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.
ObjectiveTo explore expression of Mdm2 in the estrogen receptor α (ERα)-positive breast cancer tissues and fibroadenoma of breast tissues, and to explore the effect of MDM2-siRNA on cell proliferation, colony formation, and apoptosis for MCF-7 cells. Methods① Seventy eight ERα-positive breast cancer patients identified by histopathological examination, who underwent surgery in our hospital from June 2012 to October 2015, as well as 10 fibroadenoma of breast patients underwent surgery in the same period, were collected retrospectively to determine the expression of Mdm2, then explore the relationship between the expression of Mdm2 and clinical pathological characteristics of ERα-positive breast cancer patients. ② MCF-7 cells were divided to MDM2-siRNA group (added with MDM2-siRNA), negative control group (added with negative siRNA), and blank control group (added without any reagent). Expression of Mdm2, cell proliferation rate, number of colony formation, and apoptosis rate were determined in the MCF-7 cells of 3 groups. Results① No one of fibroadenoma of breast patients was found positive expression of Mdm2 (0/10), and 38 of 78 ERα-positive breast cancer patients were found the positive expression of Mdm2 (48.7%), which is higher than that of fibroadenoma of breast tissues (χ2=12.357, P=0.000). In ERα-positive breast cancer patients, expression of Mdm2 was related with TNM staging and number of metastasic lymph node (P < 0.050), the positive expression rate of Mdm2 was higher in patients with later TNM staging or more metastasic lymph node. ② Cell proliferation rates on 2, 3, and 4 days after transfection, expression level of Mdm2, and number of colony formation were all lower (P < 0.050), but the apoptosis rate was higher in MDM2-siRNA group (P < 0.050), comparing with negative control group and blank control group. But there was no significant difference between negative control group and blank control group on aforementioned indexes (P > 0.050). ConclusionMdm2 is a diagnostic marker in ERα-positive breast cancer patients, and treatment targeting it might has a certain therapeutic value.
ObjectiveTo establish MCF-7 cell lines with different ERα/ERβ expression level and observe their biological behaviors. MethodsERα or ERβ gene were silenced by RNA interference, and the cell lines with different ERα or ERβ expression level were obtained in MCF cell lines. MTT assay, flow cytometry, RT-PCR, double layer softagar clony formation test, and Matrigel adhesion assay were used to detect the abilities of cell proliferation, apoptosis, tumorigenesis, and adhesion. ResultsThe stable expression cell lines with ERαlow/ERβhigh or ERαhigh/ERβlow were established successfully. After ERα gene knockdown, MCF-7 grew slowly and was arrested at phase G0-G1. Apoptosis of MCF-7 was induced and the capacity of tumorigenesis and adhesion in vitro were weakened. However, the characteristics mentioned above except for adhesion changed to the opposite sides after ERβ gene knockdown. ConclusionsThe ERα gene silence can inhibit the formation of tumor, however the ERβ gene silence can promote tumor growth, invasion, and metastasis. Therefore, may be a useful approach on the breast cancer therapy.
ObjectiveTo review recent studies on the roles of estrogen receptor β in breast cancer. MethodsThe literatures in recent years on the biological function, variant isoforms of estrogen receptor and its possible roles in breast cancer were reviewed. ResultsERβ was a new member of the superfamily of steroid receptors, it might play an important role in breast tumor genesis, tumor progression, prognosis and reaction to the endocrine therapy in breast cancer. ConclusionERβ is a new prognostic marker in breast cancer.
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.
Objective To explore the effect of exogenous estrogen receptor β1 (ERβ1) gene on the expression of p53 as well as the changes of apoptosis in MDA-MB-231 cell line and to investigate the biological role of ERβ1 in breast cancer. Methods Recombinant eukaryotic expressing vector containing ERβ1 cDNA was transfected into human breast cancer cell MDA-MB-231 by using cationic liposome LipofectamineTM 2000. The expression levels of p53 and ERβ1 in mRNA and protein were evaluated by real-time PCR and Western blot, respectively. Cell growth curve was used to detect the changes of cell proliferation ability. Cell apoptosis was detected by flow cytometry. Results After transfected with vector containing ERβ1 cDNA, proliferation ability of MDA-MB-231 cell decreased and the expression levels of both ERβ1 and p53 in both mRNA and protein increased (Plt;0.01). Rate of cell apoptosis increased in ERβ1 upregulation groups （Plt;0.01）. Conclusion ERβ1 can induce apoptosis and inhibit the growth of MDA-MB-231 cells by upregulating p53 expression.
ObjectiveTo summarize progression of growth factor receptor (GFR) signaling pathway in endocrineresistant breast cancer. Method Literatures about mechanisms of GFR signaling pathway in the development of endocrineresistant breast cancer were reviewed. ResultsThe crosstalk between GFR and estrogen receptor (ER) signaling pathway had been reported to be involved in the development of endocrine-resistant breast cancer. Interrupting this signaling pathway could overcome endocrine therapy resistance. Many clinical trails had shown that the utilizing endocrine therapy combined with GFR inhibitors could obviously increase the survival rate of patients with breast cancer. ConclusionSeveral agents targeting GFR signaling pathways show a great potential for treatment of patients with breast cancer.
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.
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.
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.