human lung cancer a549 cells  (ATCC)

Journal: bioRxiv

Article Title: Scalable longitudinal imaging and transcriptomics of cells in dynamic enclosures

doi: 10.64898/2026.05.05.723030

Figure Lengend Snippet: A: classification of CCEs in different phenotypes based on the analysis of longitudinal imaging data. Red: CellTrace™ Far Red, blue: Annexin V, green: EGFR. B: UMAP based on the transcriptomic data from 10,604 CCEs containing A549 cells treated with 10 µM Olmutinib. The colors represent different transcriptomic clusters. C: UMAP based on the transcriptomic data (same as panel B) colored according to the imaging-derived CCE classification in panel A. 2,328 CCEs that could not be accurately classified were excluded from the analysis. D: proportion of CCEs (y axis) belonging to each imaging-based phenotype (indicated by the color) within each gene expression cluster (x axis). E: Upset plot showing overlap of significant GSEA pathway enrichments across three classification strategies. The combination of transcriptomic clustering with imaging classification identified 15 unique pathways not found in either single-modality strategy. F: significant interaction effects (p_adj < 0.05) between RNA clusters and imaging phenotypes on the prediction of drug resistance pathway modules (G2M checkpoint, E2F targets, MYC targets, DNA repair, EMT) (see Methods). The daughter cell resistant phenotype showed 7 out of 14 total significant interactions, indicating that pathway activities are maximally explained by the combination of transcript state and the daughter cell resistant phenotypic classification. G: Confusion matrix for elastic net prediction of imaging phenotypes from gene expression. H: STRING PPI network for top 50 positive coefficient genes (associated with daughter cell resistance). I: STRING PPI network for top 50 negative coefficient genes (inversely associated with daughter cell resistance). J: Selected differentially expressed genes between expression-defined clusters (x axis). The color represents the average expression (scaled per gene) and the size of the circle indicates the percentage of CCEs expressing the gene. Cluster 2 showed strong enrichment for cell division pathways and overexpressed the proliferation marker TOP2A. Cluster 3 exhibited activation of multiple EGFR bypass pathways with overexpression of EPHA7 (64), HGF (65), ERBB2 (66), and AXL(67), all capable of activating MAPK signaling independently of EGFR. Cluster 5 displayed enrichment of p53 targets, including upregulation of quiescence-associated genes such as GADD45A, REDD1, ATF3, SFN, and BTG2.

Article Snippet: Human lung cancer A549 cells were purchased from ATCC (CCL-185), and cultured in DMEM supplemented with 10% FBS and 1% Pen-Strep.

Techniques: Imaging, Derivative Assay, Gene Expression, Expressing, Marker, Activation Assay, Over Expression

Journal: Frontiers in Oncology

Article Title: Selaginella doederleinii -derived extracellular vesicle-like particles suppress lung cancer with ferroptosis-associated changes and modulation of the FABP4/PPARG/GPX4 axis

doi: 10.3389/fonc.2026.1829211

Figure Lengend Snippet: Internalization of SD-EVLPs and its inhibitory effects on lung cancer cell proliferation (A) Internalization of SD-EVLPs by lung cancer cells; (B, C) CCK-8 assays assessing the effects of SD-EVLPs on lung cancer cell viability; (D–G) EdU assays evaluating the proliferation of A549 and NCI-H1299 cells; (H–I) Colony formation assays assessing the proliferative capacity of A549 and NCI-H1299 cells. Data are presented as the mean ± SEM, n = 3 independent experiments. Compared with the control group, * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: Human lung cancer cell lines A549 (Cat. No.: CL-0016) and NCI-H1299 (Cat. No.: CL-0165) were purchased from Wuhan Procell Life Science & Technology Co., Ltd. Four-week-old male BALB/c nude mice (SPF grade) were purchased from Hunan Silaike Jingda Laboratory Animal Co., Ltd. (Changsha, China), with the Animal Production License No.: SCXK (Xiang) 2021-0002.

Techniques: CCK-8 Assay, Control

Journal: Frontiers in Oncology

Article Title: Selaginella doederleinii -derived extracellular vesicle-like particles suppress lung cancer with ferroptosis-associated changes and modulation of the FABP4/PPARG/GPX4 axis

doi: 10.3389/fonc.2026.1829211

Figure Lengend Snippet: SD-EVLPs inhibit migration and invasion of lung cancer cells (A–D) Wound healing assays assessing the effect of SD-EVLPs on the migration of A549 and NCI-H1299 cells; (E, F) Transwell assays evaluating the invasion ability of A549 and NCI-H1299 cells; (G–I) Western blot analysis of E-cadherin and N-cadherin protein expression. Data are presented as the mean ± SEM, n = 3 independent experiments. Compared with the control group, * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: Human lung cancer cell lines A549 (Cat. No.: CL-0016) and NCI-H1299 (Cat. No.: CL-0165) were purchased from Wuhan Procell Life Science & Technology Co., Ltd. Four-week-old male BALB/c nude mice (SPF grade) were purchased from Hunan Silaike Jingda Laboratory Animal Co., Ltd. (Changsha, China), with the Animal Production License No.: SCXK (Xiang) 2021-0002.

