luad cell lines  (ATCC)

Journal: Frontiers in Immunology

Article Title: Multi-omics profiling identifies ADAM9 as a key efferocytosis driver in lung adenocarcinoma

doi: 10.3389/fimmu.2026.1772167

Figure Lengend Snippet: Effects of ADAM9 knockdown in macrophage cells. (A) Relative mRNA expression of ADAM9 in LUAD tissues and adjacent tissues. (B) ADAM9 expression in LUAD tissues evaluated by IHC. (C, D) ADAM9 expression in M2 macrophages transfected with siRNA. (E) RT-qPCR analysis of M2 polarization markers in si-ADAM9-transfected M2 macrophages. (F) ATP content assay in M2 macrophages transfected with si-ADAM9. (G) ADAM9 mRNA expression in normal bronchial epithelial cells and LUAD cell lines. (H) Transwell migration assay showing the migratory ability of A549 and H1975 cells co-cultured with M2 macrophages. (I, J) EdU assay detecting the proliferative capacity of LUAD cells co-cultured with M2 macrophages. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001.

Article Snippet: The human LUAD cell lines (A549, H1975, H460, H1299, SPCA-1), bronchial epithelial cells (BEAS-2B), and THP-1 were purchased from the American Type Culture Collection (ATCC; Manassas, VA, USA).

Techniques: Knockdown, Expressing, Transfection, Quantitative RT-PCR, Transwell Migration Assay, Cell Culture, EdU Assay

Journal: International Journal of Genomics

Article Title: USP44 Stabilizes MAOB via Deubiquitination to Inhibit Cisplatin Resistance in Lung Adenocarcinoma

doi: 10.1155/ijog/7433804

Figure Lengend Snippet: Bioinformatic analysis of DDP resistance–related genes in LUAD. (A) Volcano plot depicting DEGs in DDP‐resistant cells. (B) Venn diagram illustrating the intersection between genes from the GSE157692 dataset and DDP resistance–related targets, identifying 345 overlapping core genes. (C) KEGG pathway enrichment analysis of the core genes. (D–F) GO enrichment analysis for BP, CC, and MF.

Article Snippet: The parental LUAD cell lines (A549 and PC9) and their corresponding DDP‐resistant derivatives (A549‐DDP and PC9‐DDP) were obtained from Procell Biotechnology Co., Ltd. (Wuhan, China).

Techniques:

Journal: International Journal of Genomics

Article Title: USP44 Stabilizes MAOB via Deubiquitination to Inhibit Cisplatin Resistance in Lung Adenocarcinoma

doi: 10.1155/ijog/7433804

Figure Lengend Snippet: Expression and prognostic analysis of MAOB in LUAD and DDP‐resistant cell lines. (A) MAOB expression in A549 and A549‐DDP cells was analyzed using the GSE157692 dataset. (B) MAOB expression in LUAD ( n = 483) and normal tissues ( n = 59) was assessed via GEPIA. (C) Transcript levels of MAOB in normal ( n = 59) and primary LUAD tumor ( n = 515) samples from TCGA were compared. (D) Kaplan–Meier survival analysis of LUAD patients stratified by MAOB expression level ( p = 0.0047). (E, F) MAOB protein levels in A549/A549‐DDP and PC9/PC9‐DDP cells were detected by Western blot. ∗ p < 0.05; ∗∗ p < 0.01.

Article Snippet: The parental LUAD cell lines (A549 and PC9) and their corresponding DDP‐resistant derivatives (A549‐DDP and PC9‐DDP) were obtained from Procell Biotechnology Co., Ltd. (Wuhan, China).

