Fig 2: The correlation between ovarian tissue stiffness and clinical characteristics. (A) Shore hardness values for normal, benign, and malignant ovarian tissues. (B) Violin plots showing HGSOC tissues hardness compared to both benign ovarian disease and normal tissues. (C) The correlation between serum HE4 levels and ovarian tissue stiffness in EOC (n = 70). (D) The correlation between serum HE4 levels and tissue stiffness in HGSOC patients (n = 46). **p < 0.01, ***p < 0.001, ****p < 0.0001, ns = not significant

Fig 3: Fibroblast activation and collagen deposition were inhibited in vivo. (A) Representative images of tumors excised from mice injected with Normal Control (NC) or sh-HE4 OVCAR3 cells (n = 5/group). (B) Tumor volume was measured over 21 days, tumors in the HE4 knockdown groups grew significantly slower compared to the control group. (C) Tumor weight at the endpoint. Tumors in the HE4 knockdown groups were significantly lighter than those in the control group. (D) Representative IHC staining of HE4 and quantification of HE4-positive areas in NC and HE4 knockdown groups (n = 5/group). (E) Representative IHC staining of and quantification of fibroblast activation markers and Collagen I positive areas (n = 5/group). *p < 0.05, **p < 0.01, ****p < 0.0001

Fig 4: Expression of HE4 levels, fibroblast activation markers and collagen in high vs. low stiffness groups. (A) Serum HE4 levels in the high stiffness group and low stiffness group (n = 11/group). (B) The protein levels of HE4 in different stiffness groups were assayed by Western blot (n = 11/group). (C) Representative IHC staining of HE4 of cancer cell in high and low groups (n = 11/group), Scale bars, 50 μm/20 μm. (D) Western blot results show that the expression of fibroblast activation marker α-SMA (n = 11/group). (E) Immunohistochemistry results demonstrate fibroblast activation markers and Collagen I of mesenchymal areas in high and low groups (n = 11/group), Scale bars, 50 μm/20 μm. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001