american type culture collection crl 4029 cells  (ATCC)

Journal: NPJ Precision Oncology

Article Title: COL3A1 high cancer-associated fibroblasts orchestrate metabolic and immune microenvironments to confer chemoresistance in breast cancer

doi: 10.1038/s41698-026-01338-9

Figure Lengend Snippet: A UMAP plot showing the cell types. B UMAP plot of CAFs colored by subsets according to COL3A1 expression. C UMAP plot of CAFs colored by chemosensitivity. D Proportion of tumor cell subsets in untreated and treated patients. E Proportion of CAFs derived from untreated and treated patients across distinct subsets. F Distribution of cell counts and proportion of CAFs across biological and clinical dimensions. G Volcano plot showing differentially expressed genes in CAFs subsets associated with chemoresistance. H UMAP plots showing the features of EMT and oxidative phosphorylation in CAFs. I UMAP plots showing the feature of drug metabolism in tumor cells. J Ro/e analysis reveals different infiltration of CAFs and T cells between untreated and treated samples. K Pseudotime trajectory analysis indicates temporal evolution of CAFs subsets between naive and treated patients. L The expression of key EMT proteins in MDA-MB-231 co-cultured with CP-H172 shNC or CP-H172 shCOL3A1 , with or without PTX treatment. M , N Representative images ( M ) and quantitative data ( N ) of MDA-MB-231 co-cultured with CP-H172 shNC or CP-H172 shCOL3A1 in transwell chamber. Scale bar, 100 μm. O Schematic of the lung metastasis model established by tail vein co-injection of MDA-MB-231 cells with CP-H172 shNC or CP-H172 shCOL3A1 . P , Q Representative images ( P ) and quantitative data ( Q ) of HE staining of lung from each group ( n = 6). Scale bars: 500 μm (top), 100 μm (bottom). R Cell viability proportion with PTX in MDA-MB-231, which were cocultured with CP-H172 shNC or CP-H172 shCOL3A1 . S Cell proliferation rate by PTX in MDA-MB-231, which were cocultured with CP-H172 shNC or CP-H172 shCOL3A1 . Student’s t test was used for ( N ), ( Q ), ( R ) and ( S ). COL3A1 high CAFs, CAFs with high COL3A1 expression; COL3A1 low CAFs, CAFs with low COL3A1 expression; COL3A1 - CAFs, COL3A1-negative CAFs; Tumor resist , chemoresistant tumor cells; tumor sen , chemosensitive tumor cells；tumor inter , tumor cells with intermediate chemosensitivity. EMT epithelial–mesenchymal transition, Ro/e ratio of observed to expected cell counts, PTX paclitaxel.

Article Snippet: The CP-H172 cell line, derived from breast cancer-associated fibroblasts (CAFs), was obtained from Procell Life Science & Technology (Wuhan, China) and cultured using CM-H172 medium according to the supplier’s instructions.

Techniques: Expressing, Derivative Assay, Phospho-proteomics, Cell Culture, Injection, Staining

Journal: NPJ Precision Oncology

Article Title: COL3A1 high cancer-associated fibroblasts orchestrate metabolic and immune microenvironments to confer chemoresistance in breast cancer

doi: 10.1038/s41698-026-01338-9

Figure Lengend Snippet: A Metabolic signature comparison among tumor subsets. B Correlation between COL3A1 and SCD expression in CAFs. C ENO1 expression across tumor subsets. D Apoptosis activity across tumor subsets. E SCD expression in CP-H172 shNC or CP-H172 shCOL3A1 . F ENO1 expression in BC cells co-cultured with CP-H172 shNC or CP-H172 shCOL3A1 . G Representative images (left) and quantification (right) of BODIPY™ 493/503 staining for lipids in MDA-MB-231 cells co-cultured with CP-H172 shNC or CP-H172 shCOL3A1 . Scale bars: 20 μm. H TEM images of MDA-MB-231 cells after co-culture with CP-H172shNC (top) or CP-H172shCOL3A1. Scale bars: 5 μm (top), 1 μm (bottom). I , J Expression of key AKT/PI3K pathway key proteins in BC cells co-cultured with CP-H172 shNC or CP-H172 shCOL3A1 , with/without PTX treatment. K SCD expression in CP-H172 treated with/without oleic acid. L ENO1 expression in BC cells treated with/without oleic acid. M , N Expression of key AKT/PI3K pathway key proteins in BC cells with/without ENO1 knocking down, treated with/without oleic acid. O Apoptosis in MDA-MB-231 co-cultured with CP-H172 shNC or CP-H172 shCOL3A1 ± PTX by flow cytometry. P Quantification of apoptosis from ( O ). Pearson correlation analysis was used for ( B ); Student’s t test was used for ( G ) and ( P ). TEM transmission electron microscopy.

Article Snippet: The CP-H172 cell line, derived from breast cancer-associated fibroblasts (CAFs), was obtained from Procell Life Science & Technology (Wuhan, China) and cultured using CM-H172 medium according to the supplier’s instructions.

Techniques: Comparison, Expressing, Activity Assay, Cell Culture, Staining, Co-Culture Assay, Flow Cytometry, Transmission Assay, Electron Microscopy

Journal: NPJ Precision Oncology

Article Title: COL3A1 high cancer-associated fibroblasts orchestrate metabolic and immune microenvironments to confer chemoresistance in breast cancer

doi: 10.1038/s41698-026-01338-9

Figure Lengend Snippet: A Overview of cell–cell interactions across cell types. B Signal input and output strength of CD99 pathway among cell types. C CD99-PILRA communication intensity in COL3A1 high vesus COL3A1 low CAFs. D Number and strength of ligand-receptor interactions between CAFs subsets and tumor cell subsets. E Top ligand-receptor interactions between CAFs subsets and chemoresistant tumor cells. F The correlation of COL3A1 with FN1, CD99, MDK, and THBS2 in CAFs. G FN1, CD99, MDK, THBS2 mRNA levels in CP-H172 shNC or CP-H172 shCOL3A1 . Pearson correlation analysis was used for ( F ); Student’s t test was used for ( G ).

