Journal: Bioactive Materials

Article Title: “Artificial platelet injection system”: a plug-and-play platelet-based lysosome-targeting chimera for targeted protein degradation

doi: 10.1016/j.bioactmat.2026.01.011

Figure Lengend Snippet: │ PD-L1 degradation efficacy in vitro and in vivo by PLT-TACs in B16F10 cells. A , Western blot analysis of PD-L1 in IFN-γ pre-treated B16F10 cells after treated with saline, PLT-anti-PD-L1, PLT-TAC l , PLT-TAC m or PLT-TAC h (at an equivalent amount of 5 μM) for 36 h (n = 3 biologically independent samples). B , Mean fluorescence intensity of levels of surface PD-L1 in IFN-γ pre-treated B16F10 after treated with saline, PLT-anti-PD-L1, PLT-TAC l , PLT-TAC m or PLT-TAC h , measured by FCM (at an equivalent amount of 5 μM) for 36 h (n = 3 biologically independent samples). C , Schematic schedule of the treatment and evaluation in C57BL/6 mice with B16F10 homografting tumor model. D , Tumor growth curves, E , tumor weights, F , images of dissected tumors, G , survival curves from treatment groups (saline, PLT-anti-PD-L1, PLT-TAC l , PLT-TAC m or PLT-TAC h ) at a dosage of 5 mg/kg (n = 6 biologically independent samples). H , Immunohistochemical images of PD-L1 in dissected B16F10 tumors after treatment. I , Mean fluorescence intensity of PD-L1 in CD45-negative tumor cells from dissected tumors after treatment (n = 4 biologically independent samples). Data are presented as mean ± SD. p values were determined by one-way ANOVA test. ns, no significance; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.

Article Snippet: Breast tumor cell line 4T1 and melanoma tumor cell line B16F10 were purchased from the American Type Culture Collection (ATCC), and cultured in DMEM supplemented with 10% FBS and 1% penicillin-streptomycin.

Techniques: In Vitro, In Vivo, Western Blot, Saline, Fluorescence, Immunohistochemical staining

Journal: bioRxiv

Article Title: Cell Type–Dependent Uptake of Extracellular Vesicles Independent of Cellular Origin

doi: 10.64898/2026.05.19.726167

Figure Lengend Snippet: Uptake of HEK293T-derived EVs by murine melanoma cell lines. (A) Quantification of EV uptake following 2 h incubation of HEK293T-derived mNG-labeled EVs with B16F10 and Yummer melanoma cells at EV concentrations of 1 × 10 9 , 5 × 10 9 , and 1 × 10 10 particles. (B) Representative flow cytometry plots corresponding to panel A. (C) Quantification of EV uptake following 4 h incubation at the indicated concentrations. (D) Representative flow cytometry plots corresponding to panel C. Data are presented as mean ± SD (n = 3 independent experiments). Statistical analysis was performed using two-way ANOVA. Statistical significance is indicated as follows: *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

Article Snippet: Human embryonic kidney cells (HEK293T), SKBR-3 human breast cancer cells, pancreatic ductal adenocarcinoma (PDAK) cells, HepG2 human hepatic cancer cells, Huh7 human hepatocellular carcinoma cells, Caco-2 human colorectal adenocarcinoma cells, and the murine melanoma cell lines B16F10 and Yummer (all obtained from ATCC) were cultured in DMEM supplemented with 10% FBS and 1% antibiotic–antimycotic solution.

Techniques: Derivative Assay, Incubation, Labeling, Flow Cytometry

Journal: bioRxiv

Article Title: Cell Type–Dependent Uptake of Extracellular Vesicles Independent of Cellular Origin

doi: 10.64898/2026.05.19.726167

Figure Lengend Snippet: Uptake of Yummer-derived EVs by murine melanoma cell lines. (A) Quantification of EV uptake following 2 h incubation of Yummer-derived mNG-labeled EVs with B16F10 and Yummer cells at EV concentrations of 1 × 10 9 and 1 × 10 10 particles. (B) Representative flow cytometry plots corresponding to panel A. (C) Quantification of EV uptake following 4 h incubation at the indicated concentrations. (D) Representative flow cytometry plots corresponding to panel C. Data are presented as mean ± SD (n = 3 independent experiments). Statistical analysis was performed using two-way ANOVA. Statistical significance is indicated as follows: ****p < 0.0001.

Article Snippet: Human embryonic kidney cells (HEK293T), SKBR-3 human breast cancer cells, pancreatic ductal adenocarcinoma (PDAK) cells, HepG2 human hepatic cancer cells, Huh7 human hepatocellular carcinoma cells, Caco-2 human colorectal adenocarcinoma cells, and the murine melanoma cell lines B16F10 and Yummer (all obtained from ATCC) were cultured in DMEM supplemented with 10% FBS and 1% antibiotic–antimycotic solution.

