Extracellular Vesicles as Mediators of Nickel-Induced Cancer Progression.
Extracellular Vesicles as Mediators of Nickel-Induced Cancer Progression.
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细胞外囊泡作为镍诱导的癌症进展的介体。
DOI：
10.3390/ijms232416111
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发表时间：
2022-12-17
影响因子：
5.6
通讯作者：
中科院分区：
文献类型：
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作者：
Emerging evidence suggests that extracellular vesicles (EVs), which represent a crucial mode of intercellular communication, play important roles in cancer progression by transferring oncogenic materials. Nickel (Ni) has been identified as a human group I carcinogen; however, the underlying mechanisms governing Ni-induced carcinogenesis are still being elucidated. Here, we present data demonstrating that Ni exposure generates EVs that contribute to Ni-mediated carcinogenesis and cancer progression. Human bronchial epithelial (BEAS-2B) cells and human embryonic kidney-293 (HEK293) cells were chronically exposed to Ni to generate Ni-treated cells (Ni-6W), Ni-transformed BEAS-2B cells (Ni-3) and Ni-transformed HEK293 cells (HNi-4). The signatures of EVs isolated from Ni-6W, Ni-3, HNi-4, BEAS-2B, and HEK293 were analyzed. Compared to their respective untreated cells, Ni-6W, Ni-3, and HNi-4 released more EVs. This change in EV release coincided with increased transcription of the EV biogenesis markers CD82, CD63, and flotillin-1 (FLOT). Additionally, EVs from Ni-transformed cells had enriched protein and RNA, a phenotype also observed in other studies characterizing EVs from cancer cells. Interestingly, both epithelial cells and human umbilical vein endothelial (HUVEC) cells showed a preference for taking up Ni-altered EVs compared to EVs released from the untreated cells. Moreover, these Ni-altered EVs induced inflammatory responses in both epithelial and endothelial cells and increased the expression of coagulation markers in endothelial cells. Prolonged treatment of Ni-alerted EVs for two weeks induced the epithelial-to-mesenchymal transition (EMT) in BEAS-2B cells. This study is the first to characterize the effect of Ni on EVs and suggests the potential role of EVs in Ni-induced cancer progression.
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影响因子：
13.3
作者：
Huang H;Zhu J;Li Y;Zhang L;Gu J;Xie Q;Jin H;Che X;Li J;Huang C;Chen LC;Lyu J;Gao J;Huang C
通讯作者：
Huang C
DOI：
10.1039/c2mt20074k
发表时间：
2012-08
期刊：
Metallomics : integrated biometal science
影响因子：
--
作者：
Clancy HA;Sun H;Passantino L;Kluz T;Muñoz A;Zavadil J;Costa M
通讯作者：
Costa M
驱动癌症细胞外囊泡分泌的力。
DOI：
10.1016/j.neo.2020.11.011
发表时间：
2021-01
期刊：
Neoplasia (New York, N.Y.)
影响因子：
--
作者：
Bebelman MP;Janssen E;Pegtel DM;Crudden C
通讯作者：
Crudden C
影响因子：
3.7
作者：
Bhattacharya S;Pal K;Sharma AK;Dutta SK;Lau JS;Yan IK;Wang E;Elkhanany A;Alkharfy KM;Sanyal A;Patel TC;Chari ST;Spaller MR;Mukhopadhyay D
通讯作者：
Mukhopadhyay D
影响因子：
3.7
作者：
Hedlund M;Nagaeva O;Kargl D;Baranov V;Mincheva-Nilsson L
通讯作者：
Mincheva-Nilsson L