Techniques: Migration, Western Blot, Expressing, Control

Journal: Frontiers in Oncology

Article Title: Selaginella doederleinii -derived extracellular vesicle-like particles suppress lung cancer with ferroptosis-associated changes and modulation of the FABP4/PPARG/GPX4 axis

doi: 10.3389/fonc.2026.1829211

Figure Lengend Snippet: RT-qPCR and Western blot analysis of ferroptosis-related gene expression in lung cancer cells (A, B) RT-qPCR analysis of GPX4 and SLC7A11 mRNA expression in A549 cells; (C, D) RT-qPCR analysis of GPX4 and SLC7A11 mRNA expression in NCI-H1299 cells; (E–H) Western blot analysis of GPX4 and xCT protein expression in lung cancer cells; (I) TEM assessment of mitochondrial ultrastructure. Data are presented as the mean ± SEM, n = 3 independent experiments. Compared with the control group, * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: Human lung cancer cell lines A549 (Cat. No.: CL-0016) and NCI-H1299 (Cat. No.: CL-0165) were purchased from Wuhan Procell Life Science & Technology Co., Ltd. Four-week-old male BALB/c nude mice (SPF grade) were purchased from Hunan Silaike Jingda Laboratory Animal Co., Ltd. (Changsha, China), with the Animal Production License No.: SCXK (Xiang) 2021-0002.

Techniques: Quantitative RT-PCR, Western Blot, Gene Expression, Expressing, Control

Journal: Frontiers in Oncology

Article Title: Selaginella doederleinii -derived extracellular vesicle-like particles suppress lung cancer with ferroptosis-associated changes and modulation of the FABP4/PPARG/GPX4 axis

doi: 10.3389/fonc.2026.1829211

Figure Lengend Snippet: SD-EVLPs modulate the FABP4/PPARG/GPX4-associated pathway in lung cancer cells (A–D) RT-qPCR analysis of FABP4 and PPARG mRNA expression in A549 and NCI-H1299 cells; (E–H) Western blot analysis of FABP4 and PPARG protein expression in A549 and NCI-H1299 cells. Data are presented as the mean ± SEM, n = 3 independent experiments. Compared with the control group, * P < 0.05, ** P < 0.01, and *** P < 0.001.

Article Snippet: Human lung cancer cell lines A549 (Cat. No.: CL-0016) and NCI-H1299 (Cat. No.: CL-0165) were purchased from Wuhan Procell Life Science & Technology Co., Ltd. Four-week-old male BALB/c nude mice (SPF grade) were purchased from Hunan Silaike Jingda Laboratory Animal Co., Ltd. (Changsha, China), with the Animal Production License No.: SCXK (Xiang) 2021-0002.

Techniques: Quantitative RT-PCR, Expressing, Western Blot, Control

Journal: Cells

Article Title: Arsenic-Induced PPARγ, with the Coordinated Action of p62, Inhibits Apoptosis and Necroptosis and Activates the DNA Damage Response in A549 Lung Cancer Cells, Leading to Carcinogenesis

doi: 10.3390/cells15080659

Figure Lengend Snippet: Expression of proteins associated with apoptosis and cell cycle regulation in NaAR-exposed A549 cells. ( a ) A549 cells were exposed to increasing concentrations of NaAR for 18 h, and morphological alterations were examined by phase-contrast microscopy. Nuclear staining was performed using Hoechst 33342, and fluorescence images were captured with Nikon Eclipse TE300 microscope (200×). ( b ) A549 and H1299 cells were treated with the indicated concentrations of NaAR for 18 h, followed by cell collection and lysis. Protein expression levels were analyzed by immunoblotting. ( c ) A549 cells were treated under the same conditions, and cell lysates were subjected to immunoblot analysis to evaluate target protein expression, β-actin used as a loading control. Arrows indicate non-apoptotic chromatin changes. Data represent results from at least three independent experiments. The arrows indicate large-scale segmented chromatin.