Techniques: Derivative Assay, Incubation, Labeling, Flow Cytometry

Journal: bioRxiv

Article Title: ME1 Programs Latent Effector Capacity and Grounds a Mathematical Model of Reversible T Cell Exhaustion

doi: 10.64898/2026.05.05.722814

Figure Lengend Snippet: (A) Schematic illustrating the generation of CD8-specific ME1 transgenic (ME1 Tg) mice. (B) Representative flow cytometry showing tdTomato expression as a surrogate for ME1 overexpression in CD8 + tumor-infiltrating lymphocytes (TILs). (C–D) Average growth curves of B16F10 tumors in control and CD8-ME1 Tg mice treated with PBS (C) or combined anti-PD-1/anti-PD-L1 antibodies (100 μg each per dose) administered every other day starting on day 6 (arrow) after tumor implantation. Tumor growth was analyzed by two-way ANOVA (D, n = 6, **P < 0.01). (E) Tumor sizes were measured at endpoint. Data were analyzed using an unpaired two-tailed t test (n = 4–8, ***P < 0.001). One of two independent experiments is shown. (F) Flow cytometric analysis of granzyme B (GZMB) protein expression in CD8 + TILs cells from B16F10 tumors in ME1 Tg and control mice on day 12. Data were analyzed using an unpaired two-tailed Student’s t test ( * P< 0.05; n = 5 mice per group).

Article Snippet: B16F10 murine melanoma cell line was purchased from ATCC (CRL-6475) and cultured using DMEM complete medium.

Techniques: Transgenic Assay, Flow Cytometry, Expressing, Over Expression, Control, Tumor Implantation, Two Tailed Test

Journal: Frontiers in Molecular Biosciences

Article Title: Tumor-directed evolution of VSVΔ51M produces novel viruses with enhanced antitumor efficacy

doi: 10.3389/fmolb.2026.1656006

Figure Lengend Snippet: Scheme of viral passaging. VSVΔ51M was used to infect two cancer cell lines, B16F10 and LLC1, at an MOI of 0.1following Passage 1 (P1), was used to infect the next passage. The resultant four viruses after P10 and P30 were referred to as VSV-P10-LLC1, VSV-P10-B16F10, VSV-P30-LLC1, and VSV-P30-B16F10 throughout the study.

Article Snippet: The murine cell lines B16F10 (ATCC CRL-6475) and LLC1 (ATCC CRL-1642) used in this study were obtained from Dr. Nada Zaidan and Dr. Khalid Shah (KACST- BWH Centre of Excellence for Biomedicine, Riyadh, Saudi Arabia).

Techniques: Passaging

Journal: Frontiers in Molecular Biosciences

Article Title: Tumor-directed evolution of VSVΔ51M produces novel viruses with enhanced antitumor efficacy

doi: 10.3389/fmolb.2026.1656006

Figure Lengend Snippet: (A) B16F10 murine melanoma cells and (B) LLC1 murine lung carcinoma cells were infected with either parental VSVΔ51M or VSV-P10 variants (VSV-P10-B16F10 or VSV-P10-LLC1) at a range of multiplicities of infection (MOIs; 100 to 0.0001). Cell viability was assessed 48 h post-infection using a luminescence-based ATP assay. Statistical significance was determined by unpaired two-tailed Student’s t-test at each MOI. ****P < 0.0005; ns = not significant.

Article Snippet: The murine cell lines B16F10 (ATCC CRL-6475) and LLC1 (ATCC CRL-1642) used in this study were obtained from Dr. Nada Zaidan and Dr. Khalid Shah (KACST- BWH Centre of Excellence for Biomedicine, Riyadh, Saudi Arabia).

Techniques: Infection, ATP Assay, Two Tailed Test

Journal: Frontiers in Molecular Biosciences

Article Title: Tumor-directed evolution of VSVΔ51M produces novel viruses with enhanced antitumor efficacy

doi: 10.3389/fmolb.2026.1656006

Figure Lengend Snippet: (A) B16F10 murine melanoma cells, (B) LLC1 murine lung cancer cells (C) A549 human lung carcinoma cells, and (D) GM38 normal human fibroblasts were infected with parental VSVΔ51, VSV-P30-B16F10, or VSV-P30-LLC1 at a range of multiplicities of infection (MOIs; 0.0001–100). Cell viability was assessed 48 h post-infection using the CellTiter-Glo luminescence assay. Statistical significance for the B16F10 (A) and LLC (B) panels was determined using an unpaired two-tailed Student’s t -test, while significance for the A549 (C) panel was assessed using two-way ANOVA followed by multiple unpaired t -tests with false discovery rate (FDR) correction for multiple comparisons. Asterisks (*) denote comparisons between VSVΔ51M and VSV-P30-B16F10, and daggers (†) denote comparisons between VSVΔ51M and VSV-P30-LLC1. The levels of significance are indicated as follows: P < 0.05 (* or †), P < 0.01 (** or ††), P < 0.001 (*** or †††), and P < 0.0001 (**** or ††††).

