Article Snippet: The wild-type (WT) human lung epithelial A549 cells were from the American Type Culture Collection (ATCC).

Techniques: Infection, Plex Assay, Comparison

Cytosolic C3 contributes to cytokine release after stimulation of different receptors. ( A - F ) Levels of cytokine secretion measured by ELISA in supernatants from WT, C3 KO and C3 ΔATG1 A549 cells after infection with bacteria are reduced in cells lacking C3. IL-8 secretion after infection with M. catarrhalis ( A ), IL-6 after infection Y. enterocolitica ( B ), RANTES secretion after infection with M. catarrhalis ( C ), RANTES secretion after infection with Y. enterocolitica ( D ), MCP-1 secretion after infection with M. catarrhalis ( E ), and MCP-1 secretion after infection with Y. enterocolitica ( F ). ( G - M ) Levels of cytokine secretion in supernatants from WT, C3 KO and C3 ΔATG1 A549 cells are reduced in cells lacking C3 after stimulation of TLR or TNFR, but not after IL-1R stimulation. IL-8 secretion after treatment with Pam3CSK4 ( G ), IL-6 secretion after treatment with TNF ( H ), sICAM-1 release after treatment with Pam3CSK4 ( I ), sICAM-1 release after TNF treatment ( J ), IL-8 secretion after poly(I: C) treatment ( K ), MCP-1 secretion after poly(I: C) treatment ( L ), and IL-8 secretion after IL-1β treatment ( M ). Results are shown as mean ± SD of independent experiments. Each dot represents an average of at least three clones in one biological repeat. The cytokine secretion levels of untreated cells were subtracted from the values of treated cells. One-way ANOVA with Tukey´s multiple comparison test, matched measures within experiment for C-F and I-M. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns: not significant

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Intracellular C3 regulates the immune response to infection via NF-κB signaling

doi: 10.1007/s00018-025-05975-4

Figure Lengend Snippet: Cytosolic C3 contributes to cytokine release after stimulation of different receptors. ( A - F ) Levels of cytokine secretion measured by ELISA in supernatants from WT, C3 KO and C3 ΔATG1 A549 cells after infection with bacteria are reduced in cells lacking C3. IL-8 secretion after infection with M. catarrhalis ( A ), IL-6 after infection Y. enterocolitica ( B ), RANTES secretion after infection with M. catarrhalis ( C ), RANTES secretion after infection with Y. enterocolitica ( D ), MCP-1 secretion after infection with M. catarrhalis ( E ), and MCP-1 secretion after infection with Y. enterocolitica ( F ). ( G - M ) Levels of cytokine secretion in supernatants from WT, C3 KO and C3 ΔATG1 A549 cells are reduced in cells lacking C3 after stimulation of TLR or TNFR, but not after IL-1R stimulation. IL-8 secretion after treatment with Pam3CSK4 ( G ), IL-6 secretion after treatment with TNF ( H ), sICAM-1 release after treatment with Pam3CSK4 ( I ), sICAM-1 release after TNF treatment ( J ), IL-8 secretion after poly(I: C) treatment ( K ), MCP-1 secretion after poly(I: C) treatment ( L ), and IL-8 secretion after IL-1β treatment ( M ). Results are shown as mean ± SD of independent experiments. Each dot represents an average of at least three clones in one biological repeat. The cytokine secretion levels of untreated cells were subtracted from the values of treated cells. One-way ANOVA with Tukey´s multiple comparison test, matched measures within experiment for C-F and I-M. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns: not significant

Article Snippet: The wild-type (WT) human lung epithelial A549 cells were from the American Type Culture Collection (ATCC).

Techniques: Enzyme-linked Immunosorbent Assay, Infection, Bacteria, Clone Assay, Comparison

$Cytokine gene transcription and NF-κB pathway activation are dependent on cytosolic C3. mRNA levels for IL-6 are decreased in C3 KO A549 cells compared to WT and C3 ΔATG1 cells after infection with Y. enterocolitica , or treatment with TNF ( A ). Similar is observed for mRNA levels for IL-8 after infection with M. catarrhalis or Y. enterocolitica , however treatment with TNF or Pam3CSK4 does not reach significance ( B ). NF-κB activation assessed using luciferase reporter assay is decreased in C3 KO compared to WT and C3 ΔATG1 cells after treatment with Pam3CSK4 ( C ) or infection with M. catarrhalis ( D ). Representative Western blot showing NF-κB (p65 subunit) translocation to the nucleus ( E ) with quantification in ( F ). C3 KO cells are characterized by diminished translocation of p65 to the nucleus compared to WT and C3 ΔATG1;- and + indicate no treatment and treatment with Pam3CSK4, respectively. A similar result was obtained upon infection with M. catarrhalis , a representative blot of nuclear fractions shown in ( G ) with quantification in ( H ). Representative Western blot analysis showing decreased phosphorylation of IKK in lysates from C3 KO cells compared to WT; - and + indicate no treatment and treatment with Pam3CSK4 ( I ) or M. catarrhalis ( K ) with quantification in ( J ) and ( L ), respectively. Each dot represents one biological repeat for one clone ( A , B ) or an average of two clones in one biological repeat ( C - L ). One-way ( C , D ) or Two-way ( A , B , F , H , J , L ) ANOVA with Tukey´s multiple comparison test, matched measures within the experiment. *p< 0.05, **p < 0.01, ***p < 0.001, ns: not significant$

