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首页> 外文期刊>Cell and Tissue Research >PKC inhibition increases gap junction intercellular communication and cell adhesion in human neuroblastoma.
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PKC inhibition increases gap junction intercellular communication and cell adhesion in human neuroblastoma.

机译：PKC抑制增加人类神经母细胞瘤中的间隙连接细胞间通讯和细胞粘附。

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摘要

Gap junction intercellular communication and cell-cell adhesion are essential for maintaining a normal cellular phenotype, including the control of growth and proliferation. Loss of either cell-cell adhesion or communication is common in cancers, while restoration of function is associated with tumor suppression. Protein kinase C (PKC) isozymes regulate a broad spectrum of cellular functions including growth and proliferation, and their overexpression has been correlated with carcinogenesis. Consequently, PKC inhibitors are currently undergoing clinical trials as an anti-cancer agents although the precise cellular alterations induced by PKC inhibitors remain to be elucidated. In the current study, the effects of PKC inhibitors on cell interactions were investigated using human neuroblastoma (IMR32, SKNMC, and SHSY-5Y) cell lines. An analysis of intercellular communication revealed an increase in gap junctional coupling with PKC inhibition. The observed increase in coupling was not associated with a change in Connexin 43 distribution or an alteration of phosphorylation status of the protein. There was also an increase in cell-cell adhesion with PKC inhibitor treatment as indicated by a cell aggregation assay. Therefore, the growth suppressive abilities of PKC inhibition on tumors may be due to the cancer suppressive effects of increased gap junction intercellular communication and cell-cell adhesion.
机译：间隙连接的细胞间通讯和细胞间粘附对于维持正常的细胞表型至关重要，包括控制生长和增殖。细胞间粘附或沟通的丧失在癌症中很常见，而功能的恢复与肿瘤抑制有关。蛋白激酶C（PKC）同工酶调节广泛的细胞功能，包括生长和增殖，并且它们的过表达与致癌作用相关。因此，尽管由PKC抑制剂诱导的确切细胞改变仍有待阐明，但PKC抑制剂目前正在作为抗癌药进行临床试验。在当前的研究中，使用人类神经母细胞瘤（IMR32，SKNMC和SHSY-5Y）细胞系研究了PKC抑制剂对细胞相互作用的影响。细胞间通讯的分析表明，间隙连接偶联与PKC抑制作用增加。观察到的偶联增加与连接蛋白43分布的改变或蛋白质磷酸化状态的改变无关。如细胞聚集测定所表明的，用PKC抑制剂处理的细胞间粘附也增加。因此，PKC抑制肿瘤的生长抑制能力可能归因于间隙连接细胞间通讯增加和细胞间粘附的抑制作用。

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