Ahani Elnaz, Fereydouni Mohammad, Motaghed Mona, Kepley Christopher L
Department of Nanoengineering, Joint School of Nanoscience and Nanoengineering, North Carolina Agricultural and Technical State University, Greensboro, NC 27401, USA.
Department of Nanoscience, Joint School of Nanoscience and Nanoengineering, University of North Carolina at Greensboro, Greensboro, NC 27401, USA.
Cancers (Basel). 2022 Jun 14;14(12):2944. doi: 10.3390/cancers14122944.
Mast cells (MCs) are found in practically all tissues where they participate in innate and adaptive immune responses. They are also found in and around tumors, yet their interactions with cancer cells and the resulting impact on cancer cell growth and metastasis are not well understood. In this study, we examined a novel mechanism of IgE-FcεRI-mediated, intercellular communication between human adipose-derived mast cells (ADMC) and cancer cells. The formation of heterotypic tunneling nanotubes (TnT) and membrane structures between MCs and tumor cells in vitro was examined using microscopy and a diverse array of molecule-specific indicator dyes. We show that several MC-specific structures are dependent on the specific interactions between human tumor IgE-sensitized MCs and antigens on the tumor cell surface. The formation of TnT, membrane blebs and other MC-specific structures paralleled FcεRI-degranulation occurring within 30 min and persisting for up to 24 h. The TnT-specific adhesion of FcεRI-activated MCs to tumor cells was characterized by the transport of the MC granule content into the tumor cells, including tryptase and TNF-α. This interaction led to apoptosis of the tumor cells, which differs from previous studies examining tissue cells within the cancer microenvironment. The formation of heterotypic TnT results in stimulation of an invasive tumor cell phenotype and increased tumor cell invasion and chemoresistance of the cancer cells. These studies describe a heretofore-unrecognized mechanism underlying IgE-mediated interactions and FcεRI-activated MC-mediated killing of tumor cells through the formation of TnT.
肥大细胞(MCs)几乎存在于所有参与固有免疫和适应性免疫反应的组织中。在肿瘤内部及其周围也能发现它们,然而它们与癌细胞的相互作用以及对癌细胞生长和转移的影响尚未完全明确。在本研究中,我们探究了一种由IgE-FcεRI介导的、人脂肪源性肥大细胞(ADMC)与癌细胞之间的新型细胞间通讯机制。利用显微镜和一系列分子特异性指示染料,检测了体外MCs与肿瘤细胞之间异型隧道纳米管(TnT)和膜结构的形成。我们发现,几种MC特异性结构依赖于人类肿瘤IgE致敏的MCs与肿瘤细胞表面抗原之间的特异性相互作用。TnT、膜泡及其他MC特异性结构的形成与30分钟内发生并持续长达24小时的FcεRI脱颗粒平行。FcεRI激活的MCs与肿瘤细胞的TnT特异性黏附表现为MC颗粒内容物向肿瘤细胞的转运,包括组织蛋白酶和肿瘤坏死因子-α。这种相互作用导致肿瘤细胞凋亡,这与之前研究癌症微环境中组织细胞的结果不同。异型TnT的形成导致侵袭性肿瘤细胞表型的刺激以及癌细胞侵袭和化疗耐药性的增加。这些研究描述了一种迄今为止未被认识的机制,该机制是IgE介导的相互作用以及FcεRI激活的MCs通过形成TnT介导肿瘤细胞杀伤的基础。