Table 1 Studies suggesting that MSCs inhibit hematologic malignancy by decreasing tumor cell proliferation in vitro

Mouse BM-MSC

Erythroleukemia (FBL3), ALL (P388), and B-lymphoma (A20)

2 × 10⁴

1:0.4, 1:1, 1:4, 1:10

Induction of cell cycle arrest and apoptosis of tumor cells

Song et al. [22]

Human BM-stromal cell line (HFCL)

AML (U937, HL-60, and HL-60/VCR)

2 × 10⁴

—

Induction of specific gene expression, leading to cell cycle blockage

Liang et al. [32]

Human BM-MSC

CML (BV173 and K562), AML (KG1a), and T-ALL (Jurkat)

5 × 10³

1:1, 1:5, 1:10, 1:100

Transient arrest of tumor cells in G1 phase

Ramasamy et al. [23]

Human BM-MSC

CML (K562 and BV173)

1 × 10⁶

1:10

—

Zhang et al. [54]

Human BM-MSC and CML patient’s BM-MSC

CML (K562 and patient’s cells)

—

1:10

Regulation of apoptosis-related protein expression and activation of the Wnt signaling pathway

Han et al. [71]

Human BM-MSC

CML (BV173) and T-ALL (Jurkat)

1 × 10⁶

1:5, 1:10, 1:50, 1:100

Induction of cell cycle arrest of leukemic cells

Sarmadi et al. [33]

Leukemia patient’s BM-MSC

CML (K562)

1 × 10⁵

1:10

Induction of cell cycle arrest of leukemic cells

Wei et al. [34]

Human UC-MSC

AML (HL-60) and CML (K562)

1 × 10⁴

1:1, 1:5, 1:10

Activation of p38 MAPK and induction of cell cycle arrest of leukemic cells

Tian et al. [35]

Human UC-MSC

CML (K562)

5 × 10³

MSC secretome used

Paracrine signaling by the secretome

Hendijani et al. [72]

Human AT-MSC

AML (HL-60) and CML (K562)

1 × 10⁶

1:10

Secretion of DKK-1 by NANOG

Zhu et al. [74]

Human BM-MSC

CML (patient’s cells)

1 × 10⁴

1:0.1, 1:1, 1:10

Production of IFN-ɑ

Zhang et al. [75]

Human UC-MSC

T-ALL (Jurkat)

2 × 10⁶

1:10

Activation of Notch signaling pathway

Yuan et al. [76]