ObjectiveTo explore the associations between estrogen receptor α (ESR1) gene intron 1 PvuⅡ (?397 T/C, rs2334693), XbaⅠ (?351 A/G, rs9340799) polymorphisms and premature ovarian failure (POF).MethodsLiterature published before February 2021 were retrieved in PubMed, Web of Science, China National Knowledge Infrastructure, Wanfang, and CQVIP databases, according to the inclusion and exclusion criteria developed before. Odds ratio (OR) and 95% confidence interval (CI) were used for data analysis, the Q test and I2 statistic were used for heterogeneity analysis. Random-effect model or fixed-effect model was used according to I2 value. All analyses were performed by RevMan 5.3 software.ResultsSix case-control studies were included in this meta-analysis. For the associations between ESR1 gene intron 1 PvuⅡ polymorphisms and POF, there was no statistical difference in TT vs. CC model [OR=0.72, 95%CI (0.31, 1.70), P=0.46], TC vs. CC model [OR=1.09, 95%CI (0.83, 1.43), P=0.54], recessive model [OR=1.08, 95%CI (0.68, 1.70), P=0.74], or dominant model [OR=0.77, 95%CI (0.42, 1.42), P=0.41]. For the associations between ESR1 gene intron 1 XbaⅠ polymorphisms and POF, there was no statistical difference in AA vs. GG model [OR=0.88, 95%CI (0.44, 1.75), P=0.72], AG vs. GG model [OR=1.23, 95%CI (0.84, 1.79), P=0.29], recessive model [OR=1.14, 95%CI (0.81, 1.61), P=0.44], or dominant model [OR=0.75, 95%CI (0.41, 1.35), P=0.34], either. No statistical difference was found in the ethno-based subgroup analyses (P>0.05). Most models had obvious heterogeneities.ConclusionsCurrent evidence can’t confirm the associations between ESR1 gene PvuⅡ, XbaⅠ polymorphisms and POF. High-quality, multi-central and large-sample studies are still necessary to support this conclusion.
ObjectiveTo investigate the relationship between the polymorphisms of estrogen receptor α (ERα) gene PvuⅡ, XbaⅠ and breast hyperplasia. MethodsPolymerase chain reaction-restriction fragment length polymorphism was used to detect the polymorphisms of ERα gene PvuⅡ, XbaⅠ in breast hyperplasia patients (study group, n=89) and healthy controls (control group, n=35). ResultsThe differences of the genotypic frequency and allele frequency of the ERα gene Xba Ⅰ were significant between the study group and the control group (Plt;0.05). According to analysis of the odds ratio (OR), the risk of developing breast hyperplasia for X allele carriers was 0.551 as compared with x allele carriers. But there was no significant difference for the gene polymorphism of PvuⅡ between the study group and the control group (Pgt;0.05). ConclusionThe polymorphisms of XbaⅠof ERα gene is associated with breast hyperplasia and the mutant gene increases breast hyperplasia risk.
Objective To study the relationship between the expression of apoptosisrelated gene bclx,bax and estrogen receptor (ER) in primary gallbladder carcinoma (PGC) and its clinical significance. MethodsImmunohistochemistry of labeled dextran polymer (LDP) with EnvisionTM system was used to detect ER and gene bclx and bax. ResultsThe positive rate of bclx,bax and ER were 72.3%,66.0% and 59.6% in 47 cases with primary gallbladder carcinoma and 40.0%,93.3% and 93.3% in 6 cases with gallbladder adenomahyperplastic. The expression of bax and ER in PGC was significantly lower than that in gallbladder adenomahyperplastic (P＜0.05),the expression of bclx was significantly higher in PGC than that in the latter (P＜0.05).The expression of bclx and ER in well differentiated PGC was significantly higher than that in moderately, poorly differentiated PGC (P＜0.05); bax expression in well differentiated PGC was lower. ER and bax expression in male PGC was significantly lower than that in female PGC （P＜0.01）, the expression of bclx in male PGC was higher (P＜0.05).ER was more highly expressed in smaller PGC than in larger one (P＜0.05). ER and bax, bclx were not different between various clinical stages and ages (P＞0.05,respectively). Conclusion The expression ER, apoptosisrelated gene bclx and bax have correlation with differentiation and sex in PGC, their levels shows significance in the prognosis of PGC.