Article Snippet: Human lung cancer cell lines A549 (CCL-185 TM ), H1299 (CRL-1803 TM ), and H460 (HTB-177 TM ) were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Expressing, Microscopy, Staining, Fluorescence, Lysis, Western Blot, Control

Journal: Cells

Article Title: Arsenic-Induced PPARγ, with the Coordinated Action of p62, Inhibits Apoptosis and Necroptosis and Activates the DNA Damage Response in A549 Lung Cancer Cells, Leading to Carcinogenesis

doi: 10.3390/cells15080659

Figure Lengend Snippet: NaAR-induced cell death and DNA damage is dependent on PARP-1 activation. ( a ) A549 cells were treated with increasing NaAR concentrations for 18 h or with 65 µM NaAR for up to 24 h. Target proteins in the cell lysates were then evaluated using immunoblotting. ( b ) Immunoblot of target proteins from A549 cells exposed to 65 µM NaAR for 18 h, with or without 50 µM NAD+ pretreatment for 2 h. ( c ) Hoechst 33342-stained cells. Lung cancer cells cultured on coverslips were treated with 65 µM NaAR for 18 h, with or without 50 µM NAD+ or 10 μM 3-AB pretreatment for 2 h, respectively. Scale bar: 25 µm. ( d ) Immunoblot of target proteins from A549 cells exposed to 65 µM NaAR for 18 h, with or without 10 μM 3-AB pretreatment for 2 h. β-Actin was used as the loading control.

Article Snippet: Human lung cancer cell lines A549 (CCL-185 TM ), H1299 (CRL-1803 TM ), and H460 (HTB-177 TM ) were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Activation Assay, Western Blot, Staining, Cell Culture, Control

Journal: Cells

Article Title: Arsenic-Induced PPARγ, with the Coordinated Action of p62, Inhibits Apoptosis and Necroptosis and Activates the DNA Damage Response in A549 Lung Cancer Cells, Leading to Carcinogenesis

doi: 10.3390/cells15080659

Figure Lengend Snippet: NaAR exposure induces K63-linked RIP1-mediated NF-κB activation and MLKL downregulation. ( a , b ) Immunoblot of target proteins from A549 cells treated with increasing concentrations of NaAR for 18 h. ( c ) Immunoblot of target proteins from A549 cells exposed to 65 µM NaAR for 18 h, with or without 50 µM NAD + pretreatment for 2 h. ( d ) Immunoblot of target proteins from A549 cells exposed to 65 µM NaAR for 18 h, with or without 10 μM 3-AB pretreatment for 2 h. β-Actin was used as the loading control.

Article Snippet: Human lung cancer cell lines A549 (CCL-185 TM ), H1299 (CRL-1803 TM ), and H460 (HTB-177 TM ) were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Activation Assay, Western Blot, Control

Journal: Cells

Article Title: Arsenic-Induced PPARγ, with the Coordinated Action of p62, Inhibits Apoptosis and Necroptosis and Activates the DNA Damage Response in A549 Lung Cancer Cells, Leading to Carcinogenesis

doi: 10.3390/cells15080659

Figure Lengend Snippet: NaAR induces polyUb-PPARγ, and PPARγ knockdown leads to PARP-1 hyperactivation and necroptosis. ( a ) Immunoblot of PPARγ proteins from A549 cells treated with increasing NaAR concentrations for 18 h or with 65 µM NaAR for up to 24 h. ( b ) Immunoblot of target proteins from cells transfected with negative control (NC) or PPARγ siRNAs and then exposed to 65 µM NaAR for 18 h. ( c ) Cells were transfected with NC or PPARγ siRNAs and then exposed to NaAR as described in b, and the nuclei were stained with Hoechst 33342. Images were acquired with a fluorescence microscope. Scale bar: 25 µm. β-Actin was used as the loading control.

Article Snippet: Human lung cancer cell lines A549 (CCL-185 TM ), H1299 (CRL-1803 TM ), and H460 (HTB-177 TM ) were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Knockdown, Western Blot, Transfection, Negative Control, Staining, Fluorescence, Microscopy, Control

