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.
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 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.
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.
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.
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.
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 observe the action and correlation of p16 and estrogen receptor (ER) in papillary thyroid cancer (PTC).Methods Using immunohistochemical method, the p16 and ER in 50 cases of PTC were detected. Results The expression of p16 and ER was associated with the cellular differentiation, the lymphatic metastasis and prognosis in PTC. Conclusion It is helpful to detect the p16 protein and ER for analyzing the cellular differentiation degree and prognosis in PTC.
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.
Objective To investigate the express of ERβ protein in female slow transit constipation (STC) patients. Methods Immunohistochemistry and Western blot technique were used to detect the distribution and expression of estrogen receptor β (ERβ) protein of 20 patients with STC and 20 aged-matched controls. Results ERβ expressions were detected in mucous layer, myenteric nerve plexus and submucous nerve plexus in two groups. In comparison with the control group, the expression of ERβ protein of STC group was much lower (Plt;0.01). The expression of ERβ protein of sigmoid colon in STC group was significantly lower than that in control group (Plt;0.05). Conclusion The expression of ERβ protein decreased in myenteric and submucous nerve plexus of sigmoid colon tissues may involve in the pathogenesis of STC.