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 ...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.展开更多
目的：测定雌激素受体α36（ERα36）在甲状腺乳头状癌（PTC）原发灶中的表达,探讨其临床意义.方法：免疫组织化学显色检测ERα36和ERα66在PTC组织中的表达.结果：PTC组织中,ERα36和ERα66均特异性表达于肿瘤细胞,ERα36表达水平高于E...目的：测定雌激素受体α36（ERα36）在甲状腺乳头状癌（PTC）原发灶中的表达,探讨其临床意义.方法：免疫组织化学显色检测ERα36和ERα66在PTC组织中的表达.结果：PTC组织中,ERα36和ERα66均特异性表达于肿瘤细胞,ERα36表达水平高于ERα66（67.6％vs 20.6％）;45岁以上患者ERα36阳性率高于45岁以下患者（95.2％ vs 55.3％）.PTC组织中ERα36和ERα66的表达与性别、淋巴结转移情况无关.结论：ERα36与PTC密切相关,较ERα66更有可能在PTC发生与发展中发挥重要作用.展开更多
Background Estrogen receptor （ER）-negative breast cancer cells are more aggressive than ER-positive cells. Elevated levels of cyclooxygenase-2 （COX-2） and vascular endothelial growth factor-C （VEGF-C） expression...Background Estrogen receptor （ER）-negative breast cancer cells are more aggressive than ER-positive cells. Elevated levels of cyclooxygenase-2 （COX-2） and vascular endothelial growth factor-C （VEGF-C） expression have been detected in cultured human breast cancer cells and are associated with negative hormone receptor status. In this study, we created ERα stable transfectants in MDA-MB-231 cells to explore the effect of ERα on cell growth and COX-2 and VEGF-C expression.Methods The green fluorescent protein （GFP）-ERα plasmids were stably transfected into ER-negative MDA-MB-231 cells. The proliferation and migration of untransfected MDA-MB-231 cells, ERα-transfected MDA-MB-231 cells and ER-positive MCF-7 cells were determined. The expression of COX-2, and the levels of VEGF-C mRNA and the VEGF-C secretion concentration were assayed in these cell lines.Results The proliferation and migration capacities of ERα-tranfected MDA-MB-231 cells were significantly decreased （P 〈0.05）. The expression of COX-2 was significantly lower in ERa-tranfected MDA-MB-231 cells than in untranfected MDA-MB-231 cells. The mRNA and protein levels of VEGF-C were lower in ERa-tranfected MDA-MB-231 cells than in untransfected MDA-MB-231 cells （P〈0.05）.Conclusions ERα stable transfection inhibits proliferation and migration capacities of MDA-MB-231 cells and decreases expression of COX-2 and VEGF-C. The decreases of proliferation and migration capacities may be related to suppression of COX-2 and VEGF-C expression.展开更多
Objective: The novel estrogen receptor-α (ER-α) variant ER-α36 is reported to be functional in the es-trogen signaling pathway and is related to tamoxifen resistance in breast cancer. However, ER-α36 tends to be a...Objective: The novel estrogen receptor-α (ER-α) variant ER-α36 is reported to be functional in the es-trogen signaling pathway and is related to tamoxifen resistance in breast cancer. However, ER-α36 tends to be a favorable factor for survival in patients without tamoxifen therapy. To investigate the mechanisms behind this paradox, we determined the differences between the transcriptional profiles of ER-α36 and full-length ER-α (ER-α66) in breast cancers and matched normal tissues. Methods: We analyzed ER-α36 and ER-α66 messenger RNA ( mRNA) levels in 74 pairs of breast cancers and matched normal tissues using a real-time quantitative polymerase chain reaction (PCR) assay, and correlated the results with their clinicopathological characteristics. Results: Breast cancers expressed lower ER-α36 mRNA levels than matched normal tissues regardless of their ER-α66 expression status. Down-regulation of ER-α36 mRNA was correlated with local progression, lymph node metastasis, and advanced cancer stage. The level of ER-α66 mRNA was lower in ER-α negative breast cancers compared with matched normal tissues. No differences in ER-α66 mRNA levels were observed during cancer progression. Conclusion: Down-regulation of ER-α36 is associated with carcinogenesis and progression of breast cancer.展开更多
文摘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.
