Fig 2: Engraftment of iSwGOs functionally repopulated damaged skin. a) Schematic diagram representing the experimental procedure; b) Starch–iodine sweat tests on paw skin of thermal-injured mice showed that only paws of iSwGO-treated mice responded by displaying indigo-black dots at day 21 after transplantation; c) Starch–iodine assessment of newly formed SwGs in the defect regions of thermally injured mice at day 30 after SGM, iSwGC and iSwGO treatment. The number of mice positive for starch-iodine reaction increased in a time-dependent manner. After 30 days treatment with iSwGOs, 34.4 ± 13.0% of the recipient mice (n = 60 per group) exhibited sweat production as compared with those treated with iSwGCs (13.3 ± 10.6%, n = 60), SGM (0, n = 60) and vehicle control (0, n = 60). Data are mean ± SD of 6 independent experiments; d) H&E staining was conducted to visualize SGM-, iSwGC-, iSwGO-treated wounds at day 21 post-injury. Emerging glandular structures were seen in the dermis of iSwGO-treated mice. Dotted line represents the ridges of epidermis where the sweat pores open. Note that the rete ridges in iSwGO-engrafted paw skin were elongated and intertwined with underlying dermal tissues comparable to those derived from normal skin. Scale bar = 100 µm; e) Immunofluorescence and quantification of SwG marker expression in nascent glands at day 21 after iSwGO transplantation (left). EDA-GFP+ cells were seen in the newly generated glandular structures. Newly emerged glands showed typical SwG morphological features and expressed SwG specific markers, for example, ductal markers CK5 and CK10, luminal markers AQP5, CK18, and myoepithelial markers CK5 and a-SMA. Scale bar = 25 µm. Quantification (right) involved > 150 cells from 3 independent experiments, and GFP+ cells within the duct, luminal, and myoepithelial domain were measured, respectively; f) Immunofluorescence of human-specific histone protein expression in nascent SwGs at day 21 after iSwGO transplantation. Scale bar = 25 µm; g) Wound healing curves for quantification of the wound coverage at different times in SGM-, iSwGC-, iSwGO-treated mice (n = 15, 3 independent experiments). Mice treated with DMEM/F-12 were vehicle controls. Data are mean ± SD; * p < 0.05, ** p < 0.01, *** p < 0.001.

Fig 3: Correlation between ULBP1+ cells and PD-L1+ cells in HCC. (A) The expression of ULBP1 in HCC (left). HE staining of tumor and peritumor tissues in HCC (right). (B–D) The proportion of ULBP1+ (B), CK18+ (C) and CD56+ (D) cells in HCC. ULBP1+ and CK18+ cells were more distributed in tumor tissues, while CD56+ cells were more distributed in peritumor tissues. (E) Colocalization ULBP1, CK18 and CD56 in HCC. (F, G) The proportion of ULBP1+CD56+ cells was much less than that of ULBP1+CK18+ cells in tumor tissues (F) or peritumor tissues (G). (H) The proportion of ULBP1+CK18+ cells was significantly higher in tumor tissues than in peritumor tissues. (I) The proportion of CD56+ cells in the low ULBP1 group was lower than that in the high ULBP1 group in tumor tissues, but no significant difference was observed in peritumor tissues. (J) Colocalization of ULBP1, PD-L1, CK18 and CD56 in HCC. (K, L) The proportion of ULBP1+ cells in the low or high PD-L1 group in tumor (K) and peritumor tissues (L). (M, N) The proportion of PD-L1+ cells in the low or high ULBP1 group in tumor (M) and peritumor tissues (N). * p < 0.05, ** p < 0.01 and *** p < 0.001. HE, hematoxylin and eosin.

Fig 4: Expression of CXCL1, CD177 and LCN2 in prostate tissues and correlation with biochemical recurrence free survival in prostate cancer cases. a Representative images (magnification 200X) of CXCL1 (a~c), CD177 (d~f) and LCN2 (g~i) expression in normal prostate tissues, cancerous lesion and para-carcinoma tissue (PCT). Red arrows: tumor foci; yellow arrows: prostate stroma. b Representative images (magnification 200X) of AMACR (red, expressed in carcinoma epithelium), CK18 (white, expressed in prostate glandular epithelium), CXCL1 (cyan) and LCN2 (orange) co-staining in normal prostate tissues, carcinoma tissue and PCT observed by PerkinElmer Tyramide Signal Amplification system. c Semi-quantitative data of CXCL1, LCN2 and CD177 expression in normal prostate (n = 19) and prostate cancer (n = 118) are shown in scatter plots. p value was determined by Mann–Whitney test, asterisks indicate *p < 0.05, ***p < 0.001. d Kaplan-Meier and log-rank test were used to evaluate CXCL1 expression alone (a) or CXCL1-LCN2 co-expression (b) and biochemical recurrence free survival. High expression level of CXCL1 (CXCL1 High vs. Negative expression p < 0.001) and high co-expression of CXCL1-LCN2 (High-High/High-Medium vs. Negative/Low/Medium expression p < 0.0001) predicted early biochemical recurrence after radical prostatectomy

Fig 5: Ovalbumin is able to downregulate a-SMA biosynthesis in MDA-MB-231 cells.Phase contrast microscopy. (A): confluent MCF-7 cells in OV condition (day 7). (B): confluent MDA-MB-231 cells in OV condition (day 7): OV-treated cells did not form acini or duct-like structures in both cell lines. (C) and (D): representative western blot showing the levels of the protein ß-casein in MCF-7 and MDA-MB-231 cells respectively, after 5 days. (E) and (F): representative western blot showing the levels of the proteins E-cadherin, CK18, and a-SMA in MDA-MB-231 cells, after 5 days; a-tubulin was used as a loading control. Ctrl (control), EW (egg white), and OV (ovalbumin).