Table 4.
The role of CA-MSCs in increasing tumor metastasis by different mechanisms.
| MSCs source | Cancer type | Result | Molecular Mechanism | Reference |
|---|---|---|---|---|
| Human BM-MSCs | Breast cancer cells | Activate metastasis | By upregulating lysyl oxidase production | (181) |
| BM-MSCs | Breast cancer cells and mice | MSC facilitates breast cancer cells’ entry into bone marrow | Through Tac1-mediated regulation SDF-1α)/CXCR4 axis | (160) |
| BM-MSCs | Prostate cancer | Enhance prostate cancer cells’ metastatic capability and cancer stem cell population | Through secreting CCL5 to inhibit androgen receptor signaling | (169) |
| Human BM-MSCs | Human carcinoma cell lines and nude mice | Promote stem cell–like phenotype in carcinoma cells | PGE2 and IL-1 induce the production of IL-8 and IL-6 by MSCs | (25) |
| VEGFR1-positive hematopoietic bone marrow progenitors | Melanoma cells and lung carcinoma cells | Prepare an appropriate environment for colonization of circulating cancer cells |
By Expressing VEGFR and with the contribution of CXCL12 and fibronectin | (193) |
| Human BM-MSCs | Hepatocellular carcinoma | Induces tumor growth and metastasis | Via MAPK pathway and enhancing the expression of TNF-α, IL-6, and integrin α5 | (173) |
| Human BM-MSCs | Breast cancer cells | Activate metastasis | By stimulating the hypoxia-inducible factors (HIFs) | (207) |
| Human adipose stromal cells | Breast cancer cells | Enhance migration and invasion | By producing IL-6 | (208) |
| Human BM-MSCs | Breast carcinoma spheroids | Increase metastasis | with degradation of E-cadherin via activating ADAM10 | (188) |
| MSC derived from different human tissues | Glioblastoma | Elevate the migratory and invasive potency of glioblastoma cells | By producing TGF-β1 | (174) |