ObjectiveTo explore the effects of exogenous estrogen receptor β1 (ERβ1) gene on the expression of human telomerase reverse transcriptase (hTERT) as well as the changes of proliferation ability in MDA-MB-231 cell line by transfecting recombinant eukaryotic expressing vector containing ERβ1 cDNA into human breast cancer MDA-MB-231 cell. MethodsRecombinant eukaryotic expressing vector containing ERβ1 cDNA was transfected into human breast cancer MDA-MB-231 cell by using cationic liposome as transfecting agent (acted as pcDNA3.1ERβ1 transfection group), empty vector group and non-transfection group acted as controls. The expression levels in both the mRNA and protein of both the ERβ1 and hTERT were tested by real-time PCR and Western blot, respectively. The change of proliferation ability in MDA-MB-231 cell was displayed by cell growth curve, and the change of cell apoptosis was detected by flow cytometry. ResultsThe expression level of ERβ1 mRNA in the pcDNA3.1-ERβ1 transfection group (0.449±0.077) significantly increased as compared with the nontransfection group (0.153±0.035) or the empty vector group (0.160±0.020), P=0.001 or P=0.000. The expression level of ERβ1 protein in the pcDNA3.1-ERβ1 transfection group (0.847±0.065) significantly increased as compared with the non-transfection group (0.356±0.050) or the empty vector group (0.390±0.030), P=0.001 or P=0.000. The expression level of hTERT mRNA in the pcDNA3.1-ERβ1 transfection group (0.127±0.020) significantly decreased as compared with the non-transfection group (0.283±0.025) or the empty vector group (0.283±0.049), P=0.001 or P=0.002. The expression level of hTERT protein in the pcDNA3.1-ERβ1 transfection group (0.147±0.023) significantly decreased as compared with the non-transfection group (0.783±0.025) or the empty vector group (0.802±0.019), P=0.001 or P=0.002. The rate of cell apoptosis in the pcDNA3.1-ERβ1 transfection group 〔(6.15±0.94)%〕 was higher than that in the non-transfection group 〔(1.41±0.42)%〕， P=0.001. Cell proliferation curve showed that proliferation ability significantly decreased in the pcDNA3.1-ERβ1 transfected groups as compared with the non-transfection group (Plt;0.05). ConclusionERβ1 could inhibit cell growth of human breast cancer MDA-MB-231 cell by down-regulating the expression of hTERT.
Objective To investigate the expressions of C-erbB-2, estrogen receptor (ER) and progesterone receptor (PR) in breast cancer tissues and to explore their relationship with patients-age, tumor size, lymph node metastasis, histopathological type and the stage of cancer. Methods The expressions of C-erbB-2, ER and PR in 83 cases of breast cancer tissues were detected by immunohistochemistry and the clinical significance was statistically analyzed. Results The positive expression rate of C-erbB-2, ER and PR in 83 cases of breast cancer tissues were 78.3%, 56.6% and 55.4%, respectively. The expressions of C-erbB-2, ER and PR were not correlated to patients’ age, tumor size, histopathological type and the stage of cancer (Pgt;0.05). While the expression of C-erbB-2 rather than ER and PR was correlated to lymph node metastasis (P＜0.05) and the correlation was positive (r=0.387, P＜0.05). Conclusion The positive expression of C-erbB-2 is one of lymph node metastasis factors for breast cancer patients. Combined detection of ER and PR expression may be helpful to clinical treatment and predict prognosis for breast cancer patients.
Objective To investigate the correlation of the polymorphism of the estrogen receptor alpha gene Pvu II site and coronary heart disease (CHD) in Chinese population. Methods Such databases as CBM, CNKI, Wangfang database, VIP, MEDLINE, The Cochrane Library, EMbase, Springer, and Ovid were searched from their establishment date to November of 2010 to collect the case-control studies on the correlation of estrogen receptor alpha gene polymorphism Pvu II sites with coronary heart disease of the Chinese. The quality of included studies was evaluated, the available data was extracted, and then the RevMan5.0 software was used for Meta analyses. Results Nine case-control studies were included, involving 1 464 cases with coronary heart disease and 1 203 cases in the control group. The results of Meta-analyses showed that, as to the correlation of the polymorphism of ER alpha gene Pvu II site T/C and CHD, there was no significant difference in the risk of CHD between people with different genotypes, i.e. the C allele versus T allele (OR=0.95, 95%CI 0.77 to 1.17, P=0.63), genotype of (TC + CC) versus TT (OR=0.97, 95%CI 0.73 to 1.28, P=0.81), genotype of TC versus TT (OR = 0.93, 95%CI 0.68 to 1.26, P=0.64), genotype of CC versus TT (OR=0.86, 95%CI 0.57 to 1.31, P=0.49). Conclusion Estrogen receptor alpha gene polymorphism Pvu II site are not associated with the coronary heart disease in Chinese population.
