Comparison of produced fish protein hydrolysate from viscera and head of silver carp (Hypophthalmichthys molitrix) using alcalase enzyme and internal tissue enzymes

In the present study, hydrolysed protein of viscera and head of Silver carp (Hypophthalmichthys molitrix) was compared using Alcalase enzyme and internal tissue enzymes at 2 and 4 hours. The result indicated that product by Alcalase (Treatment 1) had significantly higher protein and rate of hydrolysates than that produced by internal tissue enzymes (Treatment 2). So, the highest mean (±SD) protein (68.10±1.33) was related to treatment 1-head (with Alcalase enzyme) after 4 hours and the highest rate of hydrolysates (29.36±1.35) was related to treatment 1-head (with Alcalase enzyme) after 4 hours. The result indicated that rate of hydrolysates raised as time of hydrolysates increased. However the intensity and rate of hydrolysates is reduced. The highest rate of hydrolysates occurred at 120 minutes in the first. This mode was similar for two treatments. The result can be considered as the Alcalase was preferred to internal enzyme

Co-evolution of matrisome and adaptive adhesion dynamics drives ovarian cancer chemoresistance

Due to its dynamic nature, the evolution of cancer cell-extracellular matrix (ECM) crosstalk, critically affecting metastasis and treatment resistance, remains elusive. Our results show that platinum-chemotherapy itself enhances resistance by progressively changing the cancer cell-intrinsic adhesion signaling and cell-surrounding ECM. Examining ovarian high-grade serous carcinoma (HGSC) transcriptome and histology, we describe the fibrotic ECM heterogeneity at primary tumors and distinct metastatic sites, prior and after chemotherapy. Using cell models from systematic ECM screen to collagen-based 2D and 3D cultures, we demonstrate that both specific ECM substrates and stiffness increase resistance to platinum-mediated, apoptosis-inducing DNA damage via FAK and β1 integrin-pMLC-YAP signaling. Among such substrates around metastatic HGSCs, COL6 was upregulated by chemotherapy and enhanced the resistance of relapse, but not treatment-naïve, HGSC organoids. These results identify matrix adhesion as an adaptive response, driving HGSC aggressiveness via co-evolving ECM composition and sensing, suggesting stromal and tumor strategies for ECM pathway targeting. </p