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European Collection of Authenticated Cell Cultures normal human foreskin fibroblasts (bj)
Normal Human Foreskin Fibroblasts (Bj), supplied by European Collection of Authenticated Cell Cultures, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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normal human foreskin fibroblasts (bj) - by Bioz Stars, 2026-10

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Article Title: Heterocyclic androstane derivatives targeting hormone-related cancers: Synthesis, bioactivity and docking studies.
Article Snippet: Insertion of a heterocyclic ring into the steroid core could enhance bioactivity, improve selectivity and reduce side effects in potential drugs for cancer therapy.. The present study describes the synthesis of new thiazoline, thiadiazoline and thiazolidinone steroid compounds combined with lactone, lactam or pyridine moieties.. These steroid hybrid molecules may be potential candidates for drug design, with improved biological activity and bioavailability.

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A Progression-Free Survival Kaplan–Meier curves according to CFH expression in the KIRC TCGA cohort ( n = 508). B UMAP displaying CFH expression across labelled Seurat clusters from 20 different ccRCC primary tumors . C Dot plot displaying CFH scaled mean expression levels (dot color) and percentage of cells (dot size) within each Seurat cluster. D Hematoxylin-eosin (H&E) section of a representative primary ccRCC tumor used for spatial transcriptomic analysis (left); Same section displaying labelled spots for CFH and fibroblast signature high and low categories (middle), or CA9 high and low categories (right). Scale bar 1 mm. E Immunofluorescence of CA9 (pink), alpha-SMA (orange) and Factor H (white) of a ccRCC primary tumor. F alpha-SMA (orange) positive CAF presenting positive FH staining (white). G ccRCC cancer cells positive for CA9 (pink) and for FH (white) staining. F , G Nuclei are stained with DAPI (blue).

Journal: Communications Biology

Article Title: Intracellular complement Factor H promotes tumor progression through modulation of cell cycle and actin cytoskeleton

doi: 10.1038/s42003-026-09807-4

Figure Lengend Snippet: A Progression-Free Survival Kaplan–Meier curves according to CFH expression in the KIRC TCGA cohort ( n = 508). B UMAP displaying CFH expression across labelled Seurat clusters from 20 different ccRCC primary tumors . C Dot plot displaying CFH scaled mean expression levels (dot color) and percentage of cells (dot size) within each Seurat cluster. D Hematoxylin-eosin (H&E) section of a representative primary ccRCC tumor used for spatial transcriptomic analysis (left); Same section displaying labelled spots for CFH and fibroblast signature high and low categories (middle), or CA9 high and low categories (right). Scale bar 1 mm. E Immunofluorescence of CA9 (pink), alpha-SMA (orange) and Factor H (white) of a ccRCC primary tumor. F alpha-SMA (orange) positive CAF presenting positive FH staining (white). G ccRCC cancer cells positive for CA9 (pink) and for FH (white) staining. F , G Nuclei are stained with DAPI (blue).

Article Snippet: Primary Normal Human Dermal Fibroblasts (NHDF, Promocell C-12302), the human dermal fibroblast cell line BJ (ATCC CRL-2522) and two ccRCC cell lines (A498 and Caki-1, ATCC HTB-44 & HTB-46, respectively, both p53 wild type, the first being VHL mutated, but not the second one) were employed.

Techniques: Expressing, Immunofluorescence, Staining

$A FH western blot with plasma purified FH along with lysates and SN from A498 and Caki-1 ccRCC cells (left and center, respectively), and BJ fibroblasts (right). B Western blot FH gene silencing validation in lysates from A498 cell (left), Caki-1 cells (center left), BJ fibroblasts (center right) and NHDF primary fibroblasts (right). C Western blot FH gene silencing validation in SN from A498 cell (left), Caki-1 cells (center left), BJ fibroblasts (center right) and NHDF primary fibroblasts (right). D FH quantification by ELISA on the different subcellular BJ fibroblasts’ fractions. Average +/- SD, all data points are presented. E FH and compartment-specific proteins western blot for the different cell fractions in BJ fibroblasts (left), NHDF fibroblasts (center left), A498 cells (center right) and Caki-1 cells (right). Cyto = cytosol fraction, Orga = organelle fraction and Nuc = nuclear fraction. All gel images represent bands from the same experimental run, with separation into two boxes when unrelated intermediate lanes were present in the original blot. F – H Partial co-localization of FH with the nuclear staining: F Confocal microscopy evidencing staining for FH (red, rabbit anti-FH polyclonal, ProteinTech), the nuclear staining (DAPI, blue) and the actin cytoskeleton (phalloidin, green) in A498. G Chromogen staining by immunohistochemistry for FH (Ox24 monoclonal anti-FH, brown) and nuclei (blue) of a section of a ccRCC patient tumor. Scale bar of the main image – 100 µm and of the insert, 50 µm. H Immunofluorescent staining for FH (red, rabbit anti-FH polyclonal, ProteinTech), tumor cells (CA9, white) and nuclei (DAPI) in a section of a ccRCC patient tumor. G , H The inserts represent a zoomed image.$