文摘目的：测定雌激素受体α36（ERα36）在甲状腺乳头状癌（PTC）原发灶中的表达,探讨其临床意义.方法：免疫组织化学显色检测ERα36和ERα66在PTC组织中的表达.结果：PTC组织中,ERα36和ERα66均特异性表达于肿瘤细胞,ERα36表达水平高于ERα66（67.6％vs 20.6％）;45岁以上患者ERα36阳性率高于45岁以下患者（95.2％ vs 55.3％）.PTC组织中ERα36和ERα66的表达与性别、淋巴结转移情况无关.结论：ERα36与PTC密切相关,较ERα66更有可能在PTC发生与发展中发挥重要作用.
基金This work was supported by a grant from the National Natural Science Foundation of China （No. 30600588）.
文摘Background Estrogen receptor （ER）-negative breast cancer cells are more aggressive than ER-positive cells. Elevated levels of cyclooxygenase-2 （COX-2） and vascular endothelial growth factor-C （VEGF-C） expression have been detected in cultured human breast cancer cells and are associated with negative hormone receptor status. In this study, we created ERα stable transfectants in MDA-MB-231 cells to explore the effect of ERα on cell growth and COX-2 and VEGF-C expression.Methods The green fluorescent protein （GFP）-ERα plasmids were stably transfected into ER-negative MDA-MB-231 cells. The proliferation and migration of untransfected MDA-MB-231 cells, ERα-transfected MDA-MB-231 cells and ER-positive MCF-7 cells were determined. The expression of COX-2, and the levels of VEGF-C mRNA and the VEGF-C secretion concentration were assayed in these cell lines.Results The proliferation and migration capacities of ERα-tranfected MDA-MB-231 cells were significantly decreased （P 〈0.05）. The expression of COX-2 was significantly lower in ERa-tranfected MDA-MB-231 cells than in untranfected MDA-MB-231 cells. The mRNA and protein levels of VEGF-C were lower in ERa-tranfected MDA-MB-231 cells than in untransfected MDA-MB-231 cells （P〈0.05）.Conclusions ERα stable transfection inhibits proliferation and migration capacities of MDA-MB-231 cells and decreases expression of COX-2 and VEGF-C. The decreases of proliferation and migration capacities may be related to suppression of COX-2 and VEGF-C expression.
基金Project supported by the National Basic Research Program (973) of China (No. 2009CB521704)the National Natural Science Foundation of China (No. 30772510)+2 种基金the Ministry of Health of China (No. WKJ2006-2-008)the Department of Science and Technology of Zhejiang Province (No. 2007C24011)the Natural Science Foundation of Zhejiang Province (No. R206060), China
文摘Objective: The novel estrogen receptor-α (ER-α) variant ER-α36 is reported to be functional in the es-trogen signaling pathway and is related to tamoxifen resistance in breast cancer. However, ER-α36 tends to be a favorable factor for survival in patients without tamoxifen therapy. To investigate the mechanisms behind this paradox, we determined the differences between the transcriptional profiles of ER-α36 and full-length ER-α (ER-α66) in breast cancers and matched normal tissues. Methods: We analyzed ER-α36 and ER-α66 messenger RNA ( mRNA) levels in 74 pairs of breast cancers and matched normal tissues using a real-time quantitative polymerase chain reaction (PCR) assay, and correlated the results with their clinicopathological characteristics. Results: Breast cancers expressed lower ER-α36 mRNA levels than matched normal tissues regardless of their ER-α66 expression status. Down-regulation of ER-α36 mRNA was correlated with local progression, lymph node metastasis, and advanced cancer stage. The level of ER-α66 mRNA was lower in ER-α negative breast cancers compared with matched normal tissues. No differences in ER-α66 mRNA levels were observed during cancer progression. Conclusion: Down-regulation of ER-α36 is associated with carcinogenesis and progression of breast cancer.
