Extended Data Fig. 3: CAFs promote patient-specific CRC remodeling.
From: Patient-derived mini-colons enable long-term modeling of tumor–microenvironment complexity
a, Brightfield time-course images showing CAF invasion of the stromal hydrogel and CRC-CAF interaction at the CRC mini-colon (patient #MS). The zoomed-in areas are indicated with dashed squares. Scale bar, 200 μm. b, Brightfield and fluorescence composite images of drug responses in CRC mini-colons with and without CAFs treated with SN-38 (patient #NW). Green fluorescence signal indicates cancer cells. Time after drug treatment initiation is indicated on the left. Scale bar, 100 μm. c, Size of tumors in CRC mini-colons treated with SN-38 under the indicated conditions (patient #NW). *P = 0.0486, **P = 0.0097 (two-way ANOVA and Sidak’s multiple comparisons test; n = 3 mini-colons per condition). d, Brightfield and immunofluorescence images of a CAF-induced invasive front in a CRC mini-colon (patient #MS). Magenta and cyan fluorescence signals indicate laminin-5 (laminin-332) and DAPI stainings, respectively. Scale bar, 40 μm. e, Brightfield image showing a 40-day-old CRC mini-colon (patient #MS) co-cultured with autologous CAFs. Scale bar, 100 μm. f, Brightfield images of conventional organoid cultures (patient #MS) in the absence and presence of autologous CAFs. Scale bar, 150 μm. g-i, Quantitation of invasive front reach (g), mini-colon area (h), and epithelium thickness (i) of CRC mini-colons from patient #MS cultured in the absence and presence of autologous CAFs. *P = 0.0251, ***P < 0.0001 (two-way ANOVA and Sidak’s multiple comparisons test; n = 24 invasive fronts (g), 3 mini-colons (h), and 18 inter-crypt epithelium sections (i) for each group). In c, and g-i, data represent mean ± SEM.