Objective To study the relations between the expression of estrogen receptor (ER), progesterone receptor (PR) and tumor infiltration and metastasis in thyroid carcinoma. Methods By using immunohistochemical staining (SABC method), the expressions of ER and PR in 100 cases of thyroid carcinomas and 28 cases of benign thyroid lesions were studied. Results The positive rate of ER and PR expressions were 67.0% and 62.0% respectively in thyroid carcinomas, they had correlation with cell differentiation and type of histology but positive expressions did not relate to age and sex. The positive rate of ER and PR in the non-metastasized group was 75.4% and 70.5%, significantly higher than that of the metastasized group in which were 53.8% and 48.7% (Ｐ＜0.05). Conclusion The results suggest that the expressions of ER and PR are related to tumor differentiation and may indicate a poor prognosis.
ObjectiveTo analyze the phasic changes of bone mass, bone turnover markers, and estrogen levels at different time points after glucocorticoid (GC) intervention in rat and their correlation. MethodsThirty-four female 3-month-old Sprague Dawley rats were randomly divided into the following 3 groups:baseline group (n=6), dexamethasone (DXM) group (n=14), and control group (n=14). Rats were injected with DXM at the dose of 0.75 mg/kg, twice a week for 12 weeks in DXM group, with salt solution lavage in control group, and no treatment was given in baseline group. The body mass, adrenal weight, and uterus weight were measured. Bone mineral density (BMD), bone mineral content (BMC), and bone area (BA) of lumbar vertebral and femurs were detected by dual energy X-ray absorptiometry. Meanwhile, the serum levels of N-terminal propeptide of type I procollagen (PINP), C-terminal cross-linking telopeptide of type I collagen (β-CTX), and estrogen levels were determined by ELISA before experiment in baseline group and at 4, 8, and 12 weeks after experiment in control and DXM groups. At last, the correlation was analyzed among body weight, BMD, PINP, β-CTX, estrogen levels, and GC intervention duration of DXM group. ResultsThe body mass, adrenal weight, and uterus weight in DXM group were significantly lower than those in baseline group and control group at all the time points (P<0.05). The levels of PINP and β-CTX elevated slowly in DXM group, significant difference was found at 12 weeks (P<0.05), but no significant difference at the 4 and 8 weeks (P>0.05) when compared with those in baseline group and control group. The estrogen level in DXM group was significantly lower than that in baseline group and control group at all the time points (P<0.05). BMD, BMC, and BA of lumbar vertebral and femurs in DXM group were significantly lower than those in control group at all the time points after GC intervention (P<0.05). Loss of bone mass of L2 and femoral trochanteric region in DXM group was the lowest of all ranges of interest (ROIs). BMC and BA of lumbar vertebrae and BA of femoral shaft in DXM group at 4 weeks were significantly lower than those in baseline group (P<0.05). But there was no significant difference in BMD, BMC, and BA of other lumbar vertebrae and femurs' ROIs between DXM group and baseline group at all the time points (P>0.05). After GC intervention, BMD of lumbar vertebrae and femurs had negative correlation with PINP and β-CTX (P<0.05) and positive correlation with estrogen level (P<0.05). ConclusionThe bone mass decreases rapidly at the early stage after GC intervention and then maintains a low level with time, the levels of bone turnover markers show a progressive increase, and the estrogen levels show a decrease trend. In addition, body weight, the levels of bone turnover markers and estrogen are associated with the change of bone mass.
Objective：To investigate the role of 17beta; estradiol on th e expressi on of vascular endothelial growth factor (VEGF) and on the releasing rate of lac tate dehydrogenase (LDH) in cultured anoxiainjured human retinal pigment epit h eliual (RPE) cells. Methods:Established the anoxiainjuried m odel of human RPE c ells with Cobalt Chloride (CoCl2) after RPE cells were pretreated with 17beta;E 2 and tamoxife, 17beta;E2 antagonist. The expression of VEGF mRNA was detecte d by re v erse transcriptionpolymerase chain reaction technique (RTPCR). The cultured RP E cells were divided into four groups: normal control group, anoxiainjured gro u p, 17beta;E2 pretreatment group and 17beta;E2 with tamoxifen pretreatment grou p. The releasing rate of LDH was detected by chromatometry. The expression of VEGF pro tein were detected by cellular immunohistochemistry. Results:T he expression of VEGF and LDH releasing rate were higher in anoxiainjured grou p than that in nor m al control group (P＜0.05), and were lower in 17beta;E2 pretreatment group than th at in anoxiainjured group （P＜0.05）. When the effect of 17beta;E2 was o bstructe d by tamoxifen, the expression of VEGF and LDH releasing rate increased but didn prime;t differ much from which in anoxiainjured group (P＞0.05). Conc lusion:The ex pression of VEGF increases in anoxiainjured human RPE cells. 17beta;E2 can do wnr egulate the expression of VEGF and decrease the releasing rate of LDH, which can be blocked by tamoxifen.
