luad lines a549  (Procell Inc)

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