Fig 1: Ridge trace curve of the association between Ln UACR, OC, and the clinical parameters. (A–C) y = Ln UACR as dependent variables in all (A), male (B), and post-menopausal female (C) patients, and x1–x7 = OC, ADPN, P1NP, β-CTx, Ln HbA1c, Ln miR-154-5p, and CTGF as the independent variables, respectively; (D–F) y = OC as dependent variables in all (D), male (E), and post-menopausal female (F) patients, and x1–x7 = Ln UACR, ADPN, P1NP, β-CTx, Ln HbA1c, Ln miR-154-5p, and CTGF as the independent variables, respectively. UACR, urinary albumin excretion rate; HbA1c, glycated hemoglobin A1c; ADPN, adiponectin; P1NP, procollagen type 1 N-terminal propeptide; β-CTx, β-C-terminal telopeptide of type I collagen; CTGF, connective tissue growth factor; OC, osteocalcin.
Fig 2: Scatter dot plots between OC and (A) Ln UACR, (B) Ln HbA1c, (C) ADPN, (D) P1NP, (E) β-CTx, (F) CTGF, (G) Ln miR-154-5p. UACR, urinary albumin excretion rate; HbA1c, glycated hemoglobin A1c; ADPN, adiponectin; P1NP, procollagen type 1 N-terminal propeptide; β-CTx, β-C-terminal telopeptide of type I collagen; CTGF, connective tissue growth factor; OC, osteocalcin.
Fig 3: Scatter dot plots between Ln miR-154-5p and (A) Ln UACR, (B) Ln HbA1c, (C) ADPN, (D) P1NP, (E) β-CTx, (F) CTGF, (G) OC. UACR, urinary albumin excretion rate; HbA1c, glycated hemoglobin A1c; ADPN, adiponectin; P1NP, procollagen type 1 N-terminal propeptide; β-CTx, β-C-terminal telopeptide of type I collagen; CTGF, connective tissue growth factor; OC, osteocalcin.
Fig 4: Scatter dot plots between Ln UACR and (A) Ln miR-154-5p, (B) Ln HbA1c, (C) ADPN, (D) P1NP, (E) β-CTx, (F) CTGF, (G) OC. UACR, urinary albumin excretion rate; HbA1c, glycated hemoglobin A1c; ADPN, adiponectin; P1NP, procollagen type 1 N-terminal propeptide; β-CTx, β-C-terminal telopeptide of type I collagen; CTGF, connective tissue growth factor; OC, osteocalcin.
Fig 5: CL8‐M6P3 blocks communication between malignant cells and CAFs. a,b) Immunofluorescence images of BT549/CAF and MDA‐MB‐231/CAF coculture 3D bioprinting models after CL8‐M6P3 or FG‐3019 treatment. c,d) GSEA showed enriched pathways in breast CAFs after CTGF treatment. e) The heatmap of DEGs related to iCAF and myCAF biomarkers in breast CAFs after CTGF treatment, with or without CL8‐M6P3 (n = 3). f) Cytokines assays of CAFs after treatment as (e). g, h) Correlation analysis of IL‐6 and CTGF, as well as IL‐8 and CTGF, in breast cancers using a public data (http://timer.comp‐genomics.org/timer/). i) IL‐6 and IL‐8 expression levels in breast CAFs after CTGF treatment (n = 3). j) CTGF expression in BT549 after IL‐6 treatment (n = 3). k) A schematic diagram showing CTGF‐mediated cellular crosstalk between TNBC cells and CAFs. l) CTGF knockdown decreased IL‐6 and IL‐8 expression in breast CAFs within co‐culture models (n = 3). m) CL8‐M6P3, and FG‐3019 treatment decreased IL‐6 and IL‐8 expression in CAFs within mono‐culture models (n = 3). The P values were calculated by one‐way ANOVA. For (i,j,l,m), the quantified data from different experiments were presented as the mean ± SD.
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