Introduction
Type/site of the tumor | Comments | Ref |
---|---|---|
Non-small cell lung cancer (NSCLC) | MCs were accumulated in tumors, and both MCT and MCTC were abundant in tumors of patients with extended survival. | [13] |
Hodgkin’s lymphoma | Higher rates of MC infiltration in tumors were related to a worse relapse-free survival of patients. | [14] |
Colorectal cancer | Infiltration of tryptase-positive MCs is an oncogenic event in colorectal cancer with poor prognosis. Tryptase activates PAR-2 receptor which activation promotes the progression of colorectal cancer. | [15] |
Oral squamous cell carcinoma (OSCC) | A significantly higher MC density was observed in lesions compared with control. The presence of MCs in tumors was associated with a better prognosis. | [16] |
Breast cancer | The number of tryptase+ MCs in tumors was significantly higher than that of peritumoral and non-tumoral controls | |
Prostate cancer | Intratumoral MCs were found protective against prostate cancer recurrence. | [10] |
CD117+ MCs showed a denser accumulation in prostate adenocarcinoma (PCa) in comparison with benign prostate tissues that were correlated with the levels of serum prostate-specific antigen (sPSA) and the tumor progression and aggressiveness. | [19] | |
Cutaneous T cell lymphomas (CTCL) | Infiltration and accumulation of MCs were observed in different rates around CTCL. They accumulate mostly in the area immediately around the tumor. | [20] |
Clear-cell renal cell carcinoma (ccRCC) | Infiltrated MC density was negatively correlated with the size of the tumor and reported as a predictor of cancer-specific survival and relapse-free survival in nonmetastatic ccRCC. | [11] |
Gastric cancer (GC) | MC density was increased in well-differentiated GC. | [21] |
Tryptase-positive MCs have a role in angiogenesis in the primary tumor and in LNs of patients with metastatic GC. | [22] | |
Endometrial carcinoma | An increased number of MCs were observed in different stages in which grade III showed the highest MC accumulation. Tryptase-positive MC accumulation was in correlation with angiogenesis and tumor progression. | [23] |
Renal cell carcinoma (RCC) | MC infiltration was correlated with angiogenesis and the progression of tumors | |
Pancreatic cancer | Increased level of MC-released tryptase in plasma and TME correlates with tumor angiogenesis. | [26] |
Thyroid carcinoma | MCD was significantly increased in tumors. Higher rate of MC infiltration was correlated with extrathyroidal extension | [27] |
Renal cancer | An inverse correlation was found between the count of accumulated MCs in the peritumorous region and 5-year postoperative patient survival. MCD had a correlation with the tumor size and angiogenesis within peritumorous zone. | [28] |
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] |
Mediator | Involved stage(s) | Comments | Ref |
---|---|---|---|
Chymase | Angiogenesis Development of tumor | Induces the proliferation of endothelial cells, induces in vitro vascular tube formation, and degrades the matrix of connective tissue to provide space for neovascular development | [24] |
Tryptase | Angiogenesis Tumor cell proliferation Metastasis | Nonclassical proangiogenic mediator Acts in a paracrine manner Tryptase degrades ECM components and activates MMPs Stimulates the proliferation of endothelial cells and promotes the activation of plasminogen activator | [35] [35] [36] [37] |
VEGF | Angiogenesis | Acts as a classical proangiogenic factor | [35] |
Histamine | Tumor cell proliferation Angiogenesis | Promotes the proliferation of tumor cells Promotes angiogenesis by acting on both H1 and H2 receptors | [10] [38] |
TNF-α | Promoting inflammation | Recruits other immune cells including neutrophils to the tumor site | [39] |
MMP9 | Development of tumor | Promotes tumor invasiveness, mobilizes VEGF from ECM, and supports neoangiogenesis Capable of degrading fibronectin and type IV, V, VII, and X collagens | [38] |
MMP-2 | Tissue remodeling Development of tumor | Promotes tissue remodeling during neovascularization Capable of degrading fibronectin and type IV, V, VII, and X collagens | [24] [38] |
Tissue inhibitors of metalloproteinases (TIMPs) | Tissue remodeling | Promote tissue remodeling during neovascularization | [24] |
Nerve growth factor (NGF) | Angiogenesis Development of tumor | Promotes angiogenesis in vivo Induces proliferation of ECs in vitro | [38] |
S1P | Development of tumor | S1P activates NF-κB and links inflammation with cancer Contributes to the accumulation of Tregs and tumor development Regulates the activity and expression of HIF1α, the main regulator of hypoxia in tumor | [42] |