Table 3.
MSCs-based delivery of TRAIL in human tumor cells.
| TRAIL form | Cancer | Main result | Ref |
|---|---|---|---|
| Soluble (s) | Glioblastoma | Paclitaxel priming the of MSCs-TRAIL promoted antitumor functions of their secretome in CFPAC-1 and U87-MG cells (in vitro) | (183) |
| Pancreatic cancer | |||
| Soluble | Neuroblastoma | MSCs-TRAIL-induced apoptosis in neuroblastoma cells (in vitro and in vivo) | (184) |
| Recombinant | NSCLC | MSCs-TRAIL resulted in significant tumor cell inhibition in NSCLC-derived cancer stem cells (in vitro) | (185) |
| Recombinant | Breast | MSCs-TRAIL-induced cell death in a resistant type of breast cancer cells, MCF-7 (in vitro) | (186) |
|
Soluble
Full Length (FL) |
Prostate cancer | MSC-sTRAIL showed more prominent anti-tumor effects than MSC-FL-TRAIL when used combined with AKT inhibitors in LNCaP, C4-2B, and PC3 cells (in vitro) | (187) |
| Recombinant | SCC | MSCs-TRAIL-induced apoptosis in H357 and A549 cells (in vitro) | (188) |
| Lung cancer | |||
| Soluble | Lung cancer | MSCs-TRAIL systemic injection into mice models resulted in a significant reduction in metastatic tumor burden with frequent eradication of metastases | (189) |
| SCC | |||
| Breast cancer | |||
| Cervical cancer | |||
| Soluble | Pancreatic cancer | MSCs-TRAIL and their secretome stimulated apoptosis in PANC1, HP62, ASPC1, TRM6, and BXPC3 cells (in vitro) | (190) |
| Full Length | Esophageal cancer | MSCs-TRAIL supported the inhibition of the proliferation and induced apoptosis in Eca-109 cells (in vitro) | (191) |
| Full Length | Breast cancer | MSCs-TRAIL systemic injection led to the reduced tumor burden in mice models | (192) |
| Full Length | Multiple myeloma | MSCs-TRAIL systemic injection resulted in decreased the tumor burden by specific induction of apoptosis in multiple myeloma cells as showed by caspase-3 activation in mice models | (193) |
| Recombinant | Lung cancer | MSCs-TRAIL systemic injection supported tumor growth inhibition in A549 xenograft mouse model | (194) |
| Soluble | Liver cancer | MSCs-TRAIL secretome led to the apoptosis induction in HepG2 cells (in vitro) | (195) |
| Recombinant | Multiple myeloma | MSCs-TRAIL in combination with bortezomib significantly stimulated myeloma cell apoptosis by caspase-8 activation (in vitro) | (196) |
| Soluble | Liver cancer | MSCs-TRAIL subcutaneous injection inhibited tumor growth and significantly increased survival in mice models mediate by up-regulating caspase 3 activation | (197) |
| Recombinant | NSCLC | MSCs-TRAIL administration caused a reduction in tumor size, tumor weight, and circulating tumor cells in the xenograft model | (198) |
| Recombinant | Glioblastoma | MSCs-TRAIL-induced apoptosis in C6 cells (in vitro) | (199) |
| Recombinant | Glioma | MSCs-TRAIL administration resulted in reduced tumor burden in glioma Fischer 344 rats | (200) |
| Recombinant | Mesothelioma | MSCs-TRAIL supported a reduction in malignant pleural mesothelioma tumor growth by an improvement in tumor cell apoptosis in xenograft models | (201) |
| Soluble | Various tumors | MSCs-FL-TRAIL showed superiority over MSCs-sTRAIL in terms of inducing anti-tumor effects in lung cancer lines, malignant pleural mesothelioma lines, colon cancer lines, renal cancer lines, oral squamous cell carcinoma line, and breast adenocarcinoma line (in vitro) | (202) |
| Full Length | |||
| Full Length | Glioma | MSCs-TRAIL caused potent induction of apoptosis in gliomas cells leading to the reduced tumor burden in xenograft models | (203) |
| Soluble | Glioma | MSCs-TRAIL intratumoral injection supported inhibited tumor growth and prolonged the survival of glioma-bearing mice | (204) |
| Soluble | RCC | Complete regression of metastatic RCC by multiple infusion of MSCs expressing dodecameric TRAIL and HSV-TK into tumor-bearing mice | (205) |
TRAIL, Tumor necrosis factor-related apoptosis-inducing ligand; MSCs, Mesenchymal stem/stromal cells; NSCLC, Non-small cell lung cancer; SCC, Squamous cell carcinoma; RCC, Renal cell carcinoma; HSV-TK, Herpes simplex virus-thymidine kinase.