Article Snippet: The CP-H172 cell line, derived from breast cancer-associated fibroblasts (CAFs), was obtained from Procell Life Science & Technology (Wuhan, China) and cultured using CM-H172 medium according to the supplier’s instructions.

Techniques:

Journal: NPJ Precision Oncology

Article Title: COL3A1 high cancer-associated fibroblasts orchestrate metabolic and immune microenvironments to confer chemoresistance in breast cancer

doi: 10.1038/s41698-026-01338-9

Figure Lengend Snippet: Schematic diagram of the xenograft model. MDA-MB-231 cells were either injected alone or coinjected with CP-H172 shNC or CP-H172 shCOL3A1 at a ratio of 1:3 into immunodeficient mice. A , B Photographs of tumors in each group. C – E Tumor growth curves ( C ), tumor weights ( D ), and body weight changes of mice ( E ) in each group ( n = 6). F , G Representative images ( F ) and quantitative data ( G ) of IHC for SCD and ENO1 in tumor samples from each group ( n = 6). Scale bar, 100 μm. H Correlation between COL3A1 and SCD, ENO1 expression based on IHC staining. I Representative ultrasound images from clinical samples. G – K Representative IHC images of COL3A1, SDC1, and ENO1 in CR ( G ) and non-CR patients ( K ). L Expression levels of COL3A1, SDC1, and ENO1 in CR and non-CR patients. M Kaplan–Meier analysis showing that high COL3A1 expression is associated with poor DFS in our cohort. Student’s t test was used for ( C ), ( D ), ( E ) and ( G ). Wilcox rank-sum test was used for ( L ). IHC immunohistochemistry, CR complete response, DFS disease-free survival.

Article Snippet: The CP-H172 cell line, derived from breast cancer-associated fibroblasts (CAFs), was obtained from Procell Life Science & Technology (Wuhan, China) and cultured using CM-H172 medium according to the supplier’s instructions.

Techniques: Injection, Expressing, Immunohistochemistry

Journal: Nature Communications

Article Title: Coronaviruses reprogram the tRNA epitranscriptome to favor viral protein expression

doi: 10.1038/s41467-026-69700-w

Figure Lengend Snippet: A – C Representative western blots showing siRNA-mediated knockdown of ELP3 (mcm⁵U/mcm⁵s ≤ U pathway), QTRT1 (Q pathway), and NSUN2 (m⁵C pathway) in HCoV-OC43–infected A549 cells (MOI 0.1). HCoV-OC43 N protein (NP) levels were measured by western blot at 48 hpi. A non-targeting siRNA (siRNA-scr) was used as a control. D – F Quantification of ELP3, QTRT1, NSUN2, and viral NP protein levels in siRNA-treated cells relative to non-targeting siRNA (scr) controls. Vinculin and GAPDH were used as loading controls. Measurements were obtained from independent biological replicates ( n = 4 for panel D; n = 2 for panels E and F ). Statistical significance was assessed using a two-sided, nonparametric Mann–Whitney U test (unpaired). D ELP3 levels: p = 0.003 for mock siRNA-scr vs mock siRNA-ELP3; p = 0.0137 for HCoV-OC43 siRNA-scr vs HCoV-OC43 siRNA-ELP3; NP levels: p = 0.0057 for HCoV-OC43 siRNA-scr vs HCoV-OC43 siRNA-ELP3. E QTRT1 levels: p = 0.17 for mock siRNA-scr vs mock siRNA-QTRT1; p = 0.0724 for HCoV-OC43 siRNA-scr vs HCoV-OC43 siRNA-QTRT1; NP levels: p = 0.042 for HCoV-OC43 siRNA-scr vs HCoV-OC43 siRNA-QTRT1. F NSUN2 levels: p = 0.043 for mock siRNA-scr vs mock siRNA-NSUN2; p = 0.071 for HCoV-OC43 siRNA-scr vs HCoV-OC43 siRNA-NSUN2; NP levels: p = 0.91 for HCoV-OC43 siRNA-scr vs HCoV-OC43 siRNA-NSUN2. Data are presented as mean ± s.d. Individual data points are shown. G Plasmid-mediated overexpression (OVE) of ADAT2 (I pathway) and ALKBH1 (hm⁵C/f⁵C pathway) in HCoV-OC43 (MOI 0.1) infected A549 cells. HCoV-OC43 NP levels was measured by western blot at 48 hpi. Empty vector transfection (pcDNA3) was used as a control. Vinculin was used as loading control. H Quantification of viral NP protein levels from independent biological replicates in plasmid-transfected cells relative to empty vector–transfected controls. Statistical significance was assessed using a two-sided, nonparametric Mann–Whitney U test (unpaired; n = 4). Exact p-values are p < 0.0001 for HCoV-OC43–empty vs HCoV-OC43–ADAT2 overexpression (OVE) and p < 0.0001 for HCoV-OC43–empty vs HCoV-OC43–ALKBH1 overexpression (OVE). Data are presented as mean ± s.d. Individual data points are shown.

Article Snippet: A549 cells were pretreated with the ATM inhibitor CP-466722 (5 μM, MedChemExpress HY-11002) for 1 h prior to infection.

Techniques: Western Blot, Knockdown, Infection, Control, MANN-WHITNEY, Plasmid Preparation, Over Expression, Transfection