Article Snippet: The murine cell lines B16F10 (ATCC CRL-6475) and LLC1 (ATCC CRL-1642) used in this study were obtained from Dr. Nada Zaidan and Dr. Khalid Shah (KACST- BWH Centre of Excellence for Biomedicine, Riyadh, Saudi Arabia).

Techniques: Infection, Luminescence Assay, Two Tailed Test

Journal: Frontiers in Molecular Biosciences

Article Title: Tumor-directed evolution of VSVΔ51M produces novel viruses with enhanced antitumor efficacy

doi: 10.3389/fmolb.2026.1656006

Figure Lengend Snippet: C57BL/6 mice (6–8 weeks old) were injected intraperitoneally (i.p.) with 2 × 10 6 B16F10 melanoma cells that had been pre-incubated for 1 h at 37 °C with either VSVΔ51M, VSV-P30-B16F10 (MOI = 0.1; 5 × 10 5 PFU), or PBS as a negative control. Tumor progression and overall survival were monitored over time. Mice treated with VSV-P30-B16F10–infected cells exhibited significantly prolonged survival compared to both the VSVΔ51M and PBS control groups. The median survival of the VSV-P30-B16F10 group was 35 days, compared to 18 and 19.5 days in the VSVΔ51M and PBS groups, respectively. Data represent a single experiment with n = 5 mice per group. Statistical significance was assessed using the Log-rank (Mantel–Cox) test (χ 2 = 7.862, P = 0.0196), the Log-rank test for trend (χ 2 = 5.396, P = 0.0202), and the Gehan–Breslow–Wilcoxon test (χ 2 = 6.679, P = 0.0355). All analyses confirmed significant differences in survival curves ( P < 0.05).

Article Snippet: The murine cell lines B16F10 (ATCC CRL-6475) and LLC1 (ATCC CRL-1642) used in this study were obtained from Dr. Nada Zaidan and Dr. Khalid Shah (KACST- BWH Centre of Excellence for Biomedicine, Riyadh, Saudi Arabia).

Techniques: Injection, Incubation, Negative Control, Infection, Control

Journal: Frontiers in Molecular Biosciences

Article Title: Tumor-directed evolution of VSVΔ51M produces novel viruses with enhanced antitumor efficacy

doi: 10.3389/fmolb.2026.1656006

Figure Lengend Snippet: Structural comparison of VSV glycoproteins from wild-type and passaged variants, and their interaction with LDLR. (A) Surface representation of the wild-type VSVΔ51M glycoprotein (VSV WT) showing the unmutated structure. (B) Surface model of the VSV-P30-B16F10 glycoprotein, with mutation sites highlighted in yellow. (C) Surface model of the VSV-P30-LLC1 glycoprotein, with the mutation site highlighted in red. (D) Overlay of VSV-P30-B16F10 (yellow) and VSV-P30-LLC1 (red) variants mapped onto the glycoprotein surface, illustrating the spatial distribution of mutations. (E) Structural model showing the glycoproteins in complex with the LDL receptor (LDLR, shown in magenta), highlighting the proximity of the mutated residues (yellow and red) to the predicted LDLR binding interface. These structural differences may underlie the enhanced binding affinity and altered receptor interactions observed in mutant viruses.

Article Snippet: The murine cell lines B16F10 (ATCC CRL-6475) and LLC1 (ATCC CRL-1642) used in this study were obtained from Dr. Nada Zaidan and Dr. Khalid Shah (KACST- BWH Centre of Excellence for Biomedicine, Riyadh, Saudi Arabia).

Techniques: Comparison, Mutagenesis, Binding Assay

Journal: Frontiers in Molecular Biosciences

Article Title: Tumor-directed evolution of VSVΔ51M produces novel viruses with enhanced antitumor efficacy

doi: 10.3389/fmolb.2026.1656006

Figure Lengend Snippet: Structural modeling reveals enhanced interaction between VSV-P30-B16F10 and LDLR mediated by the E353K mutation. (A) Overall structure of the VSV glycoprotein (green) in complex with the LDL receptor (LDLR; magenta), shown in ribbon representation with the LDLR surface displayed in transparent grey. (B) Close-up view of the wild-type VSV-LDLR interaction highlighting residue Glu353, which forms a hydrogen bond with Cys83 of LDLR (residues indicated in red shading). (C) Surface mesh visualization of the binding interface, further illustrating the proximity of the interacting residues. (D) Structural model of the VSV-P30-B16F10 variant showing the Glu353 to Lys353 substitution (light green), which maintains the hydrogen bond with LDLR at Cys83 and is predicted to enhance binding affinity. Hydrogen bonds are indicated with dashed lines.

Article Snippet: The murine cell lines B16F10 (ATCC CRL-6475) and LLC1 (ATCC CRL-1642) used in this study were obtained from Dr. Nada Zaidan and Dr. Khalid Shah (KACST- BWH Centre of Excellence for Biomedicine, Riyadh, Saudi Arabia).

Techniques: Mutagenesis, Residue, Binding Assay, Variant Assay