Journal: Communications Biology

Article Title: Intracellular complement Factor H promotes tumor progression through modulation of cell cycle and actin cytoskeleton

doi: 10.1038/s42003-026-09807-4

Figure Lengend Snippet: A FH western blot with plasma purified FH along with lysates and SN from A498 and Caki-1 ccRCC cells (left and center, respectively), and BJ fibroblasts (right). B Western blot FH gene silencing validation in lysates from A498 cell (left), Caki-1 cells (center left), BJ fibroblasts (center right) and NHDF primary fibroblasts (right). C Western blot FH gene silencing validation in SN from A498 cell (left), Caki-1 cells (center left), BJ fibroblasts (center right) and NHDF primary fibroblasts (right). D FH quantification by ELISA on the different subcellular BJ fibroblasts’ fractions. Average +/- SD, all data points are presented. E FH and compartment-specific proteins western blot for the different cell fractions in BJ fibroblasts (left), NHDF fibroblasts (center left), A498 cells (center right) and Caki-1 cells (right). Cyto = cytosol fraction, Orga = organelle fraction and Nuc = nuclear fraction. All gel images represent bands from the same experimental run, with separation into two boxes when unrelated intermediate lanes were present in the original blot. F – H Partial co-localization of FH with the nuclear staining: F Confocal microscopy evidencing staining for FH (red, rabbit anti-FH polyclonal, ProteinTech), the nuclear staining (DAPI, blue) and the actin cytoskeleton (phalloidin, green) in A498. G Chromogen staining by immunohistochemistry for FH (Ox24 monoclonal anti-FH, brown) and nuclei (blue) of a section of a ccRCC patient tumor. Scale bar of the main image – 100 µm and of the insert, 50 µm. H Immunofluorescent staining for FH (red, rabbit anti-FH polyclonal, ProteinTech), tumor cells (CA9, white) and nuclei (DAPI) in a section of a ccRCC patient tumor. G , H The inserts represent a zoomed image.

Techniques: Western Blot, Clinical Proteomics, Purification, Biomarker Discovery, Enzyme-linked Immunosorbent Assay, Staining, Confocal Microscopy, Immunohistochemistry

$A Protein-protein interaction network analysis of common FH interacting proteins within A498 ccRCC cells and BJ fibroblasts (FH immunoprecipitated with anti-C-terminal FH mAb C18/3); STRING Tool, physical subnetwork with at least 0.4 confidence. Top 10 gene-ontology pathways for B the common FH interactors between A498 and BJ cells, C FH interacting candidates in BJ fibroblasts and D FH interactors identified in A498 ccRCC cells. E Protein-protein interaction ELISA dose-response analysis of purified FH binding to intracellular FH interacting candidates. F Validation of the co-immunoprecipitation of E2F3 and CAPZB together with FH. A498 lysate was incubated with anti-C-terminus FH mAb C18/3 (FH) or unspecific isotype control immunoglobuling G (IgG). Immunoprecipitation was then performed on protein A/G beads and proteins were eluted and probed by western blot for FH (upper line), E2F3 (middle line) and CAPZB (lower line). The validation of the target is based on its presence in the immunoprecipitates fraction with anti-FH (ip FH) but not in the one of the control IgG (ip IgG). Input: starting lysate material; SN: supernatant; ip: immunoprecipitates. G Kinetic SPR analysis using purified FH at concentrations ranging from 31.25 nM to 500 nM, twofold dilutions. FH was injected in normal (left) or low (right) ionic strength conditions on its respective FH interacting candidate coated chip for 240 s followed by 240 s dissociation. A 1:1 interaction with a drifting baseline curve was fitted to calculate kinetic parameters. The straight line represents the measured signal. The dotted one represents the kinetic fit. Curves from high to low RU values match the FH concentrations used (high FH, high RU values).$

