|Tissue/organ- derived||Normal||Lung||Lung cancer A549, H460, H1299 cells||-Developed pattern of growth similar with original human lung cancer.|||
|Breast cancer MDA-MB-231 and MCF-7 cells||-MDA-MB-231 cells undergone EMT can proliferation.|
-MCF-7 cells not undergone EMT died by apoptosis.
|Adipose tissue||Breast cancer MCF-7, BT474, SKBR3 cells||-Proliferation, underwent EMT, and increased invasion. -Increased chemoresistance via Akt.|||
|Liver||Hepatocellular carcinoma, HCCLM3 cells||-Increased uPA production and MMP-2 activity.|
-Decreased PAI-1 production.
|Hepatocellular carcinoma, HepG2 cells||-Increased expression of genes relating to hepatic functions.|||
|Liver and lung||Colorectal cancer HT-29, Caco2 and SW480 cells||-Exhibited morphology and gene expression pattern similar with metastatic sites of colorectal cancer.|
-The cells educated by dECM acquire metastatic ability.
|Cancer||Mammary grand||Breast cancer MCF-7 cells||-Underwent EMT, increased stem cell marker expression and chemoresistance.|||
|Glioblastoma||Isolated glioblastoma cells||-Increased invasive ability via HAS gene expression.|||
|A549-derived lung cancer||Breast cancer MCF-7 cells||-Cell proliferation.|
-Increased IL-8, bFGF, and VEGF production.
|Normal and cancer||Colon||Colorectal cancer SW620, SW480, HCT116 cells, normal lung fibroblasts, endothelial colony forming cells||-Increased angiogenesis and cancer cell proliferation in cancer tissue-derived dECM.|||
|Isolated monocytes||-Promoted monocyte differentiation and CCL18 production to accelerate cancer cell invasion.|||
|Colorectal cancer HT-29 cells||-Increased IL-8 production in cancer tissue-derived dECM.|||
|Breast||Breast cancer MCF-7 cells||-Suppressed proliferation, EMT and angiogenic gene expression and increased apoptosis in normal tissue-derived dECM.|
-Promoted MMP-9 production, proliferation, EMT, and angiogenic gene expression and suppressed apoptosis in cancer tissue-derived dECM.
|Lung and liver||Breast cancer LM2-4 and 4T1 cells||-Promoted cell adhesion and colonization in cancer tissue-derived dECM.|||
|Normal and fibrosis||Liver||Hepatocellular carcinoma HLF and HuH7 cells||-Promoted proliferation.|
-Promoted EMT via integrin-FAK signaling.
|Cultured-cell-derived||Cancer||Tongue (Oral carcinoma HN12 cells)||Oral carcinoma HN12 cells||-Increased chemoresistance via talin, FAK, and NF-κB-mediated signals||[71,72]|
|Normal||Fibroblasts (NIH-3T3)||Various cancer and benign cells (HCT116, NCI-H460, PA-1, COLO 205, PANC-1, MCF-7, SW620, HCT116/p53-, HS 578T, PA1/E6, MCF-10A||-Increased chemoresistance via integrin β1-dependent survival signal.|||
|Normal and cancer||Fibroblasts (NIH-3T3 cells and cancer associated fibroblasts)||Breast cancer MDA-MB-231, MCF-7, and MCF-10A cells||-Activated PI3K-Akt signaling via integrin β1.|
-Changed morphology and cell migration behaviors
|Benign tumor and cancer||Breast (MDA-MB-231, MCF-7, and MCF-10A cells)||Breast cancer MDA-MB-231, MCF-7, and MCF-10A cells||-Promoted proliferation on invasive MDA-MB-231 cell-derived dECM.|
-Suppressed proliferation on benign MCF-10A cell-derived dECM.
-Increased chemoresistance on invasive MDA-MB-231 cell-derived dECM.
|Normal and cancer||Colon (HT-29, SW480, CCD-841-CoN cells)||Colon cancer HT-29 and SW480 cells||-Increased chemoresistance on invasive HT-29 cell-derived dECM via Akt activation and ABCB1 upregulation.|
-Promoted EMT on invasive HT-29 cell-derived dECM via TGF-β signaling.