Techniques: Expressing, Western Blot

Journal: International Journal of Genomics

Article Title: USP44 Stabilizes MAOB via Deubiquitination to Inhibit Cisplatin Resistance in Lung Adenocarcinoma

doi: 10.1155/ijog/7433804

Figure Lengend Snippet: MAOB overexpression enhances DDP sensitivity in DDP‐resistant LUAD cells by inhibiting proliferation and promoting apoptosis. (A) MAOB overexpression efficiency was validated in A549‐DDP and PC9‐DDP cells via Western blot. (B, C) CCK‐8 assays were performed to determine DDP sensitivity in A549‐DDP and PC9‐DDP cells. (D–G) A549‐DDP and PC9‐DDP cells were transfected with pcDNA or MAOB‐overexpressing plasmid and divided into two subgroups: control (without DDP treatment) and DDP treatment. (D, E) Colony formation assays were conducted to assess cell proliferation in A549‐DDP and PC9‐DDP cells. (F, G) Flow cytometry analysis was used to detect cell apoptosis. Data are presented as mean ± SD from n ≥ 3 independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01.

Article Snippet: The parental LUAD cell lines (A549 and PC9) and their corresponding DDP‐resistant derivatives (A549‐DDP and PC9‐DDP) were obtained from Procell Biotechnology Co., Ltd. (Wuhan, China).

Techniques: Over Expression, Western Blot, CCK-8 Assay, Transfection, Plasmid Preparation, Control, Flow Cytometry

Journal: International Journal of Genomics

Article Title: USP44 Stabilizes MAOB via Deubiquitination to Inhibit Cisplatin Resistance in Lung Adenocarcinoma

doi: 10.1155/ijog/7433804

Figure Lengend Snippet: MAOB overexpression enhances DDP‐mediated inhibition of migration, invasion, and EMT in DDP‐resistant LUAD cells. Untreated or DDP‐treated A549‐DDP and PC9‐DDP cells were transfected with pcDNA or MAOB. (A–D) Transwell migration assay was conducted to assess cell migration and invasion. (E, F) Western blot analysis of EMT marker (E‐cadherin, N‐cadherin, and vimentin) expression levels. Data are presented as mean ± SD from n ≥ 3 independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.

Article Snippet: The parental LUAD cell lines (A549 and PC9) and their corresponding DDP‐resistant derivatives (A549‐DDP and PC9‐DDP) were obtained from Procell Biotechnology Co., Ltd. (Wuhan, China).

Techniques: Over Expression, Inhibition, Migration, Transfection, Transwell Migration Assay, Western Blot, Marker, Expressing

Journal: International Journal of Genomics

Article Title: USP44 Stabilizes MAOB via Deubiquitination to Inhibit Cisplatin Resistance in Lung Adenocarcinoma

doi: 10.1155/ijog/7433804

Figure Lengend Snippet: USP44 stabilizes MAOB via deubiquitination in DDP‐resistant LUAD cells. (A) USP44 expression in A549 and A549‐DDP cells was analyzed using the GSE157692 dataset. (B) Transcript levels of USP44 in normal ( n = 59) and primary LUAD tumor ( n = 515) samples from TCGA were compared. (C) Kaplan–Meier survival analysis of LUAD patients stratified by USP44 expression level ( p = 0.044). (D, E) Co‐IP assays in A549‐DDP and PC9‐DDP cells showed that USP44 overexpression decreased MAOB ubiquitination. (F, G) CHX chase assay was employed to assess MAOB protein stability in A549‐DDP and PC9‐DDP cells transfected with pcDNA or USP44. Data are presented as mean ± SD from n ≥ 3 independent biological replicates. ∗∗ p < 0.01; ∗∗∗ p < 0.001.

Article Snippet: The parental LUAD cell lines (A549 and PC9) and their corresponding DDP‐resistant derivatives (A549‐DDP and PC9‐DDP) were obtained from Procell Biotechnology Co., Ltd. (Wuhan, China).

