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首页> 外文期刊>Journal of biochemical and molecular toxicology >SP3 is associated with migration, invasion, and Akt/PKB signalling in MDA-MB-231 breast cancer cells
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SP3 is associated with migration, invasion, and Akt/PKB signalling in MDA-MB-231 breast cancer cells

机译：SP3与MDA-MB-231乳腺癌细胞中的迁移，侵袭和AKT / PKB信号相关联

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摘要

Specificity proteins (SPs) have pro-oncogenic functions in cancer cells, ranging from cancer cell proliferation, migration, invasion, and angiogenesis. There is strong evidence that several antineoplastic drugs target depletion of SP proteins via different pathways. However, the mode of action of SP3 and the underlying consequences of its depletion are not well understood. Here, we demonstrate that SP3 is over-expressed in invasive breast cancer cells vs normal counterparts. The gene expression analysis from The Cancer Genome Atlas datasets indicated that SP3 is strongly correlated with Akt signalling-related proteins, G protein subunit alpha 13, and RAB33B (RAB33B, member RAS oncogene family). RNA interference of SP3 decreased active phosphorylation of Akt at serine and threonine sites. These findings indicate that SP3 exhibits a pro-oncogenic function, which clearly fits the description of an nononcogene addiction gene. Future analyses are prompted to uncover the SP3 gene regulation function and to reveal downstream targets of SP3 in breast cancer.
机译：特异性蛋白（SPs）在癌细胞中具有促癌功能，包括癌细胞增殖、迁移、侵袭和血管生成。有强有力的证据表明，几种抗肿瘤药物通过不同途径靶向SP蛋白的耗竭。然而，SP3的作用方式及其耗竭的潜在后果尚不清楚。在这里，我们证明了SP3在浸润性乳腺癌细胞和正常乳腺癌细胞中过度表达。来自癌症基因组图谱数据集的基因表达分析表明，SP3与Akt信号相关蛋白、G蛋白亚单位α13和RAB33B（RAB33B，RAS癌基因家族成员）密切相关。SP3的RNA干扰降低了丝氨酸和苏氨酸部位Akt的活性磷酸化。这些发现表明SP3具有促癌功能，这显然符合非癌基因成瘾基因的描述。未来的分析将揭示SP3基因的调节功能，并揭示SP3在乳腺癌中的下游靶点。

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