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.