Journal: Cells

Article Title: Arsenic-Induced PPARγ, with the Coordinated Action of p62, Inhibits Apoptosis and Necroptosis and Activates the DNA Damage Response in A549 Lung Cancer Cells, Leading to Carcinogenesis

doi: 10.3390/cells15080659

Figure Lengend Snippet: The stability of PPARγ in NaAR-exposed A549 cells is regulated by proteasomes. ( a , b ) Immunoblot of target proteins from A549 cells exposed to 65 µM NaAR for 18 h, with 25 nM LMB or DMSO pretreatment for 2 h. ( c ) Immunoblot of target proteins from cells treated with 65 µM NaAR for 18 h in the presence of 25 nM LMB or 5 µM MG132 or both inhibitors. β-Actin was used as the loading control. ( d ) Immunoblot of target proteins from cells treated as described in ( a ) and ( b ) and subjected to subcellular fractionation into nucleus-rich, cytosolic, and particulate fractions. The purities of the nuclear, autophagosome, mitochondrial, and cytosolic fractions were determined by immunoblotting for HDAC1, LC3-II, SOD2, and β-actin, respectively (n = 3). ( e ) Cells on coverslips were treated as in ( a , b ), fixed, and stained with PPARγ (green) and p53 (red), followed by FITC- and rhodamine-conjugated secondary antibodies. The arrows indicate p53 in the cytosol. Nuclei were counterstained with Hoechst 33342 (blue) and images were acquired by fluorescence microscopy. Arrows indicate apoptotic nuclei. Scale bar: 25 µm.

Article Snippet: Human lung cancer cell lines A549 (CCL-185 TM ), H1299 (CRL-1803 TM ), and H460 (HTB-177 TM ) were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Western Blot, Control, Fractionation, Staining, Fluorescence, Microscopy

Journal: Cells

Article Title: Arsenic-Induced PPARγ, with the Coordinated Action of p62, Inhibits Apoptosis and Necroptosis and Activates the DNA Damage Response in A549 Lung Cancer Cells, Leading to Carcinogenesis

doi: 10.3390/cells15080659

Figure Lengend Snippet: p62 regulates p53 stability in NaAR-exposed A549 cells. ( a ) Immunoblot of p62 proteins from A549 cells treated with increasing concentrations of NaAR for 18 h or with 65 µM NaAR for up to 24 h. ( b , c ) Immunoblot of target proteins from cells transfected with negative control (NC) or p62 siRNAs and then exposed to 65 μM NaAR for 18 h. β-Actin was used as the loading control (n = 3).

Article Snippet: Human lung cancer cell lines A549 (CCL-185 TM ), H1299 (CRL-1803 TM ), and H460 (HTB-177 TM ) were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Western Blot, Transfection, Negative Control, Control

Journal: Cells

Article Title: Arsenic-Induced PPARγ, with the Coordinated Action of p62, Inhibits Apoptosis and Necroptosis and Activates the DNA Damage Response in A549 Lung Cancer Cells, Leading to Carcinogenesis

doi: 10.3390/cells15080659

Figure Lengend Snippet: Subcellular localization of p62, p53, and PPARγ and their interactions in NaAR-exposed A549 cells. ( a ) Immunoblot of target proteins from cells treated with 65 μM NaAR for 18 h in the presence of either 25 nM LMB or DMSO. ( b , d ) Cells on coverslips were treated as in part ( a ), fixed, and stained with p62, p53, and PPARγ antibodies. Nuclei were counterstained with Hoechst 33342 (blue), and images were obtained by fluorescence microscopy. Scale bar: 25 µm. ( c ) Immunoblots of p62, p53, and PPARγ from cells treated with 65 µM NaAR for 12 h. After immunoblotting for p62 (input), 800 µg of the remaining protein was used for immunoprecipitation with p62 antibody, followed by immunoblotting for p62, p53, and PPARγ. β-Actin was used as the loading control (n = 3).

Article Snippet: Human lung cancer cell lines A549 (CCL-185 TM ), H1299 (CRL-1803 TM ), and H460 (HTB-177 TM ) were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Western Blot, Staining, Fluorescence, Microscopy, Immunoprecipitation, Control

Journal: Cells

Article Title: Arsenic-Induced PPARγ, with the Coordinated Action of p62, Inhibits Apoptosis and Necroptosis and Activates the DNA Damage Response in A549 Lung Cancer Cells, Leading to Carcinogenesis

doi: 10.3390/cells15080659

Figure Lengend Snippet: Sodium arsenite (NaAR) induces polyubiquitination of PPARγ, which promotes DNA damage responses while suppressing apoptosis and necroptosis through NF-κB activation and MLKL downregulation. Disruption of PPARγ or modulation of PARP-1 activity shifts the balance toward necroptosis or apoptosis. p53 and p62 cooperate with PPARγ to regulate cell fate in A549 cells.

Article Snippet: Human lung cancer cell lines A549 (CCL-185 TM ), H1299 (CRL-1803 TM ), and H460 (HTB-177 TM ) were obtained from the American Type Culture Collection (ATCC, Rockville, MD, USA).

Techniques: Activation Assay, Disruption, Activity Assay