Journal: Communications Biology

Article Title: Intracellular complement Factor H promotes tumor progression through modulation of cell cycle and actin cytoskeleton

doi: 10.1038/s42003-026-09807-4

Figure Lengend Snippet: A Protein-protein interaction network analysis of common FH interacting proteins within A498 ccRCC cells and BJ fibroblasts (FH immunoprecipitated with anti-C-terminal FH mAb C18/3); STRING Tool, physical subnetwork with at least 0.4 confidence. Top 10 gene-ontology pathways for B the common FH interactors between A498 and BJ cells, C FH interacting candidates in BJ fibroblasts and D FH interactors identified in A498 ccRCC cells. E Protein-protein interaction ELISA dose-response analysis of purified FH binding to intracellular FH interacting candidates. F Validation of the co-immunoprecipitation of E2F3 and CAPZB together with FH. A498 lysate was incubated with anti-C-terminus FH mAb C18/3 (FH) or unspecific isotype control immunoglobuling G (IgG). Immunoprecipitation was then performed on protein A/G beads and proteins were eluted and probed by western blot for FH (upper line), E2F3 (middle line) and CAPZB (lower line). The validation of the target is based on its presence in the immunoprecipitates fraction with anti-FH (ip FH) but not in the one of the control IgG (ip IgG). Input: starting lysate material; SN: supernatant; ip: immunoprecipitates. G Kinetic SPR analysis using purified FH at concentrations ranging from 31.25 nM to 500 nM, twofold dilutions. FH was injected in normal (left) or low (right) ionic strength conditions on its respective FH interacting candidate coated chip for 240 s followed by 240 s dissociation. A 1:1 interaction with a drifting baseline curve was fitted to calculate kinetic parameters. The straight line represents the measured signal. The dotted one represents the kinetic fit. Curves from high to low RU values match the FH concentrations used (high FH, high RU values).

Techniques: Immunoprecipitation, Enzyme-linked Immunosorbent Assay, Purification, Binding Assay, Biomarker Discovery, Incubation, Control, Western Blot, Injection

A IPA comparison analysis of common predicted upstream regulators in siFH vs siC treated A498, Caki-1 and BJ cells. Top 3 upstream regulators across cell lines are annotated and a heatmap with their activation z-score in siFH is presented. B Protein-protein interaction network analysis of common FH interacting proteins and p53; STRING Tool, physical subnetwork with at least 0.4 confidence. C TP53 expression fold change (siFH/siC) for A498, Caki-1 and BJ cells. GSEA plots for the p53 pathway (hallmark gene set) comparing siFH vs siC treated D A498 ccRCC cells, E Caki-1 ccRCC cells and F BJ fibroblasts. Western blot analysis of G total p53 and H phosphorylated p53 S46 levels in the lysates of siC and siFH treated A498 ccRCC cells, Caki-1 ccRCC cells and BJ fibroblasts. I Immunofluorescence staining of p53 (light yellow) and nuclei (blue) of siC (left), siTP53 (left center), siFH (right center) or siTP53 + siFH (right) treated A498 cells (top row) and BJ fibroblasts (bottom row). Arrows indicate representative nuclei positive for p53 staining. The scale bar in the insert is of 100 µm and of the main image – 500 µm. J Evaluation of proliferation (left panels) and mortality (right panels) of siC, siTP53, siFH and siTP53 + siFH treated A498 (top row) and BJ (bottom row) cells. Cell proliferation is shown as inversed Fold Change of CFSE geometric means and mortality is represented as the Fold Change of DAPI stained dead cells. Exact p values indicated on the figures. Brown–Forsythe and Welch ANOVA tests plus post-hoc Tamhane’s T2 multiple comparisons test.