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Intracellular C3 regulates the immune response to infection via NF-κB signaling

doi: 10.1007/s00018-025-05975-4

Figure Lengend Snippet: Cytokine gene transcription and NF-κB pathway activation are dependent on cytosolic C3. mRNA levels for IL-6 are decreased in C3 KO A549 cells compared to WT and C3 ΔATG1 cells after infection with Y. enterocolitica , or treatment with TNF ( A ). Similar is observed for mRNA levels for IL-8 after infection with M. catarrhalis or Y. enterocolitica , however treatment with TNF or Pam3CSK4 does not reach significance ( B ). NF-κB activation assessed using luciferase reporter assay is decreased in C3 KO compared to WT and C3 ΔATG1 cells after treatment with Pam3CSK4 ( C ) or infection with M. catarrhalis ( D ). Representative Western blot showing NF-κB (p65 subunit) translocation to the nucleus ( E ) with quantification in ( F ). C3 KO cells are characterized by diminished translocation of p65 to the nucleus compared to WT and C3 ΔATG1;- and + indicate no treatment and treatment with Pam3CSK4, respectively. A similar result was obtained upon infection with M. catarrhalis , a representative blot of nuclear fractions shown in ( G ) with quantification in ( H ). Representative Western blot analysis showing decreased phosphorylation of IKK in lysates from C3 KO cells compared to WT; - and + indicate no treatment and treatment with Pam3CSK4 ( I ) or M. catarrhalis ( K ) with quantification in ( J ) and ( L ), respectively. Each dot represents one biological repeat for one clone ( A , B ) or an average of two clones in one biological repeat ( C - L ). One-way ( C , D ) or Two-way ( A , B , F , H , J , L ) ANOVA with Tukey´s multiple comparison test, matched measures within the experiment. *p< 0.05, **p < 0.01, ***p < 0.001, ns: not significant

Article Snippet: The wild-type (WT) human lung epithelial A549 cells were from the American Type Culture Collection (ATCC).

Techniques: Activation Assay, Infection, Luciferase, Reporter Assay, Western Blot, Translocation Assay, Phospho-proteomics, Clone Assay, Comparison

Plating efficiencies of H358 and A549 cells grown under normoxia (20% O 2 ) and hypoxia (1% O 2 ) after either 48 h (immediate) or 72 h (late) of pre-incubation.

Journal: International Journal of Molecular Sciences

Article Title: DNA Damage and Inflammatory Response of p53 Null H358 Non-Small Cell Lung Cancer Cells to X-Ray Exposure Under Chronic Hypoxia

doi: 10.3390/ijms252312590

Figure Lengend Snippet: Plating efficiencies of H358 and A549 cells grown under normoxia (20% O 2 ) and hypoxia (1% O 2 ) after either 48 h (immediate) or 72 h (late) of pre-incubation.

Article Snippet: H358 cells (human, male, lung adenocarcinoma, p53 null, KRAS-mutated) and A549 cells (human, male, lung adenocarcinoma, p53 wildtype—wt, KRAS-mutated) were obtained from LGC Genomics (Berlin, Germany) [ ].

Techniques:

Comparison of D 0 and oxygen enhancement ratio (OER) between H358 (this study) and A549 cells [ <xref ref-type=

17 ] following X-ray exposure under normoxia and hypoxia." width="100%" height="100%">

Journal: International Journal of Molecular Sciences

Article Title: DNA Damage and Inflammatory Response of p53 Null H358 Non-Small Cell Lung Cancer Cells to X-Ray Exposure Under Chronic Hypoxia

doi: 10.3390/ijms252312590

Figure Lengend Snippet: Comparison of D 0 and oxygen enhancement ratio (OER) between H358 (this study) and A549 cells [ 17 ] following X-ray exposure under normoxia and hypoxia.

