Fig. 7.

Stat3 as a target to abrogate lung colonization. a, b Colony forming efficiency of T24 and metastatic PDX model upon treatment with Napabucasin (Stat3 inhibitor, 1μM) in ASMC-conditioned media. Full colonies were allowed to form for 14 days, before the administration of vehicle or Napabucasin for an additional 7-day period. Live colonies were stained with the MTT assay for quantifications. c Assessment of metastatic lung colonization in T24 and metastatic PDX models upon treatment with Napabucasin for six weeks. 1 × 10⁶ cancer cells were injected via tail-vein. Napabucasin treatment (intraperitoneal injection, 20 mg kg⁻¹) started 72 h post-injection (T24 model, n = 6; PDX model, n = 6). BLI signals were measured weekly. BLI images at the experimental endpoint (after 6 weeks treatment) with respective quantitative intensities are shown. d Immunohistochemical analysis of stem/progenitor and differentiation markers (CK14 and CK18) in vehicle and Napabucasin treated lung sections from mice injected with T24 cancer cells via tail-vein. e Gene expression analysis of stemness markers (CK14, SOX5, SOX9 and HOXA4) in lung sections of vehicle and Napabucasin-treated mice tail-vein injected with T24 cancer cells. Statistical analysis: a two-tailed, unpaired student’s t-test. Error bar: mean ± SEM. ^*p < 0.05, ^**p < 0.01