luad cell lines  (Procell Inc)

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: Frontiers in Oncology

Article Title: TSPAN32 as a biomarker associated with radiotherapy and immune microenvironment remodeling in lung adenocarcinoma

doi: 10.3389/fonc.2026.1724489

Figure Lengend Snippet: Overexpression of TSPAN32 inhibits proliferation and migration of lung cancer cells and enhances their radiosensitivity. (A) 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showing TSPAN32 knockdown (si-TSPAN32) promotes while overexpression (oe-TSPAN32) suppresses A549 and H1299 cell proliferation. (B, C) Wound healing assay revealing the effect of TSPAN32 on cell migration. B: Representative images of wound closure in A549 and H1299 cells at 24 h after wounding; C: Quantification. (D, E) Clonogenic assay: surviving fraction after irradiation in TSPAN32-overexpressing vs control cells. D: Representative images; E: Quantification. (F) Apoptosis in A549 and H1299 cells after TSPAN32 modulation and 4 Gy X−ray irradiation. (G-I) Subcutaneous A549 xenografts: TSPAN32 overexpression markedly slowed tumor growth. G: Representative tumors; H: Final tumor weights; I: Growth curves over time. pcDNA3.1+ serves as the control group; oe-TSPAN32 refers to the overexpression group, abbreviated as OE; si-TSPAN32 represents the TSPAN32-targeted interference group (small interfering RNA), abbreviated as SI. * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: The normal lung cell BEAS-2B, LUAD cell lines A549 and H1299, and the Human Embryonic Kidney 293T cells (HEK-293T) were obtained from American Type Culture Collection (ATCC).

Techniques: Over Expression, Migration, MTT Assay, Knockdown, Wound Healing Assay, Clonogenic Assay, Irradiation, Control, Small Interfering RNA

Journal: Frontiers in Oncology

Article Title: TSPAN32 as a biomarker associated with radiotherapy and immune microenvironment remodeling in lung adenocarcinoma

doi: 10.3389/fonc.2026.1724489

Figure Lengend Snippet: The regulatory mechanism of TSPAN32 in LUAD through stabilization of PTEN. (A) KEGG enrichment analysis of differentially expressed genes. (B) Gene set enrichment analysis (GSVA) of high- and low-risk groups based on risk scores. Green: low-risk group; Orange: high-risk group. (C) GSEA analysis showing pathways enriched in the low-risk group, with significance threshold set at FDR q < 0.05. (D) Co-immunoprecipitation data for the TSPAN32-PTEN interaction. (E) Real-time quantitative PCR (RT-qPCR) analysis of the expression levels of TSPAN32, PTEN, AKT, FOXO1, PD-L1 , and VEGF genes in A549 and H1299 cells after TSPAN32 overexpression. (F) RT-qPCR analysis of the expression levels of TSPAN32, PTEN, AKT, FOXO1, PD-L1 , and VEGF genes in subcutaneous tumor tissues of nude mice. (G) Western blotting (WB) analysis of PTEN and AKT protein expression levels in A549 and H1299 cells after TSPAN32 overexpression. (H) WB analysis of PTEN, AKT, and mTOR protein expression levels in A549 and H1299 cells after ionizing radiation (4 Gy). (I) Schematic diagram illustrating the role of the TSPAN32-PTEN signaling pathway in regulating the sensitivity of LUAD.

Article Snippet: The normal lung cell BEAS-2B, LUAD cell lines A549 and H1299, and the Human Embryonic Kidney 293T cells (HEK-293T) were obtained from American Type Culture Collection (ATCC).

Techniques: Immunoprecipitation, Real-time Polymerase Chain Reaction, Quantitative RT-PCR, Expressing, Over Expression, Western Blot