Voltage-gated sodium channel (Na_v) expression in non-excitable cells has raised questions regarding their non-canonical roles. Interestingly, a growing body of evidence also points towards the prevalence of aberrant Na_v expression in malignant tumors, potentially opening a new therapeutic window. In this study, the transcriptional consequences of channel inhibition were investigated in non-small cell lung carcinoma H460 and neuroblastoma SH-SYSY cell lines, that both express Na_v1.7. Channel activity was blocked by the application of both selective, ProTx-II, and non-selective, tetrodotoxin, inhibitors. Global gene expression profiling did not point to any statistically significant inhibition-associated perturbation of the transcriptome. A small subset of genes that showed relatively consistent changes across multiple treatments were further assayed in the context of a multiplex bead expression array which failed to recapitulate the changes seen in the global array. We conclude that there is no robust transcriptional signature associated with the inhibition of two sodium channel expressing cancer cell lines and consequently sodium channel inhibition will not lend itself to therapeutic approaches such as transcription-based drug repurposing.

电压门控性钠通道（Na _v）在非兴奋性细胞中的表达提出了有关其非规范作用的疑问。有趣的是，越来越多的证据主体还指向朝向异常的Na的患病率_v表达在恶性肿瘤中，潜在地打开一个新的治疗窗。在这项研究中，研究了通道抑制在非小细胞肺癌H460和神经母细胞瘤SH-SYSY细胞系中均表达Na _v1.7。通道活性被选择性ProTx-II和非选择性河豚毒素抑制剂的应用所阻断。全局基因表达谱分析未指出转录组的任何统计学上显着的抑制相关扰动。在多重珠子表达阵列的背景下，进一步分析了在多次处理中显示出相对一致的变化的一小部分基因，但未能概括在整体阵列中看到的变化。我们得出的结论是，没有与抑制两种表达钠通道的癌细胞系相关的强大的转录特征，因此钠通道的抑制作用不会使其自身适用于基于转录的药物再利用等治疗方法。