Techniques: Expressing, Co-Immunoprecipitation Assay, Over Expression, Ubiquitin Proteomics, Transfection

Journal: International Journal of Genomics

Article Title: USP44 Stabilizes MAOB via Deubiquitination to Inhibit Cisplatin Resistance in Lung Adenocarcinoma

doi: 10.1155/ijog/7433804

Figure Lengend Snippet: MAOB knockdown reverses the effects of USP44 overexpression on DDP resistance, proliferation, apoptosis, migration, invasion, and EMT in LUAD cells. A549‐DDP and PC9‐DDP cells were divided into three groups: pcDNA + siNC, USP44 + siNC, and USP44 + siMAOB. (A, B) Western blot was used to validate the efficiency of MAOB knockdown in USP44‐overexpressing A549‐DDP and PC9‐DDP cells. (C) Colony formation assay was used to assess cell proliferation. (D) Flow cytometry analysis of cell apoptosis. (E, F) Transwell assay was performed to evaluate cell migration and invasion. (G, H) Western blot analysis of E‐cadherin, N‐cadherin, and vimentin expression. Data are presented as mean ± SD from n ≥ 3 independent biological replicates. ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001.

Article Snippet: The parental LUAD cell lines (A549 and PC9) and their corresponding DDP‐resistant derivatives (A549‐DDP and PC9‐DDP) were obtained from Procell Biotechnology Co., Ltd. (Wuhan, China).

Techniques: Knockdown, Over Expression, Migration, Western Blot, Colony Assay, Flow Cytometry, Transwell Assay, Expressing

Journal: Translational Lung Cancer Research

Article Title: TLR7 induces autophagy in non-small cell lung cancer tumor cells and influences anti-tumors responses in patients

doi: 10.21037/tlcr-2025-aw-1173

Figure Lengend Snippet: Identification of genes correlated with autophagy in lung tumor cells. (A) Strategy of our analysis. A public data cohort of 516 adenocarcinoma NSCLC patients from TCGA (TCGA-LUAD) was used, and a WGCNA analysis was applied to the cohort. Correlation studies were realized between the different module and the autophagy genes from the HAD (232 genes) and the autophagy GC (99 genes). (B) Assessment of Correlation Strength in Modules from HAD and GC: this evaluation ranges from weakly correlated modules, depicted in green, to strongly correlated modules, illustrated in red. (C) Representation of GS for autophagy relative to its MM in the blue module. (D) Association network of genes in the blue module with an MM >0.8, analyzed using STRING software. Nodes with a GS >0.5 or GS >0.6 are depicted in red and dark red, respectively. (E) Selection of the top 10 genes in the blue module with a node degree >30, ranked according to their GS score. (F) A public data cohort of 38 lung tumor patients ( GSE111907 ), each with sorted cell types from the TME, was utilized. Only adenocarcinoma NSCLC patients were selected for analysis (n=22). Correlation studies between autophagy genes and TLRs genes expression were conducted for all cell types, including malignant, pan-immune, fibroblast, and endothelial cells. (G) Graph representing the level of TLRs expression in function of the cell type composing the TME. (H) Graph representing the level of correlation of autophagy genes with each TLRs genes expression in function of the cell type composing the TME. GC, GeneCard; GS, gene significance; HAD, Human Autophagy Database; MM, module membership; NSCLC, non-small cell lung cancer; TCGA-LUAD, The Cancer Genome Atlas-lung adenocarcinoma; TLR, toll-like receptor; TME, tumor microenvironment; WGCNA, weighted gene co-expression network analysis.

Article Snippet: The human LUAD cell line A549 (ATCC CCL-185, RRID: CVCL_0023), lung squamous cell carcinoma (ATCC HTB-58, RRID: CVCL_0630) and the murine LUAD cell line LLC (ATCC CRL-1642, RRID: CVCL_0391) were cultured in DMEM/F-12 medium (Gibco, Waltham, MA, USA) supplemented with 10% fetal bovine serum (FBS; Eurobio Scientific, Les Ulis, France), 1% non-essential amino acids, 1% HEPES buffer, 1% L-glutamine, and 1% sodium pyruvate (all from Gibco).

Techniques: Software, Selection, Expressing