Table 3 Studies suggesting that MSCs aggravate hematologic malignancy by suppressing tumor cell apoptosis in vitro

From: Mesenchymal stem cells in suppression or progression of hematologic malignancy: current status and challenges

Isolated MSC

Tumor cell

Tumor cell no. (cells)

MSC:tumor cell ratio

Proposed mechanism

Reference

Human BM-MSC

B-ALL (patient’s cells)

1 × 106

—

Secretion of soluble factors by MSCs

Manabe et al. [103]

Human BM-MSC

CLL (patient’s cells)

4 × 105, 2 × 106

—

Cell-to-cell contact of tumor cells with MSCs

Panayiotidis et al. [104]

Human BM-MSC

B-CLL (patient’s cells)

2 × 106

—

Increased Bcl-2 expression by direct contact between leukemic cells and stromal cells

Lagneaux et al. [105]

Human BM-MSC

B-ALL (patient’s cells)

1 × 105

1:10

Activation of Notch-3 and -4 signaling when tumor cells are in contact with MSCs

Nwabo Kamdje et al. [106]

Human stromal cell line (HS-5)

AML (patient’s cells)

4–6 × 105

1:4~1:6

Direct cell-to-cell interactions regulating antiapoptotic effects, not including Bcl-2

Garrido et al. [107]

Mouse stromal cell line (MS-5)

AML (HL-60 and patient’s cells)

5 × 105

—

Increased Bcl-2 expression

Konopleva et al. [108]

Human BM-MSC

BCP-ALL (patient’s cells)

—

—

Secretion of PGE2 from MSCs

Naderi et al. [109]

Leukemia patient’s BM-MSC

CML (K562)

1 × 105

1:10

Activation of the PI3K-Akt-Bad pathway

Wei et al. [34]

Human UC-MSC

T-ALL (Jurkat)

2 × 106

1:10

Activation of the Notch signaling pathway

Yuan et al. [76]

Human BM-MSC

CML (BV173)

1 × 106

1:10

Transient cell cycle arrest conferring increased leukemic cell survival by preserving their proliferative ability

Ramasamy et al. [23]

  1. MSC mesenchymal stem cell, BM bone marrow, AML acute myeloid leukemia, CML chronic myeloid leukemia, UM umbilical cord, T-ALL T cell acute lymphoblastic leukemia, CLL chronic lymphocytic leukemia, PI3K phosphoinositide 3-kinase, PGE2 prostaglandin E2