Lactose-functionalized dendrimers arbitrate the interaction of galectin-3/MUC1 mediated cancer cellular aggregation.
Lactose-functionalized dendrimers arbitrate the interaction of galectin-3/MUC1 mediated cancer cellular aggregation.
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乳糖官能化的树枝状聚合物仲裁了半乳糖素3/MUC1介导的癌细胞聚集的相互作用。
DOI：
10.1002/cbic.201402134
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发表时间：
2014-09-22
期刊：
影响因子：
--
通讯作者：
Cloninger MJ
中科院分区：
文献类型：
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作者：
Michel AK;Nangia-Makker P;Raz A;Cloninger MJ
通过使用乳糖官能化的聚（酰胺基胺）树枝状聚合物作为可调的多价平台，我们研究了癌细胞聚集在三个不同的细胞系（A549，DU-145和HT-1080）与半乳糖凝集素-3。我们发现小乳糖官能化的G（2）-树枝状聚合物1抑制半乳糖凝集素-3诱导的癌细胞聚集。相比之下，树枝状聚合物4（具有100个碳水化合物端基的较大的第6代树枝状聚合物）通过半乳糖凝集素-3途径引起癌细胞聚集。该研究表明，细胞聚集的抑制发生，因为1提供了半乳糖凝集素-3的竞争性结合位点（与其推定的癌细胞配体MUC 1上的TF-抗原相比）。相反，树枝状聚合物4为半乳糖凝集素-3结合提供了过量的配体;这导致细胞的交联和聚集增加。
By using lactose-functionalized poly(amidoamine) dendrimers as a tunable multivalent platform, we studied cancer cell aggregation in three different cell lines (A549, DU-145, and HT-1080) with galectin-3. We found that small lactose-functionalized G(2)-dendrimer 1 inhibited galectin-3-induced aggregation of the cancer cells. In contrast, dendrimer 4 (a larger, generation 6 dendrimer with 100 carbohydrate end groups) caused cancer cells to aggregate through a galectin-3 pathway. This study indicates that inhibition of cellular aggregation occurred because 1 provided competitive binding sites for galectin-3 (compared to its putative cancer cell ligand, TF-antigen on MUC1). Dendrimer 4, in contrast, provided an excess of ligands for galectin-3 binding; this caused crosslinking and aggregation of cells to be increased.