ObjectiveTo review the recent progress in research on the role of estrogen and estrogen receptor on the onset and progression of adolescent idiopathic scoliosis (AIS). MethodsThe recently published clinical and experimental 1iterature at home and abroad on abnormality of estrogen and its receptor in AIS was reviewed and summarized. ResultsThere are many abnormal changes of estrogen and estrogen receptor in most AIS patients, including higher serum estrogen concentration, unusual cellular response to estrogen, late age at menarche, and gene polymorphisms of estrogen receptor, which are closely associated with AIS predisposition, curve severity, and scoliosis progression. ConclusionEstrogen and its receptor participate in the onset and progression of AIS by certain mechanisms, but exact mechanism remains indefinite, which needs further research to better define the role of estrogen and its receptor in AIS.
Objective:To observe the inhibited effect and its mechani sm of estro gen on lightinduced apoptosis of retinal photoreceptor cells. Methods:Twenty female Sprague-Dawley rats were randomly divided into two groups: ovariectomized (OV) group and OV and estrogen (E2) replacement (OV+E2) group, with 10 rats in each group. All of the rats were exposed to the cyclic illumination under 12 hou r light and 12 hour dark condition with the light intensity of (600plusmn;35.4) lx ( a total of 14 times). All of the right eyes were extracted and the thickness of r etinal outer nuclear layer (ONL) was measured. Terminal deoxynucleotidyl Transfe rasemediated dUTP nick end labeling (TUNEL) method was used to evaluate positi v e apoptosis cells in ONL. The expression of nitric oxide synthase (NOS) in retin al cells was detected by immunohistochemistry with image analysis method. Results:The thickness of ONL in OV group was obviously thinner than that in the OV+ E2 group. The number of positive apoptosis of the cells was (0.0275plusmn;0.0069) c el ls/mu;m2 in OV group and (0.0162plusmn;0.0054) cells/mu;m2 in OV+E2group; the di fferen ce between the two groups was significant (t=4.1370，P=0.0012). The values o f in tegral optical density of NOS positively stained cells in retinal inner nuclear layer was (0.3675plusmn;0.0662) in the OV group and (0.2941plusmn;0.0350) in OV+E2 group ; the difference between the two groups was significant (t=3.4885, P=0.0031). Conclusion:Estrogen can protect retina from light injuries by regu lating NOS synthesis and inhibiting apoptosis of photoreceptor cells.
ObjectiveTo summarize the relevant studies of pharmacological mechanism of tamoxifen and its influence on ovary function in order to provide information and evidence for the therapy of breast cancer. MethodsPapers published from January 1950 to January 2014, were retrieved in MedLine, OVID, CBM, CNKI databases using the keywords on tamoxifen, drug metabolism, ovary, sex hormone, etc, 1286 papers were retrieved in English literatures, and 621 in Chinese literatures. Criteria of paper adoption:①The clinical and basic studies about metabolism of tamoxifen, metabolic effect of tamoxifen, and gene polymorphism of CYP2D6.②The role played by estrogen receptor and protein cofactors in tamoxifen effect.③The clinical and basic studies about tamoxifen induced ovulation, caused endometrial thickening, changed sex hormone levels. According to the above criteria, 152 papers were selected, and 77 papers out of them were finally analyzed and reviewed. Results①The tamoxifen metabolite 4-OH-N-tamoxifen was the main working component, the decreased levels could predict the poor prognosis.②The CYP2D6 gene polymorphism could affect the metabolic effect of tamoxifen and the therapeutic effect of patients with breast cancer.③The metabolic effect of tamoxifen needed the participation of the estrogen receptors and protein cofactors.④Tamoxifen could affect the reproductive system function through the estrogen receptor of H-P-O axis, ovary, and endometrium. ConclusionsMetabolic effect of tamoxifen is regulated by gene, it could affect reproductive system functions through estrogen receptor. the mechanism that tamoxifen cowld affect the hormone levels and wherther it could reflect the ovarian function by monitering the hormone levels continuously for patients with breast cancer need to be researched.
Objective To study the effects of estrogen and progesterone and their receptors on the development of gallstone (GS) and primary gallbladder carcinoma (PGC), and probe to the relationship between the biological characteristic of PGC and female hormone and their receptors. Methods The study of PGC related to female hormone was reviewed by history document and experimental study in resently. Results The female hormone influenced human body extensively: they acted on not only the target organs, but also the nontarget organs with their receptors. The action was brought about by their receptors expression. The action intensity was dependent on not only the serum level of female hormone but also their corresponding receptors distributing in organs. The carcinogenic mechanism of estrogen was more clear with the discovery of estrogen-regulating-proteins. Conclusion The estrogen play an important role in the onset and development of GS and PGC. Estrogen and progestrone can inhance the patients′ susceptibility to the cholesterol gallstone and become a high risk factor in causing PGC through inducing their corresponding receptors expression in the gallbladder. Evaluating the effects of estrogen-estrogen receptor-estrogen-regulating-protein on biological characteristic of PGC is significant in guiding clinical endocrine treatment.