Techniques: Comparison

Expression of p53 target genes in H358 cells under hypoxia (mock-irradiated cells: H0 vs. N0; cells exposed to 8 Gy X-rays H8 vs. N8), and after X-irradiation (8 Gy) under normoxia (N8 vs. N0) or hypoxia (H8 vs. H0). DEGs in H358 cells within each group comparison ( <xref ref-type=

Section 2.6.1 ) were evaluated using the p53 target genes listed in KEGG’s database (KEGG ID: hsa04115). Log2FC values highlighted in bold are significant. ‘NA’ represents no gene expression data." width="100%" height="100%">

Journal: International Journal of Molecular Sciences

Article Title: DNA Damage and Inflammatory Response of p53 Null H358 Non-Small Cell Lung Cancer Cells to X-Ray Exposure Under Chronic Hypoxia

doi: 10.3390/ijms252312590

Figure Lengend Snippet: Expression of p53 target genes in H358 cells under hypoxia (mock-irradiated cells: H0 vs. N0; cells exposed to 8 Gy X-rays H8 vs. N8), and after X-irradiation (8 Gy) under normoxia (N8 vs. N0) or hypoxia (H8 vs. H0). DEGs in H358 cells within each group comparison ( Section 2.6.1 ) were evaluated using the p53 target genes listed in KEGG’s database (KEGG ID: hsa04115). Log2FC values highlighted in bold are significant. ‘NA’ represents no gene expression data.

Techniques: Expressing, Comparison

Luteolin inhibited the proliferation and migration of NSCLC cell lines. (A, B) The CCK8 assay demonstrated that luteolin inhibited the viability of A549 cells and H460 cells in both concentration- and time-dependent manner. (C, D) Colony formation assay showed that luteolin inhibited the proliferation of A549 cells. (E, F) Wound healing assay showed that luteolin inhibited the migration of A549 cells in a concentration-dependent manner. All data were presented as mean ± SE of three independent experiments. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001 compared with control group (luteolin 0 μM).

Journal: Frontiers in Oncology

Article Title: Mechanism of luteolin against non-small-cell lung cancer: a study based on network pharmacology, molecular docking, molecular dynamics simulation, and in vitro experiments

doi: 10.3389/fonc.2024.1471109

Figure Lengend Snippet: Luteolin inhibited the proliferation and migration of NSCLC cell lines. (A, B) The CCK8 assay demonstrated that luteolin inhibited the viability of A549 cells and H460 cells in both concentration- and time-dependent manner. (C, D) Colony formation assay showed that luteolin inhibited the proliferation of A549 cells. (E, F) Wound healing assay showed that luteolin inhibited the migration of A549 cells in a concentration-dependent manner. All data were presented as mean ± SE of three independent experiments. * P <0.05; ** P <0.01; *** P <0.001; **** P <0.0001 compared with control group (luteolin 0 μM).

Article Snippet: The human p53 wild-type (wt) NSCLC cell lines A549 and H460 were procured from Procell Life Science & Technology Co., Ltd.

Techniques: Migration, CCK-8 Assay, Concentration Assay, Colony Assay, Wound Healing Assay, Control

a Immunoblot analysis of p53, p21, and total and phosphorylated (p) forms of EGFR, ERK, and AKT in PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cells. β-actin was examined as a loading control. b Cell proliferation curves for PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cells determined with a colorimetric assay. c Immunoblot analysis of EGFR signaling as well as of p53 and p21 in PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cells treated with 100 nM osimertinib for 0, 6, 24, or 72 h. d Viability of PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cells exposed to the indicated concentrations of osimertinib for 72 h as determined with a colorimetric assay. Data in ( b ) and ( d ) are means ± SEM of triplicates from one experiment and are representative of three independent experiments.

Journal: NPJ Precision Oncology

Article Title: TP53 gain-of-function mutations promote osimertinib resistance via TNF-α–NF-κB signaling in EGFR -mutated lung cancer

doi: 10.1038/s41698-024-00557-2

Figure Lengend Snippet: a Immunoblot analysis of p53, p21, and total and phosphorylated (p) forms of EGFR, ERK, and AKT in PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cells. β-actin was examined as a loading control. b Cell proliferation curves for PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cells determined with a colorimetric assay. c Immunoblot analysis of EGFR signaling as well as of p53 and p21 in PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cells treated with 100 nM osimertinib for 0, 6, 24, or 72 h. d Viability of PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cells exposed to the indicated concentrations of osimertinib for 72 h as determined with a colorimetric assay. Data in ( b ) and ( d ) are means ± SEM of triplicates from one experiment and are representative of three independent experiments.