The level of androgen receptor (AR), estrogen receptor (ER) and progesterone receptor (PR) of carcinoma and pericarcinoma tissue were determined in 30 cases of male hepatocellular carcinoma (HCC) patients operated by streptavidin peroxdase conjugated method, meanwhile used 20 patients with benign liver disease as a contrast group. The results showed that the positive rate of AR in tumor tisse was 80.0%, significantly higher than that in peritumor tissue (46.7%) and liver tissue of benign diseases (40.0%), Ｐ＜0.01, and there was no significantly difference between the latter two groups (Ｐ＞0.05). The positive rate of ER in carcinoma tissue (43.3%) was notably lower than that in pericarcinoma tissue (80.0%), Ｐ＜0.01. Statistically significantly difference wasn’t achieved in contrast with the benign diseases group (50.0%), Ｐ＞0.05. The positive rate of PR had no significantly difference among the three groups (Ｐ＞0.05). The authors suggest that sex hormone is related to initializing and developing of HCC by the action via its receptor, the level of AR and ER can be used as a prognosis determine index of HCC.
Objective To explore the clinical significance of estrogen receptor α( ERα) , estrogen receptor β( ERβ) in non-small cell lung cancer( NSCLC) .Methods EnVision method was used to detect the expressions of ERα, ERβ, vascular endothelial growth factor( VEGF) , and microvessel density( MVD) in 54 NSCLC patients, 10 patients with lung benign lesions, and 10 normal controls. The interrelation between ERα, ERβ, VEGF, and MVD was analyzed. Results No obvious expressions of ERα and ERβwere observed in the normal lung tissues and lung benign lesions. The positive expression rates of ERα, ERβ, and VEGF in NSCLC were 20. 4% ( 11/54) , 64. 8% ( 35/54) , and 64. 8% ( 35/54) , respectively. There were no significant differences between ERαin regard to clinical parameters of NSCLC. But the expression of ERβwas dependent on pathological classification and differentiation of NSCLC. The expression of ERβ was significantly higher in adenocarcinoma than in squamous cell carcinoma( P lt; 0. 05) . The expression rate of ERβin well differentiated group was significantly higher than that in low, moderately differentiated group( P lt;0. 05) . There were significant differences between VEGF in regard to lymph node metastasis and TNM stage. The expression of ERαinterrelated with VEGF and MVD with r value of 0. 4 and 0. 685 respectively ( P lt;0. 05) . There was little correlation between ERβ and VEGF, MVD( P gt; 0. 05) . Conclusion Theexpression of ERβ correlates with pathological classification and differentiation of NSCLC, suggesting its significance in evaluating the pathological classification and malignant degree of NSCLC. The expression of ERαcorrelates with VEGF and MVD, suggesting that ERαpossibly promote micro-angiogenesis of NSCLC by VEGF pathway.