Journal: Communications Biology

Article Title: Intracellular complement Factor H promotes tumor progression through modulation of cell cycle and actin cytoskeleton

doi: 10.1038/s42003-026-09807-4

Figure Lengend Snippet: A IPA comparison analysis of common predicted upstream regulators in siFH vs siC treated A498, Caki-1 and BJ cells. Top 3 upstream regulators across cell lines are annotated and a heatmap with their activation z-score in siFH is presented. B Protein-protein interaction network analysis of common FH interacting proteins and p53; STRING Tool, physical subnetwork with at least 0.4 confidence. C TP53 expression fold change (siFH/siC) for A498, Caki-1 and BJ cells. GSEA plots for the p53 pathway (hallmark gene set) comparing siFH vs siC treated D A498 ccRCC cells, E Caki-1 ccRCC cells and F BJ fibroblasts. Western blot analysis of G total p53 and H phosphorylated p53 S46 levels in the lysates of siC and siFH treated A498 ccRCC cells, Caki-1 ccRCC cells and BJ fibroblasts. I Immunofluorescence staining of p53 (light yellow) and nuclei (blue) of siC (left), siTP53 (left center), siFH (right center) or siTP53 + siFH (right) treated A498 cells (top row) and BJ fibroblasts (bottom row). Arrows indicate representative nuclei positive for p53 staining. The scale bar in the insert is of 100 µm and of the main image – 500 µm. J Evaluation of proliferation (left panels) and mortality (right panels) of siC, siTP53, siFH and siTP53 + siFH treated A498 (top row) and BJ (bottom row) cells. Cell proliferation is shown as inversed Fold Change of CFSE geometric means and mortality is represented as the Fold Change of DAPI stained dead cells. Exact p values indicated on the figures. Brown–Forsythe and Welch ANOVA tests plus post-hoc Tamhane’s T2 multiple comparisons test.

Techniques: Comparison, Activation Assay, Expressing, Western Blot, Immunofluorescence, Staining

UMAP displaying A the malignant cell states identified by reclustering, and B the proximal tubular cell signature expression across malignant cells. C Dot plot displaying significantly enriched pathways across malignant cell states, scaled mean expression levels (dot color) and percentage of cells (dot size). D Dot plot displaying CFH scaled mean expression levels (dot color) across malignant cell states. E Pseudotime trajectories of malignant cells inferred by Monocle3. Two main branches were identified: Branch 1 representing cells undergoing cell cycle progression, and Branch 2 representing cancer cell differentiation. F Expression of E2F target genes along the trajectory of Branch 1. G Expression of CFH , POLA1 , CCND2 and MKI67 genes along the trajectory of Branch 1. H Immunofluorescence of CA9 (pink), Factor H (white) and Ki67 (light blue) of a ccRCC primary tumor. Representative Ki67 and FH positive (top row), and Ki67 and FH negative (bottom row) cancer cell staining. I Evaluation of Ki67 positive cell frequency in FH positive versus negative ccRCC cancer cells. The exact p value is indicated on the figure. Wilcoxon matched-pairs signed rank test. J Overall Survival Kaplan–Meier curves according to Hedgehog cancer cell signature abundance in the KIRC TCGA cohort ( n = 508). K Proposed mode of action of intracellular FH in ccRCC fibroblasts and cancer cells. Created in BioRender. Roumenina, L. (2025) https://BioRender.com/gtfgxgw .

Journal: Communications Biology

Article Title: Intracellular complement Factor H promotes tumor progression through modulation of cell cycle and actin cytoskeleton

doi: 10.1038/s42003-026-09807-4

Figure Lengend Snippet: UMAP displaying A the malignant cell states identified by reclustering, and B the proximal tubular cell signature expression across malignant cells. C Dot plot displaying significantly enriched pathways across malignant cell states, scaled mean expression levels (dot color) and percentage of cells (dot size). D Dot plot displaying CFH scaled mean expression levels (dot color) across malignant cell states. E Pseudotime trajectories of malignant cells inferred by Monocle3. Two main branches were identified: Branch 1 representing cells undergoing cell cycle progression, and Branch 2 representing cancer cell differentiation. F Expression of E2F target genes along the trajectory of Branch 1. G Expression of CFH , POLA1 , CCND2 and MKI67 genes along the trajectory of Branch 1. H Immunofluorescence of CA9 (pink), Factor H (white) and Ki67 (light blue) of a ccRCC primary tumor. Representative Ki67 and FH positive (top row), and Ki67 and FH negative (bottom row) cancer cell staining. I Evaluation of Ki67 positive cell frequency in FH positive versus negative ccRCC cancer cells. The exact p value is indicated on the figure. Wilcoxon matched-pairs signed rank test. J Overall Survival Kaplan–Meier curves according to Hedgehog cancer cell signature abundance in the KIRC TCGA cohort ( n = 508). K Proposed mode of action of intracellular FH in ccRCC fibroblasts and cancer cells. Created in BioRender. Roumenina, L. (2025) https://BioRender.com/gtfgxgw .

