non small cell lung cancer nsclc a549 cell line  (ATCC)

Journal: Pharmaceutical Biology

Article Title: Mechanistic insight into the anti-inflammatory and lung-protective effects of Agrimonia pilosa extract via NF-κB/MAPK inhibition in ovalbumin- and lipopolysaccharide-induced respiratory inflammation models

doi: 10.1080/13880209.2026.2627661

Figure Lengend Snippet: Effects of AP on the mRNA expression of inflammatory cytokines and mediators in LPS-stimulated A549 cells. A549 cells were pretreated with AP for 1 h, followed by LPS stimulation for 24 h. The mRNA expression levels of (A) IL-1β, (B) IL-6, (C) TNF-α, (D) iNOS, (E) COX-2, and (F) MUC5AC were analyzed by qRT-PCR. The data are presented as mean ± SEM ( n = 3). # p < 0.05, ### p < 0.001 vs. normal control; * p < 0.05, *** p < 0.001 vs. LPS treated control.

Article Snippet: Cells from the human non-small cell lung cancer (NSCLC) cell line A549 were purchased from Korean Cell Line Bank (KCLB No. 10185, Seoul, Korea) and cultured in RPMI-1640 medium (10–040, Corning Inc., New York, NY, USA) supplemented with 10% fetal bovine serum (Corning Inc.) and 1% penicillin-streptomycin (Cat. No.50-195-9713, GenDEPOT Inc., Baker, TX, USA).

Techniques: Expressing, Quantitative RT-PCR, Control

Journal: Pharmaceutical Biology

Article Title: Mechanistic insight into the anti-inflammatory and lung-protective effects of Agrimonia pilosa extract via NF-κB/MAPK inhibition in ovalbumin- and lipopolysaccharide-induced respiratory inflammation models

doi: 10.1080/13880209.2026.2627661

Figure Lengend Snippet: Effects of AP on the NF-κB and MAPK signaling pathway in A549 cells. Cells were pretreated with AP for 1 h, followed by LPS stimulation for 6 h. Protein expression levels were analyzed by Western blots. Phosphorylation levels of NF-κB, p38, ERK, and JNK were evaluated to assess activation of the NF-κB and MAPK signaling pathways. β-actin was used as a loading control. Densitometric analysis of the phosphorylated proteins was normalized to total protein levels and is presented as bar graphs. The data are presented as ### p < 0.001 vs. normal control; *** p < 0.001 vs. LPS treated control.

Article Snippet: Cells from the human non-small cell lung cancer (NSCLC) cell line A549 were purchased from Korean Cell Line Bank (KCLB No. 10185, Seoul, Korea) and cultured in RPMI-1640 medium (10–040, Corning Inc., New York, NY, USA) supplemented with 10% fetal bovine serum (Corning Inc.) and 1% penicillin-streptomycin (Cat. No.50-195-9713, GenDEPOT Inc., Baker, TX, USA).

Techniques: Expressing, Western Blot, Phospho-proteomics, Activation Assay, Protein-Protein interactions, Control

Journal: Hereditas

Article Title: miR-4652-3p suppresses glutamine metabolism induced by the inflammatory microenvironment in non-small cell lung cancer by regulating MYC/SLC1A5

doi: 10.1186/s41065-026-00649-y

Figure Lengend Snippet: Enhanced glutamine metabolism in the inflammatory microenvironment promoted NSCLC cell growth. A IL-1β + TNF-α + IL-6 stimulation promotedA549 cell proliferation. B IL-1β + TNF-α + IL-6 stimulation enhanced glutamine uptake in A549 cells. C IL-1β + TNF-α + IL-6 stimulation increased α-ketoglutarate (α-KG) production in A549 cells. D IL-1β + TNF-α + IL-6 stimulation elevated ATP synthesis in A549 cells. E Glutaminase inhibitor CB-839 suppressed enzyme activity, reducing α-KG and ATP production in A549 cells. F CB-839 inhibited the enhanced proliferative capacity of A549 cells induced by IL-1β + TNF-α + IL-6 stimulation. All the experiments were independently repeated three times. * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: The human non-small cell lung cancer (NSCLC) cell line A549 and the normal lung epithelial cell line BEAS-2B were purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China).

Techniques: Activity Assay

Journal: Hereditas

Article Title: miR-4652-3p suppresses glutamine metabolism induced by the inflammatory microenvironment in non-small cell lung cancer by regulating MYC/SLC1A5

doi: 10.1186/s41065-026-00649-y

Figure Lengend Snippet: MYC increased glutamine uptake in NSCLC by transcriptionally upregulating SLC1A5. A SLC1A5 expression was upregulated in IL-1β + TNF-α + IL-6-stimulated A549 cells. B Screening identified siRNA-2 (siSLC1A5-2) as the most efficient for SLC1A5 knockdown. C SLC1A5 knockdown reduced glutamine uptake in cytokine-treated A549 cells. D Chromatin immunoprecipitation assay confirmed MYC binding to the SLC1A5 promoter. E Dual-luciferase reporter assay demonstrated MYC targeting of SLC1A5. F MYC inhibitor 10,058-F4 suppressed SLC1A5 transcription in cytokine-treated A549 cells. G 10,058-F4-mediated SLC1A5 downregulation decreased glutamine uptake in cytokine-treated A549 cells. H MYC overexpression upregulated SLC1A5 mRNA levels. I MYC overexpression-mediated SLC1A5 upregulation enhanced glutamine uptake in A549 cells. All the experiments were independently repeated three times. ns, no significant difference. * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: The human non-small cell lung cancer (NSCLC) cell line A549 and the normal lung epithelial cell line BEAS-2B were purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China).

