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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:
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:
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:
Techniques: Derivative Assay, Inhibition, Activation Assay, Generated