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ALCAM/CD166 参与了癌细胞来源的细胞外囊泡的结合和摄取。

ALCAM/CD166 Is Involved in the Binding and Uptake of Cancer-Derived Extracellular Vesicles.

机构信息

Centre for Molecular Biology "Severo Ochoa" (CSIC-UAM), Cell-Cell Communication & Inflammation Unit, 28049 Madrid, Spain.

Department of Molecular Biology, Faculty of Sciences, Instituto Universitario de Biología Molecular, Universidad Autónoma de Madrid, 28049 Madrid, Spain.

出版信息

Int J Mol Sci. 2022 May 20;23(10):5753. doi: 10.3390/ijms23105753.

DOI:10.3390/ijms23105753
PMID:35628559
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9143639/
Abstract

Colorectal cancer (CRC) and ovarian cancer (OvC) patients frequently develop peritoneal metastasis, a condition associated with a very poor prognosis. In these cancers, tumor-derived extracellular vesicles (EVs) cause immunosuppression, facilitate the direct attachment and invasion of cancer cells through the mesothelium, induce the conversion of peritoneal mesothelial cells (PMCs) into cancer-associated fibroblasts (CAFs) and transfer a more aggressive phenotype amongst cancer cells. Although the promoting role of EVs in CRC and OvC peritoneal metastasis is well established, the specific molecules that mediate the interactions between tumor-derived EVs and immune and non-immune target cells remain elusive. Here, we employed the SKOV-3 (ovarian adenocarcinoma) and Colo-320 (colorectal adenocarcinoma) human cell lines as model systems to study the interactions and uptake of EVs produced by ovarian carcinoma and colorectal carcinoma cells, respectively. We established that the adhesion molecule ALCAM/CD166 is involved in the interaction of cancer-derived EVs with recipient cancer cells (a process termed "EV binding" or "EV docking") and in their subsequent uptake by these cells. The identification of ALCAM/CD166 as a molecule mediating the docking and uptake of CRC and OvC-derived EVs may be potentially exploited to block the peritoneal metastasis cascade promoted by EVs in CRC and OvC patients.

摘要

结直肠癌（CRC）和卵巢癌（OvC）患者经常发生腹膜转移，这种情况预后极差。在这些癌症中，肿瘤来源的细胞外囊泡（EVs）引起免疫抑制，促进癌细胞通过间皮的直接附着和侵袭，诱导腹膜间皮细胞（PMCs）向癌相关成纤维细胞（CAFs）转化，并在癌细胞之间转移更具侵袭性的表型。尽管 EVs 在 CRC 和 OvC 腹膜转移中的促进作用已得到充分证实，但介导肿瘤来源的 EVs 与免疫和非免疫靶细胞之间相互作用的特定分子仍不清楚。在这里，我们使用 SKOV-3（卵巢腺癌）和 Colo-320（结直肠腺癌）人细胞系作为模型系统，分别研究卵巢癌和结直肠癌细胞产生的 EVs 的相互作用和摄取。我们确定粘附分子 ALCAM/CD166 参与了癌细胞来源的 EVs 与受体癌细胞的相互作用（称为“EV 结合”或“EV 对接”），以及随后这些细胞对它们的摄取。ALCAM/CD166 作为一种介导 CRC 和 OvC 来源的 EVs 对接和摄取的分子的鉴定，可能被潜在地利用来阻断 CRC 和 OvC 患者中由 EVs 促进的腹膜转移级联反应。

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