Techniques: Expressing, Knockdown, Chromatin Immunoprecipitation, Binding Assay, Luciferase, Reporter Assay, Over Expression

Journal: Hereditas

Article Title: miR-4652-3p suppresses glutamine metabolism induced by the inflammatory microenvironment in non-small cell lung cancer by regulating MYC/SLC1A5

doi: 10.1186/s41065-026-00649-y

Figure Lengend Snippet: Impact of the miR-4652-3p-MYC/SLC1A5 regulatory axis on NSCLC malignant phenotypes. A A549 cells exhibited enhanced proliferative capacity compared to BEAS-2B cells. B A549 cells displayed increased migratory capacity compared to BEAS-2B cells. C Compared to BEAS-2B cells, A549 cells exhibited a decrease in the level of miR-4652-3p. D Western blot analysis revealed elevated protein levels of both MYC and SLC1A5 in A549 cells compared to BEAS-2B cells. E Effects of miR-4652-3p, MYC, and SLC1A5 on NSCLC cell proliferation. F Effects of miR-4652-3p, MYC, and SLC1A5 on NSCLC cell migration. G Overexpression of MYC or SLC1A5 reversed the proliferation inhibition induced by miR-4652-3p upregulation in NSCLC cells. H Overexpression of MYC or SLC1A5 reversed the migration inhibition induced by miR-4652-3p upregulation in NSCLC cells. Effects of administering minic NC, miR mimics, miR mimics + pcMYC, or miR mimics + pcSLC1A5 on tumor volume ( I ) and weight ( J ). All the experiments were independently repeated three times. * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: The human non-small cell lung cancer (NSCLC) cell line A549 and the normal lung epithelial cell line BEAS-2B were purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China).

Techniques: Western Blot, Migration, Over Expression, Inhibition

Journal: Hereditas

Article Title: miR-4652-3p suppresses glutamine metabolism induced by the inflammatory microenvironment in non-small cell lung cancer by regulating MYC/SLC1A5

doi: 10.1186/s41065-026-00649-y

Figure Lengend Snippet: Activation of the MYC/SLC1A5 pathway reversed miR-4652-3p-mediated suppression of glutamine metabolism. A Effect of the miR-4652-3p-MYC/SLC1A5 regulatory axis on proliferation of IL-1β + TNF-α + IL-6-stimulated A549 cells. B Upregulation of miR-4652-3p suppressed glutamine uptake in cytokine-stimulated A549 cells, reversed by MYC/SLC1A5 overexpression. C Upregulation of miR-4652-3p inhibited α-KG production in cytokine-stimulated A549 cells, reversed by MYC/SLC1A5 overexpression. D Upregulation of miR-4652-3p reduced ATP production in cytokine-stimulated A549 cells, reversed by MYC/SLC1A5 overexpression. All the experiments were independently repeated three times. * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: The human non-small cell lung cancer (NSCLC) cell line A549 and the normal lung epithelial cell line BEAS-2B were purchased from Procell Life Science & Technology Co., Ltd. (Wuhan, China).

Techniques: Activation Assay, Over Expression

Journal: Journal of Translational Medicine

Article Title: Developing an antibody drug encapsulation nanoagent targeting HER2 for cancer treatment

doi: 10.1186/s12967-025-07450-x

Figure Lengend Snippet: Effects of Tr-ACT2 on a lung cancer cell model. ( A ) Effects of Tr-ACT2 on the growth of A549 cells at concentrations of 0.05 µM, 0.25 µM, and 1 µM for indicated time. Cell growth was evaluated using the MTT assay. ( B ) Representative images of A549 cell morphology at 48 h after treatment with 0.25 μM Tr-ACT2 or vehicle. Scale bar: 400 μm. ( C , D ) Western blot analysis showing the protein levels of PARP, cleaved PARP, IgG heavy chain, IgG light chain, and GAPDH in A549 cells treated with 0.25 μM Tr-ACT2 for indicated time. Protein levels are quantified by densitometry and normalized by GAPDH, versus 0 h. Data are presented as means ± SD ( n ≥ 4). p > 0.05 (ns), p < 0.05 (*), p < 0.01 (**), p < 0.001 (***), p < 0.0001 (****)

Article Snippet: Human breast cancer cell lines SKBR3, JIMT1, BT549, MDA-MB-231, and the human non-small cell lung cancer (NSCLC) cell line A549 were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA), and cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% Fetal bovine serum (FBS) and 1% Antibiotic-Antimycotic, at 37 °C and 5% CO2.

Techniques: MTT Assay, Western Blot

Journal: Journal of Translational Medicine

Article Title: Developing an antibody drug encapsulation nanoagent targeting HER2 for cancer treatment

doi: 10.1186/s12967-025-07450-x

Figure Lengend Snippet: Antitumor efficacy of Tr-ACT2 in the A549 xenograft model. ( A ) Tumor volume change over time for all mice. ( B ) Normalized body weight change over time for all mice. Data are presented as means ± SEM ( n ≥ 3)

Article Snippet: Human breast cancer cell lines SKBR3, JIMT1, BT549, MDA-MB-231, and the human non-small cell lung cancer (NSCLC) cell line A549 were obtained from the American Type Culture Collection (ATCC, Manassas, VA, USA), and cultured in Dulbecco’s Modified Eagle Medium (DMEM) supplemented with 10% Fetal bovine serum (FBS) and 1% Antibiotic-Antimycotic, at 37 °C and 5% CO2.

Techniques: