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J. Zhang, G. Li, Z. Li, X. Yu, Y. Zheng, K. Jin, H. Wang, Y. Gong, X. Sun, X. Teng, J. Cao and L. Teng, “Estrogen-Independent Effects of ER-a36 in ER-Negative Breast Cancer,” Steroids, Vol. 77, No. 6, 2012, pp. 666-673. doi:10.1016/j.steroids.2012.02.013

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• TITLE: Estrogen Receptor Alpha 36 Gene Knockdown Promote the Expression of NF-κB in PC12 Cells

  AUTHORS: Ping Zou, Chao Qu, Yihui Xu, Hongyan Li, Dannv Han, Dan Shi, Wei Zou

  KEYWORDS: NF-κB; Estrogen Receptor Alpha 36; PC12 Cells

  JOURNAL NAME: Open Journal of Endocrine and Metabolic Diseases, Vol.3 No.4B, August 6, 2013

  ABSTRACT: The nuclear transcription factors κB (NF-κB) is widely existing in various kinds of cell types in the nervous system and plays an important role in neuron apoptosis and neurodegenerative diseases. Estrogen receptor alpha 36 (ER-α36), is a novel variant of ERα (as known ER-α66) which can transduce both estrogenand antiestrogen-dependent activation of MAPK signal pathway and stimulate cell growth. Here, we aimed to detect the effect of ER-α36 gene silencing on the expression of NF-κB in normal cultured PC12 cells and to provide an experimental foundation for understanding the function of ER-α36 innerve cells. PC12 cells with ER-α36 expression knocked down by the shRNA method. Then Western blot and immunocytochemical staining were performed to detect the expression and translocation of NF-κB after transfection. The results showed that NF-κB expression was significantly higher comparing with the control group after transfection (P 0.01). Also, NF-κB subunit entered nuclear after transfection; Immunofluorescence staining and immunocytochemical staining of PC12 cells demonstrated that ER-α36 was expressed mainly on the plasma membrane and on the cell nucleus membrane. These data indicate that ER-α36 gene silencing can increase the expression of NF-κB and promote its nuclear translocation in PC12 cells.