Table 2.

Role of MCs and their mediators on the biology of cultured tumor cells lines

Cell line of tumor cells	MC mediator, source, or cell line	Brief description	Ref
KMH2 (human Hodgkin’s lymphoma cell line)	BMMCs of C57BL mice	BMMCs could proliferate KMH2 cells.	[30]
OSRC-2 cells (renal cell carcinoma cell line)	HMC-1	Co-culture with human umbilical vein endothelial cell (HUVEC) showed that HMC-1 released mediators contribute OSRC-2-induced HUVEC recruitment and promote the formation of capillary tubes.	[24]
Thyroid cell lines including Nthy-ori-3-1, TPC-1, NIM-1, BCPAP, 8505c, and CAL62	HMC-1 and LAD2	MC-released IL-8 promotes epithelial–mesenchymal transition (EMT) and stemness of cultured thyroid cancer cells through IL-8–Akt–Slug pathway.	[31]
Membranes derived from A549, H1299, SK-LMS-1, and Panc-1	HMC-1	Culturing HMC-1 with membrane fragments of tumor cells could promote phosphorylation of the MAP kinases ERK1/2 in MCs and activated them.	[32]
Lung carcinoma cell lines A549 and H520	MC chymase	Dose-dependent chymase decreased the rate of proliferation of both cell lines after 24 h post treating. It also hampered the A549 cells adhesion ability, downregulated the expression of E-cadherin	[33]
Glioma cell lines U2987MG and U3086MG	LAD2 cells	Conditioned medium obtained from human glioma cells could induce MC activation and release of IL-6, IL-8, VEGF, and TNF-α. “Tumor educated” MCs could reduce the ability of glioma cells to proliferate and migrate and self-renewal capacity through inactivation of the STAT3 signaling pathway.	[34]
Colon cancer cells HT29 and Caco2	Primary human MCs generated from CD34+ peripheral stem cells in the presence of IL-3 and SCF	In transwell migration assay, the colon cancer cells HT29 and Caco2 could recruit MCs by releasing CCL15 or SCF, respectively. MCs supported the proliferation of colon cancer cells by releasing protumorigenic mediators.	[29]