Techniques: Expressing, Cell Differentiation, Immunofluorescence, Staining

TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), fibroblast proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.

Journal: Scientific Reports

Article Title: Chitosan-dextran sulfate nanocapsules for enhanced tigecycline efficacy against non-typhoidal Salmonella enterica

doi: 10.1038/s41598-026-35229-7

Figure Lengend Snippet: TGC and/or unloaded CD NPs ameliorated the S. Typhimurium infected group induced histopathological alterations in mice’s liver tissues. Representative photomicrographs of the H&E-stained hepatic tissue sections showing the control (A), S. Typhimurium infected group (C), TGC (E), unloaded CD NPs (G), CD-TGC groups (I) and their respective higher magnifications (B, D, F, H, and J). A, B: control group displaying normal central vein (CV), hepatic cords (HC) with hepatocytes of eosinophilic granular cytoplasm (EC), rounded central single (SN) or double vesicular nuclei (DN), and kupffer cells (KC). C, D: S. Typhimurium infected group demonstrating multiple areas of variable-sized necrotic areas (NA) of coagulative necrosis (CN), severely dilated and congested sinusoid (SDS) with Kupffer cell hyperplasia (KCH). E, F: TGC group displaying moderately sized necrotic areas (MNA), moderately dilated and congested sinusoids (MDS), moderately hyperplastic Kupffer’s cells (MKC), interstitial mononuclear cell infiltration (MI), fibroblast proliferation (FP), and regenerated hepatocytes of stippling basophilic cytoplasm (BC) and pale nuclei (PN). G, H: unloaded CD NPs group showing a few scattered minute necrotic areas (mNA), intense mononuclear cell infiltration (IMI) around the portal area, and apparently normal hepatocytes (NH). I, J: CD-TGC group showed normal hepatocytes (NH), few dilated blood vessels (DBV), and a few interstitial lymphocytic aggregates (FL). Scale bars = 100 μm in A, C, E, G, I; and = 20 μm in B, D, F, H, and J. K: Bar charts demonstrate the statistical analysis of the comparative quantification of the hepatic injury scores in all studied groups. Bars carrying different superscript letters (a, b, c, d, and e) are significantly different as analyzed by the one-way ANOVA test, followed by the multiple comparisons by Duncan’s Post-hoc test ( p < 0.05). Values are the mean of 6 mice per group ± S.E.M.

Article Snippet: BJ normal human foreskin primary fibroblast cell line (ATCC CRL-2522) was used for studying safety of CD-TGC nanocapsules.

Techniques: Infection, Staining, Control

(1A) Schematic of microfluidic chip fabrication. PDMS devices were generated by soft lithography using SU-8 patterned silicon wafers, punched to create inlet/outlet ports, and irreversibly bonded to glass coverslips via oxygen plasma activation. (1B) Hydrogel loading and cell encapsulation workflow. Tumor cells and fibroblasts were co-seeded in a Matrigel/Collagen I/Hyaluronic Acid (Mat/COL/HA) matrix crosslinked with Genipin and injected into the central chamber. Devices were cultured for 6 days to allow microtissue formation prior to 4 days (96⍰h) of drug treatment. (1C) Schematic representation of the microfluidic chip layout showing the spatial distribution of tumor cells and fibroblasts within the central hydrogel chamber and adjacent side channels used for media perfusion and drug delivery. (1D) FTIR-ATR spectra (950–1730⍰cm −1 ) comparing Mat/COL/HA hydrogels with and without Genipin. Key shifts in amide I/II and C–O/C–N stretching regions indicate successful crosslinking and structural rearrangement. (1E) FTIR-ATR spectra (2450–3700⍰cm −1 ) highlighting changes in CH 2 , O–H, and N–H stretching bands. Decreases at 3284 and 2833⍰cm −1 , along with persistent signals, suggest partial retention of functional groups relevant for subsequent surface anchoring. (1F) Schematic representation of the dual-surface functionalization strategy. Plasma-activated PDMS and glass were silanized using APTES to enable covalent bonding to Genipin-crosslinked hydrogels via residual hydroxyl and amine groups.

