Journal: Journal of Bone Oncology

Article Title: Doxorubicin enhances adipogenesis in an FGF2-dependent manner and induces a tumour-promoting secretory phenotype

doi: 10.1016/j.jbo.2026.100754

Figure Lengend Snippet: Tumour cell proliferation is increased by culture with or media transfer from doxorubicin-treated adipogenic differentiated MSC and is dependent in part on FGF2. A) Proliferation of PC3 cells was assessed at 24 h, 48 h and 72 h following I) treatment with conditioned media from doxorubicin-treated BMA or II) direct seeding on top of doxorubicin-treated BMA. B) Proliferation of PC3 following direct co-culture with day 12 adipogenic differentiated MSC that were treated at day 9 of adipogenic differentiation with vehicle control or 25 nM or 50 nM doxorubicin. PC3 cells were enumerated at 24 h, 48 h and 72 h following addition to adipogenic differentiated MSC. Proliferation of PC3 treated with 30% conditioned media isolated at C) day 10 or D) day 12 from differentiated MSC treated at day 9 of adipogenic differentiation with vehicle control or 25 nM doxorubicin. E) Proliferation of PC3 in response to treatment with 30% conditioned media isolated at day 10 from adipogenic differentiating MSC following treatment at day 9 with 25 nM doxorubicin and siRNA targeting FGF2 or non-targeting control siRNA. F) Conditioned media was collected at day 10 from differentiating MSC/BMA cells treated with vehicle or 25 nM doxorubicin at day 9 of the differentiation process. K562 or 4T1 tumour cells were treated with 30% adipocyte conditioned media and were imaged and counted 48 h after addition of conditioned media. Mean cell count normalized to vehicle control is presented. In all graphs, mean cell count is normalized to cell count at 0 h prior to addition of conditioned media. Graphs show the mean ± SEM, using the statistical test two-way ANOVA in Figure B) and one-way ANOVA in Figure C), D) and E), (*p < 0.05, ***p < 0.001; ****p < 0.0001), n = 3 biological replicates each with 3 technical replicates.

Article Snippet: PC3 prostate tumour cells (ATCC CRL-1435), 4T1 breast tumour cells (CRL-2539) and K562 leukemia tumour cells (CCL-243) were obtained from the American Type Culture Collection (ATCC, Manassas, VA).

Techniques: Co-Culture Assay, Control, Isolation, Cell Characterization

Journal: bioRxiv

Article Title: Dynamic optimization of extrachromosomal DNA copy number drives tumour evolution

doi: 10.64898/2026.03.20.713026

Figure Lengend Snippet: (a) Schematics depicting hypothesized ecDNA copy number distributions of all cells, G1 cells, and parent cells giving rise to daughter cells (left). Representative images from combined IF for Aurora B Kinase and Cyclin A and DNA FISH for MYC in COLO 320DM. Cyclin A was used as a marker to identify G1 interphase cells, whose copy number should theoretically be 1n before entering S-phase and undergoing genome doubling. Aurora B Kinase was used as an identification marker for recently divided daughter cells. Copy number of parents of daughter cells was estimated by taking the average of the daughter cells’ MYC DNA FISH foci areas. Copy numbers of parent cells were compared against copy numbers of G1 interphase cells to avoid high copy number bias arising from cells past S-phase and with replicated DNA content. Scale bars, 10 µm (right). (b) Histograms depicting proportion of G1 interphase and parent cells in each copy number quintile in COLO 320DM and PC3 DM.

Article Snippet: COLO 320DM and COLO 320HSR (colorectal cancer) and the parental PC3 (prostate cancer) cell lines were obtained from ATCC.

Techniques: Marker