Basic helix-loop-helix transcription factors DEC1 and DEC2 regulate the paclitaxel-induced apoptotic pathway of MCF-7 human breast cancer cells
Basic helix-loop-helix transcription factors DEC1 and DEC2 regulate the paclitaxel-induced apoptotic pathway of MCF-7 human breast cancer cells
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DOI：
10.3892/ijmm.2011.617
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发表时间：
2011-04-01
影响因子：
5.4
通讯作者：
Kijima, Hiroshi
中科院分区：
文献类型：
--
作者：
Wu, Yunyan;Sato, Fuyuki;Kijima, Hiroshi
分化胚胎软骨细胞基因 (DEC) 1 (BHLHE40/Stra13/Sharp2) 和 DEC2 (BHLHE41/Sharp1) 是基本螺旋-环-螺旋 (bHLH) 转录因子，与细胞凋亡、细胞增殖和昼夜节律以及各种癌症中的恶性肿瘤的调节相关。然而，人们对 DEC1 和 DEC2 表达在乳腺癌中的作用知之甚少。在这项研究中，我们试图检查 DEC1 和 DEC2 在紫杉醇治疗的 MCF-7 人乳腺癌细胞中的作用。紫杉醇处理的 MCF-7 细胞中 DEC1 和 DEC2 的表达上调。在紫杉醇治疗后，通过 siRNA 敲低 DEC1 会减少裂解的聚 (ADP-核糖) 聚合酶 (PARP) 的量，而在存在和不存在紫杉醇的情况下，敲低 DEC2 会增加裂解的 PARP 的量。免疫荧光染色显示，紫杉醇处理增加了细胞核中DEC1的含量，并增加了细胞核和细胞质中DEC2的含量。这些结果表明，在人乳腺癌MCF-7细胞中，DEC1具有促凋亡作用，而DEC2对紫杉醇诱导的细胞凋亡具有抗凋亡作用。
Differentiated embryonic chondrocyte gene (DEC) 1 (BHLHE40/Stra13/Sharp2) and DEC2 (BHLHE41/Sharp1) are basic helix-loop-helix (bHLH) transcription factors that are associated with the regulation of apoptosis, cell proliferation and circadian rhythms, as well as malignancy in various cancers. However, the roles of DEC1 and DEC2 expression in breast cancer are poorly understood. In this study, we sought to examine the roles of DEC1 and DEC2 in MCF-7 human breast cancer cells that had been treated with paclitaxel. The expression of DEC1 and DEC2 was up-regulated in paclitaxel-treated MCF-7 cells. Knockdown of DEC1 by siRNA decreased the amount of cleaved poly (ADP-ribose) polymerase (PARP), after treatment with paclitaxel, whereas DEC2 knockdown increased the amount of cleaved PARP in both the presence and absence of paclitaxel. Immunofluorescent staining revealed that paclitaxel treatment increased the amount of DEC1 in the nucleus, and increased the amount of DEC2 in both the nucleus and cytoplasm. These results indicate that DEC1 has pro-apoptotic effects, whereas DEC2 has anti-apoptotic effects on the paclitaxel-induced apoptosis in human breast cancer MCF-7 cells.