Article Snippet: Five human NSCLC cell lines with EGFR activating mutations (PC-9 [ECACC #90071810], H1975 [ATCC #CRL-5908], II-18 [#RCB2093; RIKEN BioResource Research Center, Tsukuba, Japan], HCC827 [ATCC #CRL-2868], and HCC4006 [ATCC #CRL-2871]) and one human NSCLC cell line WT for EGFR (A549 [ATCC #CCL-185]) were studied.

Techniques: Western Blot, Control, Colorimetric Assay

a Time course of PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cell number during treatment with 1 μM osimertinib for up to 28 days. b Time course for the development of osimertinib resistance in PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cells. The concentration of osimertinib was gradually increased from 10 nM to 1 μM each time the cells achieved 70% confluence. Immunoblot analysis of EGFR signaling as well as of p53 and p21 during treatment with 1 μM osimertinib for up to 72 h for osimertinib-resistant PC9/p53 GOF cells ( c ) and PC9/p53 EV and PC9/p53 WT cells that had been previously treated with osimertinib for 30 days ( d ). Data in ( a ) and ( b ) are means ± SEM for triplicates from one experiment and are representative of two independent experiments.

Journal: NPJ Precision Oncology

Article Title: TP53 gain-of-function mutations promote osimertinib resistance via TNF-α–NF-κB signaling in EGFR -mutated lung cancer

doi: 10.1038/s41698-024-00557-2

Figure Lengend Snippet: a Time course of PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cell number during treatment with 1 μM osimertinib for up to 28 days. b Time course for the development of osimertinib resistance in PC9/p53 EV , PC9/p53 WT , and PC9/p53 MUT cells. The concentration of osimertinib was gradually increased from 10 nM to 1 μM each time the cells achieved 70% confluence. Immunoblot analysis of EGFR signaling as well as of p53 and p21 during treatment with 1 μM osimertinib for up to 72 h for osimertinib-resistant PC9/p53 GOF cells ( c ) and PC9/p53 EV and PC9/p53 WT cells that had been previously treated with osimertinib for 30 days ( d ). Data in ( a ) and ( b ) are means ± SEM for triplicates from one experiment and are representative of two independent experiments.

Techniques: Concentration Assay, Western Blot

Percentage cell number for PC9/p53 GOF mutant cells ( a ) as well as PC9/p53 EV , PC9/p53 WT , and PC9/p53 V218del cells ( b ) treated with 1 μM osimertinib (Osi) in the absence or presence of infliximab (1 µg/ml) for the indicated times. Viability of osimertinib-resistant PC9/p53 R248Q ( c ) and PC9/p53 R273H ( d ) cells treated with the indicated concentrations of osimertinib in the absence or presence of infliximab (1 µg/ml) for 72 h as measured by a colorimetric assay. e Immunoblot analysis of EGFR signaling as well as p53 and c-Myc expression in osimertinib-resistant PC9/p53 GOF mutant cells incubated in the absence or presence of osimertinib (100 nM) or infliximab (1 µg/ml) for 24 h. Data in ( a ) through ( d ) are means ± SEM of triplicates from one experiment and are representative of three independent experiments.

Journal: NPJ Precision Oncology

Article Title: TP53 gain-of-function mutations promote osimertinib resistance via TNF-α–NF-κB signaling in EGFR -mutated lung cancer

doi: 10.1038/s41698-024-00557-2

Figure Lengend Snippet: Percentage cell number for PC9/p53 GOF mutant cells ( a ) as well as PC9/p53 EV , PC9/p53 WT , and PC9/p53 V218del cells ( b ) treated with 1 μM osimertinib (Osi) in the absence or presence of infliximab (1 µg/ml) for the indicated times. Viability of osimertinib-resistant PC9/p53 R248Q ( c ) and PC9/p53 R273H ( d ) cells treated with the indicated concentrations of osimertinib in the absence or presence of infliximab (1 µg/ml) for 72 h as measured by a colorimetric assay. e Immunoblot analysis of EGFR signaling as well as p53 and c-Myc expression in osimertinib-resistant PC9/p53 GOF mutant cells incubated in the absence or presence of osimertinib (100 nM) or infliximab (1 µg/ml) for 24 h. Data in ( a ) through ( d ) are means ± SEM of triplicates from one experiment and are representative of three independent experiments.

Techniques: Mutagenesis, Colorimetric Assay, Western Blot, Expressing, Incubation

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1) Product Images from "Synthesis, radiolabeling, and evaluation of a 68 Ga-labeled tyrosine kinase inhibitor for detecting EGFR T790M mutations in vivo"

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