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.
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 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 summarize the research progress of distributional heterogeneity of the molecular pathology characteristics in breast cancer.
Methods The related literatures about the distribution of the molecular pathology characteristics in breast cancer were reviewed.
Results The breast cancer had the same heterogeneity as other cancers. At the same time, the molecular pathology characteristics, such as estrogen receptor (ER), progesterone receptor (PR), Ki-67, and human epidermal growth factor receptor-2 (HER-2), had the distributional heterogeneity. The distributional heterogeneity of molecular pathology characteristics in breast cancer could effect the pathologic diagnosis, the treatment, and the prognosis.
Conclusion Although there are some new techniques which were used to investigate the heterogeneity of breast cancer, but each way has some problems. The more attention should be paid to the research about the distributional heterogeneity of the molecular pathology characteristics in breast cancer.
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 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 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.
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.
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 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.
