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Table 2 Anti-tumor effects of MSCs on the biology of different types of tumors

From: Importance of the origin of mesenchymal (stem) stromal cells in cancer biology: “alliance” or “war” in intercellular signals

MSC source

Product administrated

Tumor type

Type of study

Outcome effect

References

Bone marrow

Cells

HepG2 and Huh7 hepatocarcinoma cell

In vitro

In vivo

Inhibition of cancer cell proliferation/inhibition of AKT/FOCO3a pathway

[18]

Primary human glioma cells, HUVEC endothelial cells

In vitro

Reduction in tumor volume and vascular density/reduced expression of platelet-derived growth factor (PDGF)-BB and interleukin (IL)-1β

[19]

Colorectal cancer cells

In vivo

Administration of MSCs increase the life span of carcinogen-exposed rats by attenuating both colorectal cancer initiation and progression, mediated polarization of resident immune cells which in turn interferes with tumor growth. After fractionated irradiation, MSCs inhibited residual tumor growth, protected healthy tissue and prolonged animal survival

[9]

Conditioned medium

MDA-MB-231 breast cancer cells

In vivo

Suppressed tumor growth and lung metastasis. Reduced proliferative activity of cancer cells

[20]

Non-small-cell lung carcinoma cells

In vitro

Inhibition of cell proliferation, viability and migration. Downregulation of mitogen-activated protein kinase (MAPK) signaling pathway

[21]

Extracellular vesicles

Liver Carcinoma

Kaposi’s sarcoma

Ovarian tumour cell lines

In vitro

Inhibit proliferation and promote apoptosis

[22]

Adipose tissue

Exosomes

A2780 and SKOV-3 ovarian cancer cells

In vitro

Inhibed proliferation of ovarian cancer cells. Upregulates proapoptotic molecules, induced apoptosis signalling by upregulating different pro-apoptotic signalling molecules (BAX, CASP9, and CASP3), as well as downregulating the anti-apoptotic protein BCL2. Sequencing of exosomal RNAs revealed a rich population of microRNAs (miRNAs), which exhibit anti-cancer activities by targeting different molecules associated with cancer survival, blocking the cell cycle, and activating mitochondria-mediated apoptosis signalling

[23]

Adipose tissue

Cells

U87MG or GSC1 cells

Glioblastoma cells

In vitro

In vivo

AD-hMSCs showed remarkable tropism towards the tumor, reduction in tumor growth, tumor cell proliferation, and microvascular density

[24]

Conditioned medium

PC3M-luc2 prostate cancer cells

In vitro

In vivo

Inhibit proliferation and promote apoptosis. Reduced the expression of caspase 3/7 with increased antiapoptotic protein, BclxL; effects at least mediated by miR-145 form exosomes released from ASC

[25]

Extracellular vesicles

Prostate cancer

Ovarian cancer

Glioblastoma

In vivo

In vitro

In vivo

Inhibit proliferation and promote apoptosis

[23,24,25]

Endometrial tissue

Cells

Ovarian cancer cell lines (SKOV3 cells and HO-8910 cells)

In vitro

In vivo

Attenuate tumor growth. Induce cell cycle arrest, promote apoptosis, disturb mitochondrial membrane potential and decreasing pro-angiogenic ability

[26]

Uterine cervical tissue

Conditioned medium

MCF-7 and MDA-MB-231 breast cancer cells

In vitro

In vivo

Induce cell cycle arrest, promote apoptosis, inhibited proliferation of cancer associated fibroblasts, inhibited macrophage activation, inhibit tumor cell invasion

[27]

Amniotic fluid

Cells

SKOV3 ovarian cancer cells

In vitro

Cytotoxic effect on SKOV3 and suppressed their proliferation; induction of internal and external pathways of apoptosis. Release soluble factors which cause an efficient anticancer effect; induction of its anticancer effects by stimulating the caspase cascade (caspase 3 and 8) and apoptosis. Activation of genes responsible for apoptosis (P53 and P21)

[28]

Placental chorionic villi

Cells

MDA-MB-231 breast cancer cells

In vitro

Reduce the proliferative and migratory capacity of tumor cells, inhibited the endothelial cell-associated vasculogenic capacity

[29]

Umbilical cord

Cells

Line MDA-MB-231 human breast cancer cells

In vivo

Antitumor effect. Inhibited tumor angiogenesis and induced cell apoptosis

[30]

Liver cancer cell lines HepG2 and SK-Hep-1

In vitro

In vivo

Reducing hepatoma cell growth and metastasis. Downregulation of Wnt/β-catenin signaling pathway

[31]

High-grade human glioma cell lines (SNB19 and U251) and xenograft cell lines (4910 and 5310)

In vitro

In vivo

Inhibited tumor growth. Upregulation of PTEN gene phosphatase and tensin homolog deleted on chromosome 10 (PTEN) in tumors induced cellular death through decreasing XIAP expression

[32]

Conditioned medium

MCF-7 tumor cells

In vitro

Cytotoxic effects on MCF-7 cells by induction of apoptosis

[33]

Ovarian cancer cell lines (OVCAR3 and SKOV3)

In vitro

Reduction in size of tumor spheres. Increase in the sub-G1 and G2M phases of cell cycle, inhibition of cell migration, activated caspase; decreased expression of cell cycle regulatory genes (cyclin A2, Cyclin E1), prostaglandin receptor signaling genes (EP2, EP4) and the pro-inflammatory genes (IL-6, TNF-α); cycle arrest, apoptosis

[34]

MG-63 and SKES-1 osteosarcoma cell lines

In vitro

In vivo

Decreased tumor sizes/Inhibition of mammary carcinoma and osteosarcoma cells via apoptosis and autophagy

[35]

HeLa cells

In vitro

Reduced cell viability and increased apoptosis. Increased caspase-3/7 activity, decreased mitochondrial membrane potential, and induced cell cycle arrest

[36]

MDA-MB-231 breast cancer cells

In vitro

In vivo

Suppresses breast cancer cells growth and sensitizes cancer cells to radiotherapy. Inhibition of the Stat3 signaling pathway

[37]