Abstract
BackgroundCancer cells release exosomes and can be taken up by mast cells (MCs), but the potential functional effects of MCs on tumor metastasis remain unknown.MethodExosomes were isolated from the lung adenocarcinoma cell line A549, and the uptake of PKH26-labeled exosomes by bone marrow MCs was examined via flow cytometry and fluorescence microscopy. Cytokines and tryptase in MC supernatant were analyzed using an ELISA kit, and the presence of tryptase was evaluated by Western blotting. Cell proliferation and migration were determined through CCK-8 and transwell assays. Proteins in the tryptase-JAK-STAT signaling pathway were detected by Western blotting.ResultsIn this study, we show that exosomes from A549 cells can be taken up by MCs. Moreover, A549 exosomes contain stem cell factor (SCF) to MCs and subsequently induce the activation of MCs through SCF-KIT signal transduction, which leads to MC degranulation and the release of tryptase. Tryptase accelerates the proliferation and migration of human umbilical vein endothelial cells (HUVECs) through the JAK-STAT signaling pathway.ConclusionsOur results reveal a mechanism for metastasis in which exosomes can transfer SCF to and activate MCs, which can affect the release of tryptase and the angiogenesis of HUVECs.
Highlights
Cancer cells release exosomes and can be taken up by mast cells (MCs), but the potential functional effects of MCs on tumor metastasis remain unknown
Our results reveal a mechanism for metastasis in which exosomes can transfer stem cell factor (SCF) to and activate MCs, which can affect the release of tryptase and the angiogenesis of human umbilical vein endothelial cells (HUVECs)
Highlights Exosomes derived from lung cancer cells possess SCF for binding to mast cells via KIT
Summary
Cancer cells release exosomes and can be taken up by mast cells (MCs), but the potential functional effects of MCs on tumor metastasis remain unknown. Metastasis is the leading cause of lung cancer-related deaths. Angiogenesis or vascular permeability is a characteristic of the premetastatic niche that enables tumor cell colonization and promotes metastasis. Organs of future metastasis are selectively and actively modified by the primary tumor before metastatic spread [1]. Sowing the ‘seeds’ of metastasis requires tumor-shed exosomes that enable the ‘soil’ at distant metastases promote the capture and growth of circulating tumor cells [1]. Pancreatic ductal adenocarcinomaderived exosomes initiate premetastatic niche formation in the liver [3]. Tumor-conditioned lymphatic endothelial cells promote angiogenesis in these organs for breast cancer metastasis [4]
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