luad cell lines  (ATCC)

Journal: Frontiers in Immunology

Article Title: Exosomal POSTN from cancer-associated fibroblasts drives progression of microinvasive lung adenocarcinoma: insights from single-cell and tissue exosome sequencing analysis

doi: 10.3389/fimmu.2026.1767771

Figure Lengend Snippet: Clinical evaluation of exosome-derived candidate genes and validation of POSTN in LUAD. (A) Expression levels of the five most upregulated differentially expressed mRNAs—CCL19, NHS, URB1/KIAA0539, PHLDA2, and POSTN—in tissue-derived exosomes from LUAD tissues and matched adjacent normal tissues. (B) Expression levels of CCL19, NHS, URB1, PHLDA2, and POSTN in tumor and normal lung tissues from the TCGA-LUAD cohort. (C) Kaplan–Meier overall survival analysis according to POSTN expression in LUAD. (D) Receiver operating characteristic (ROC) curves showing the diagnostic performance of the five candidate genes in LUAD. (E) Relative POSTN mRNA expression in BEAS-2B bronchial epithelial cells and LUAD cell lines (A549, H1299, HCC827, and PC9). (F) Relative POSTN mRNA expression in adjacent and LUAD tissues, and in non-metastatic and metastatic LUAD samples. (G) Tissue-derived exosomal POSTN mRNA levels in LUAD, stratified by lymph node metastasis status and pathological stage. (H) Relative serum exosomal POSTN mRNA expression in healthy controls and patients with LUAD. *Asterisks indicate statistical significance versus adjacent tissue or the non-metastatic group (** P < 0.01; *** P < 0.001), and hash symbols indicate significance between tumor subgroups ( ## P < 0.01; ### P < 0.001).

Article Snippet: Two LUAD cell lines, A549 (ATCC ® CRM-CCL-185TM) and H1299 (ATCC ® CRL-5803TM), were obtained from the Cell Bank of the Chinese Academy of Sciences (Shanghai, China).

Techniques: Derivative Assay, Biomarker Discovery, Expressing, Diagnostic Assay

Journal: Frontiers in Immunology

Article Title: Exosomal POSTN from cancer-associated fibroblasts drives progression of microinvasive lung adenocarcinoma: insights from single-cell and tissue exosome sequencing analysis

doi: 10.3389/fimmu.2026.1767771

Figure Lengend Snippet: In vitro and in vivo effects of POSTN + CAF–derived exosomes on LUAD cells. (A, B) CCK-8 assays showing the proliferation of A549 (A) and H1299 (B) cells after treatment with exosomes derived from POSTN - CAFs or POSTN + CAFs. (C) Representative images of colony formation in A549 and H1299 cells treated with exosomes from POSTN - CAFs or POSTN + CAFs. (D, E) Representative images of Transwell migration and invasion assays in A549 (D) and H1299 (E) cells treated with exosomes from POSTN - CAFs or POSTN + CAFs. (F) Tumor growth in nude mice bearing A549 or H1299 xenografts treated with PBS, POSTN - CAF–derived exosomes, or POSTN + CAF–derived exosomes. * P < 0.05, ** P < 0.01, *** P < 0.001 versus the control group; # P < 0.05, ## P < 0.01, ### P < 0.001 versus the POSTN - CAF–derived exosome group.

Article Snippet: Two LUAD cell lines, A549 (ATCC ® CRM-CCL-185TM) and H1299 (ATCC ® CRL-5803TM), were obtained from the Cell Bank of the Chinese Academy of Sciences (Shanghai, China).

Techniques: In Vitro, In Vivo, Derivative Assay, CCK-8 Assay, Migration, Control

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