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 explore the role of estrogen receptor alpha (ERα) and estrogen receptor beta (ERβ) in estrogen-induced proliferation of endometrial cancer, and explore whether metformin inhibits the proliferation of endometrial cancer cells through ERα and ERβ. Methods Stable transfected Ishikawa cells were constructed by lentivirus. The effects of down-regulated ERα and ERβ on estrogen-induced Ishikawa cell proliferation were detected by methyl thiazolyl tetrazolium assay. The effects of down-regulated ERα and ERβ on estrogen-induced Ishikawa cell cycle were detected by flow cytometry. In addition, quantitative real-time polymerase chain reaction and Western blotting assays were used to detect changes in the expression of cyclinD1 and P21 involved in cell cycle regulation. The effects of down-regulated ERα and ERβ on estrogen-induced Ishikawa cell proliferation were observed by adding metformin to estrogen treatment. Results Down-regulation of ERα inhibited the proliferation and cell cycle of Ishikawa cells (P<0.05). Down-regulation of ERα also inhibited the expression of cyclinD1 and promoted the expression of P21 (P<0.05). Down-regulation of ERα counteracted the effect of estrogen-induced cell proliferation, cell cycle, and the expression changes of cyclinD1 and P21 (P<0.05). Down-regulation of ERβ promoted the proliferation and cell cycle of Ishikawa cells (P<0.05). Down-regulation of ERβ also promoted the expression of cyclinD1 and inhibited the expression of P21 (P<0.05). Down-regulation of ERβ enhanced the effect of estrogen-induced cell proliferation, cell cycle, and the expression changes of cyclinD1 and P21 (P<0.05). Metformin inhibited the proliferation of estrogen-induced Ishikawa cells (P<0.05), while in the down-regulated ERα Ishikawa cells or down-regulated ERβ Ishikawa cells, the inhibition of metformin on Ishikawa cells disappeared (P<0.05). Conclusions ERα may promote estrogen-induced proliferation of endometrial cancer cells, while ERβ may inhibit estrogen-induced proliferation of endometrial cancer cells. In addition, ERα and ERβ may also mediate the inhibitory effect of metformin on endometrial cancer cells.
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 explore the effect of toremifene on estrogen receptor （ER） expression and tumor micro-angiogenesis in rat Lewis lung carcinoma. Methods Cell suspension of rat Lewis lung carcinoma was implanted into 40 female Wistar rats subcutaneously. The rats were randomly divided into a control group，a estradiol group （0.006 mg/mL），a low dose toremifene group （0.25 mg/mL） and a high dose toremifene group （5 mg/mL）. Tumor size was measured every 3 days and the tumor growth curve was charted. On 15th day，the tumor weight and the growth inhibition rate were measured. Immunohistochemical method was used to detect the expressions of estrogen receptor α （ERα），estrogen receptor β （ERβ），vascular endothelial growth factor （VEGF），and platelet endothelial cell adhesion molecule-1 （PECAM-1）. Integral optical density （IOD） of ERα，ERβ and VEGF was calculated by image analysis software. Quantitative method of Weidner with PECAM-1 was employed for microvessel density （MVD） count. Results Tumor size of the four groups all presented a quadratic function growth trend with time （Plt;0.05）. Tumor growth speed was slower in toremifene groups of low and high doses than that in the control group and the estradiol group. The growth inhibition rate of the estradiol group，the low dose toremifene group and the high dose toremifene group was －15.1%，22.6%，and 45.1%，respectively. The expressions of ERα，VEGF，and MVD in the estradiol group were significantly higher than those in the control group，the low dose toremifene group and the high dose toremifene group （all Plt;0.05）. The expressions of ERα，VEGF，and MVD in the low dose toremifene group were significantly lower than those in control group，but higher than those in high dose toremifene group （all Plt;0.05）.The expression of ERα was positively related to VEGF （r=0.664，Plt;0.05） and MVD（r=0.593，Plt;0.05）. Conclusion Toremifene can inhibit tumor growth，which maybe involved in inhibiting ERα mediated VEGF expression.
We determined estrogen receptor (ER), estradiol (E2) and testosterone (T) in the tissue of 50 gastric carcinomas ans 20 benign stomach diseases. The result showed that the positive rate of ER was 32.0% in gastric cancerous tissue, in which the poorly-differentiated type was higher than that of the well-differentiated type (Plt;0.05)，and still higher in BorrmannⅢ、Ⅳ types than in Borrmann Ⅰ、Ⅱ types (Plt;0.01). The determination of Er is significant for the estimation of prognosis ans endocrinal therapy after operation. E2 content showed no obvious difference betweenn gastric carcinoma, benign somach diseases ans normal gastric mucose, but T level and T/E2 ratio in gastric cancer were much higher than those in benign stomach diseases and normal gastric mucosa (Plt;0.05). IT suggested that the imbalance of E2 and T contents may related the occurence of gatric carcinoma. The E2 and T level showed no obvious difference between ER+ and ER- in gastric cancerous tissue.