Journal: bioRxiv

Article Title: Genipin-Crosslinked, Silane-Anchored 3D Tumor–Stroma Microtissues for High-Content On-Chip Drug Testing

doi: 10.1101/2025.07.03.662913

Figure Lengend Snippet: (1A) Schematic of microfluidic chip fabrication. PDMS devices were generated by soft lithography using SU-8 patterned silicon wafers, punched to create inlet/outlet ports, and irreversibly bonded to glass coverslips via oxygen plasma activation. (1B) Hydrogel loading and cell encapsulation workflow. Tumor cells and fibroblasts were co-seeded in a Matrigel/Collagen I/Hyaluronic Acid (Mat/COL/HA) matrix crosslinked with Genipin and injected into the central chamber. Devices were cultured for 6 days to allow microtissue formation prior to 4 days (96⍰h) of drug treatment. (1C) Schematic representation of the microfluidic chip layout showing the spatial distribution of tumor cells and fibroblasts within the central hydrogel chamber and adjacent side channels used for media perfusion and drug delivery. (1D) FTIR-ATR spectra (950–1730⍰cm −1 ) comparing Mat/COL/HA hydrogels with and without Genipin. Key shifts in amide I/II and C–O/C–N stretching regions indicate successful crosslinking and structural rearrangement. (1E) FTIR-ATR spectra (2450–3700⍰cm −1 ) highlighting changes in CH 2 , O–H, and N–H stretching bands. Decreases at 3284 and 2833⍰cm −1 , along with persistent signals, suggest partial retention of functional groups relevant for subsequent surface anchoring. (1F) Schematic representation of the dual-surface functionalization strategy. Plasma-activated PDMS and glass were silanized using APTES to enable covalent bonding to Genipin-crosslinked hydrogels via residual hydroxyl and amine groups.

Article Snippet: Normal human foreskin fibroblasts BJ (ATCC CRL-2522), hTERT-immortalized cancer-associated fibroblasts (PF179T), and LNCaP prostate cancer cells were obtained from the biobank of the Institute of Biomedicine, Cancer Research Unit and FICAN West Cancer Centre Laboratory, University of Turku and Turku University Hospital.

Techniques: Generated, Clinical Proteomics, Activation Assay, Encapsulation, Injection, Cell Culture, Functional Assay

(2A) Quantification of hydrogel area retention over 6 days for UT-SCC-19A and UT-SCC-44 cell lines cultured in mono- or co-culture with BJ fibroblasts. Four conditions were assessed: untreated, APTES-only, Genipin-only (500rzµM), and APTES + Genipin. Data represent mean ± SD of three biological replicates. Statistical analysis was performed using two-way ANOVA with Dunnett’s post hoc test versus untreated control. (2B) Brightfield images of UT-SCC-19A/BJ co-cultures in the central chamber at day 6, comparing Genipin-crosslinked and non-crosslinked hydrogels. Scale bar: 200⍰µm. (2C) Immunofluorescence staining of UT-SCC-19A/BJ (top) and UT-SCC-44/BJ co-cultures (bottom) after 10 days, showing Vimentin (mesenchymal marker), pan-Cytokeratin (epithelial marker), F-actin (Phalloidin), and nuclei (Hoechst 33342) stainings. Z-stack projections acquired using Zeiss LSM980 with 10× objective. Scale bar: 100⍰µm.

