tocilizumab  (Selleck Chemicals)

Journal: bioRxiv

Article Title: IL-6R blockade with tocilizumab disrupts pericyte– and tumor cell–driven IL-6/STAT3 signaling, enhancing docetaxel efficacy in ER+ breast cancer

doi: 10.64898/2026.01.29.702661

Figure Lengend Snippet: a MCF-7 and b T-47D cells were serum starved then incubated HBVP CM from 10 nM DTX with 0.1 µg/mL control IgG, 0.1 µg/mL tocilizumab, vehicle, or 10 nM DTX in combination as indicated for 24 hours. Cells were then lysed and subjected to immunoblotting using a pSTAT3 or STAT3 antibody. Fold change of pSTAT3 over total STAT3. Data is representative of n = 4 independent experiments. Mean ± s.e.m. shown. P values were calculated using a repeated measures one-way ANOVA with a ( a ) Sidak’s and ( b ) Tukey’s multiple comparisons test. * P ≤ 0.05, ** P ≤ 0.01. SimplyBlue SafeStains are shown for each representative membrane. HBVP = human brain vascular pericytes, and CM = conditioned media. DTX = docetaxel.

Article Snippet: Tocilizumab (#A2012) and human IgG isotype control (#A2051, RRID:AB_3096062)) were purchased from SelleckChem, while docetaxel (DTX) (#01885-5MG-F) and bovine serum albumin (#A193325G) were purchased from Sigma Aldrich.

Techniques: Incubation, Control, Western Blot, Membrane

Journal: bioRxiv

Article Title: IL-6R blockade with tocilizumab disrupts pericyte– and tumor cell–driven IL-6/STAT3 signaling, enhancing docetaxel efficacy in ER+ breast cancer

doi: 10.64898/2026.01.29.702661

Figure Lengend Snippet: ( a – c ) Longitudinal spheroid growth of UVABCO178 ( a ), UVABCO176 ( b ), and UVABCO179 ( c ) over 14-16 days following treatment with control IgG (black), tocilizumab (0.1 µg/mL; cyan), DTX (10 nM; light pink), or the tocilizumab + DTX combination (purple). Lines represent model-fitted exponential growth curves for spheroid area over time, derived from linear regression of log-transformed area (log(Area) ∼ day) (n = 8 – 780 organoids per patient, time point, and condition). Bliss synergy excess for the tocilizumab + DTX combination are reported in each panel. Statistical significance between treatment groups is indicated (* P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001).( d – e ) Representative immunofluorescence images of spheroids from UVABCO178 ( d ) and UVABCO179 ( e ) following treatment with control IgG, tocilizumab, DTX, or the combination. Staining includes DAPI (nuclei, white), EdU (proliferation, magenta), pSTAT3 (IL-6 signaling, red), and NucView488 (NV488; apoptosis, green). Scale bars, 100 µm. DTX = docetaxel.

Article Snippet: Tocilizumab (#A2012) and human IgG isotype control (#A2051, RRID:AB_3096062)) were purchased from SelleckChem, while docetaxel (DTX) (#01885-5MG-F) and bovine serum albumin (#A193325G) were purchased from Sigma Aldrich.

Techniques: Control, Derivative Assay, Transformation Assay, Immunofluorescence, Staining

Journal: bioRxiv

Article Title: IL-6R blockade with tocilizumab disrupts pericyte– and tumor cell–driven IL-6/STAT3 signaling, enhancing docetaxel efficacy in ER+ breast cancer

doi: 10.64898/2026.01.29.702661

Figure Lengend Snippet: a Docetaxel directly impacts pericytes within the tumor microenvironment, inducing secretion of IL-6. Pericyte-derived IL-6 engages the IL-6R complex (IL-6Rα/IL-6Rβ) on ER+ breast cancer cells, activating JAK/STAT3 signaling and promoting anti-apoptotic signaling, cancer cell survival, and chemoresistance. b Pharmacologic inhibition of IL-6R with tocilizumab disrupts IL-6 mediated signaling between pericytes and cancer cells. IL-6R blockade attenuates STAT3 activation, resulting in reduced anti-apoptotic signaling and decreased chemoresistance in ER+ breast cancer cells treated with docetaxel. Generated from BioRender.

Article Snippet: Tocilizumab (#A2012) and human IgG isotype control (#A2051, RRID:AB_3096062)) were purchased from SelleckChem, while docetaxel (DTX) (#01885-5MG-F) and bovine serum albumin (#A193325G) were purchased from Sigma Aldrich.

Techniques: Derivative Assay, Inhibition, Activation Assay, Generated

Journal: bioRxiv

Article Title: A fully human pluripotent stem cell-derived blood-brain barrier model for clinically relevant disease modeling and selection of neurotropic adeno-associated viruses

doi: 10.64898/2025.12.21.695793

Figure Lengend Snippet: ( a ) Quantification of TEER levels shows a reduction in barrier integrity following incubation with poly(I:C) and a recovery after treatment with the CAR factors (3 biological independent experiments). ( b ) Quantification of NaFl levels confirms the recovery after treatment with the CAR factors (n=3 biological independent experiments). ( c ) Representative images and reduction of human IgG+ puncta in hPSC-derived neurons following incubation with the CAR factors (5 fields; n=3 biological independent experiments). ( d ) CAR factors reverse the mesenchymal cell transition induced by Poly(I:C). ( e ) Rescue of TEER values after treatment with tocilizumab (TCZ) (n=3 biological independent experiments). ( f ) Quantification of NaFl levels confirms the recovery after treatment with the TCZ (n=3 biological independent experiments). ( g ) Representative images and quantification of human IgG+ puncta in hPSC-derived neuronal cultures following incubation with poly(I:C) with or without TCZ (5 fields; n=3 biological independent experiments). ( h ) TCZ treatment is sufficient to rescue the endothelial-specific gene expression as confirmed by qPCR analysis. Values are mean ± SEM. *p < 0.05, ****p < 0.0001. Statistical analysis is performed using one-way ANOVA followed by Tukey post-test. Scale bars, 100 µm. CAR: CHIR99021 (C), db-cAMP (A), RepSox (R); TCZ: Tocilizumab.

Article Snippet: For the CAR or tocilizumab (TCZ) treatment the medium was replaced with fresh medium with dbcAMP (Selleckchem, 250 μM), RepSox (10 μM, Sigma) and CHIR99021 (10 μM, Miltenyi), (CAR factor combination) or tocilizumab (50 ng/mL, BioXCell) for 48 hrs.

Techniques: Incubation, Derivative Assay, Gene Expression