Journal: bioRxiv

Article Title: Genipin-Crosslinked, Silane-Anchored 3D Tumor–Stroma Microtissues for High-Content On-Chip Drug Testing

doi: 10.1101/2025.07.03.662913

Figure Lengend Snippet: (2A) Quantification of hydrogel area retention over 6 days for UT-SCC-19A and UT-SCC-44 cell lines cultured in mono- or co-culture with BJ fibroblasts. Four conditions were assessed: untreated, APTES-only, Genipin-only (500rzµM), and APTES + Genipin. Data represent mean ± SD of three biological replicates. Statistical analysis was performed using two-way ANOVA with Dunnett’s post hoc test versus untreated control. (2B) Brightfield images of UT-SCC-19A/BJ co-cultures in the central chamber at day 6, comparing Genipin-crosslinked and non-crosslinked hydrogels. Scale bar: 200⍰µm. (2C) Immunofluorescence staining of UT-SCC-19A/BJ (top) and UT-SCC-44/BJ co-cultures (bottom) after 10 days, showing Vimentin (mesenchymal marker), pan-Cytokeratin (epithelial marker), F-actin (Phalloidin), and nuclei (Hoechst 33342) stainings. Z-stack projections acquired using Zeiss LSM980 with 10× objective. Scale bar: 100⍰µm.

Techniques: Cell Culture, Co-Culture Assay, Control, Immunofluorescence, Staining, Marker

(5A) Cisplatin dose– response in UT-SCC-19A and UT-SCC-44 tumor–fibroblast co-cultures embedded in native (non-crosslinked) versus Genipin-crosslinked hydrogels. (5B) Comparison of drug sensitivity in native hydrogels between cells adhered to the chip surface and cells retained within the hydrogel matrix. (5C-E) Dose–response curves for UT-SCC-19A (C) and UT-SCC-44 (E) in monoculture, co-culture with BJ fibroblasts, and co-culture with patient-derived CAFs. Each dot represents a biological replicate (n = 3), with viability expressed as % of untreated control and plotted against log-transformed cisplatin concentrations. (5F) Summary of IC 50 values calculated from nonlinear regression using the four-parameter Hill equation. Bars indicate the median IC 50 (µM), with error bars representing the interquartile range (25th–75th percentile). Individual biological replicate values (n = 3) are shown as black dots; mean IC 50 values are annotated above each bar. (5G) Representative immunofluorescence images of UT-SCC-44 in 3D monoculture and BJ co-culture following 4 days of Cisplatin treatment. Samples were stained for Vimentin (mesenchymal marker), Pan-cytokeratin (epithelial marker), Phalloidin (F-actin), and Hoechst 33342 (nuclei). Z-projected images acquired using a 10× objective on super-resolution microscopy. Scale bar = 100⍰µm. Statistical analysis: two-way ANOVA with Tukey’s post hoc test unless otherwise stated. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Journal: bioRxiv

Article Title: Genipin-Crosslinked, Silane-Anchored 3D Tumor–Stroma Microtissues for High-Content On-Chip Drug Testing

doi: 10.1101/2025.07.03.662913

Figure Lengend Snippet: (5A) Cisplatin dose– response in UT-SCC-19A and UT-SCC-44 tumor–fibroblast co-cultures embedded in native (non-crosslinked) versus Genipin-crosslinked hydrogels. (5B) Comparison of drug sensitivity in native hydrogels between cells adhered to the chip surface and cells retained within the hydrogel matrix. (5C-E) Dose–response curves for UT-SCC-19A (C) and UT-SCC-44 (E) in monoculture, co-culture with BJ fibroblasts, and co-culture with patient-derived CAFs. Each dot represents a biological replicate (n = 3), with viability expressed as % of untreated control and plotted against log-transformed cisplatin concentrations. (5F) Summary of IC 50 values calculated from nonlinear regression using the four-parameter Hill equation. Bars indicate the median IC 50 (µM), with error bars representing the interquartile range (25th–75th percentile). Individual biological replicate values (n = 3) are shown as black dots; mean IC 50 values are annotated above each bar. (5G) Representative immunofluorescence images of UT-SCC-44 in 3D monoculture and BJ co-culture following 4 days of Cisplatin treatment. Samples were stained for Vimentin (mesenchymal marker), Pan-cytokeratin (epithelial marker), Phalloidin (F-actin), and Hoechst 33342 (nuclei). Z-projected images acquired using a 10× objective on super-resolution microscopy. Scale bar = 100⍰µm. Statistical analysis: two-way ANOVA with Tukey’s post hoc test unless otherwise stated. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Techniques: Comparison, Co-Culture Assay, Derivative Assay, Control, Transformation Assay, Immunofluorescence, Staining, Marker, Super-Resolution Microscopy

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normal human foreskin fibroblasts (bj) (European Collection of Authenticated Cell Cultures)

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