OBJECTIVETo explore the expressions of trefoil factor 1 (TFF1) and trefoil factor 3 (TFF3) in prostate cancer (PCa) and prostate intraepithelial neoplasia (PIN) and their clinical significance.

METHODSUsing immunohistochemistry, we detected the expressions of TFF1 and TFF3 in the prostatic tissues of 89 cases of PCa, 50 cases of PIN, and 65 cases of benign prostate hyperplasia (BPH), and evaluated their clinical significance.

RESULTSThe positive rates of TFF1 and TFF3 expressions were 77. 53% and 48. 31% in PCa and 66.00% and 30.00% in PIN, significantly higher than 49.23% and 13. 85% in BPH (P <0. 05). The expression of TFF1 was not correlated with Gleason score (P >0. 05), while that of TFF3 was significantly higher in the PCa cases with Gleason score ≤7 than in those with Gleason score > 7 (70. 00% vs 42. 03%, P <0. 05). No significant correlation was observed between TFF1 and TFF3 expressions in PCa (P >0. 05).

CONCLUSIONThe expressions of TFF1 and TFF3 may contribute to the occurrence and progression of PCa, and therefore could be used as laboratory indexes in the diagnosis, differential diagnosis, and prognosis of PCa.

Disease Progression ; Humans ; Immunohistochemistry ; Male ; Peptides ; metabolism ; Prognosis ; Prostatic Hyperplasia ; metabolism ; Prostatic Intraepithelial Neoplasia ; metabolism ; Prostatic Neoplasms ; metabolism ; Trefoil Factor-1 ; Trefoil Factor-3 ; Tumor Suppressor Proteins ; metabolism

OBJECTIVETo observe the effect of hTFF1 fusion protein on gastric mucosal lesion in mice after burn injury.

METHODSThe pET32alpha-hTFF1 vector were transfected into E.coli Origami B (DE3), and rhTFF1 fusion protein was expressed by IPTG induction. Mice were inflicted with 30% TBSA full-thickness burn, then were divided into burn treatment (BT, with treatment of rhTEF1 fusion protein by gavage), burn control (BC, with treatment of isotonic saline by gavage), and normal control (NC) groups according to block randomized design. Gastric mucosal lesion, including appearance of gastric mucosa, injury index, pathological change, were compared between BT and BC groups before and after burn injury, and above indices in NC group were also examined.

RESULTSThe rhTFF1 fusion protein was expressed with good specificity confirmed with Western blot analysis. The gastric erosion rate was 77.8% and 22.2% respectively in BC and T group. The injury index was 6.2 +/- 2.0 and 2.0 +/- 1.2 respectively in BC and T group. Above indices in C group were 0.

CONCLUSIONThe rhTFF1 fusion protein can be expressed in E.coli expression systems, which can obviously ameliorate gastric mucosal lesion in mice after burn injury.

Animals ; Burns ; pathology ; therapy ; Disease Models, Animal ; Gastric Mucosa ; pathology ; Humans ; Mice ; Recombinant Fusion Proteins ; therapeutic use ; Trefoil Factor-1 ; Tumor Suppressor Proteins ; therapeutic use ; Wound Healing

OBJECTIVETo investigate phytoestrogenic effects of ferulic acid in ER-positive T47D and ER-negative MDA-MB231 cells in culture.

METHODT47D and MDA-MB231 human breast cancer cells were treated with ferulic acid and examined cell proliferation by means of MTT assay. Cell cycle distribution, ERalpha and ERbeta expression were treated by flow cytometer. The pS2 mRNA expressions were detected by real-time fluorescence quantitative PCR.

RESULTThe proliferations were enhanced significantly by treatment with ferulic acid on T47D cells and the proliferation effects were inhibited by adding Faslodex (1 x 10(-8) mol x L(-1)). However, there was no significant difference on the proliferation in MDA-MB-231 cells compared with solvent control group by both treatment with ferulic acid and co-treatment with Faslodex (1 x 10(-8) mol x L(-1)). Ferulic acid stimulated the amount of T47D cells in phase S and proliferation index increased significantly. The effects were inhibited by treatment with Faslodex (1 x 10(-8) mol x L(-1)), and the amount of cells in phase S and proliferation index decreased, the amount of cells in G0/G1 phase increased, cell cycle of T47D was arrested in G0/G1 phase. Ferulic acid up-regulated pS2 mRNA expressions and increased the level of ERalpha protein expression in T47D cells. Ferulic acid did not show remarkable effect to the level of ERbeta protein expression in T47D cells.

CONCLUSIONFerulic acid possessed phytoestrogenic effect by up-regulating pS2 gene expression and the receptor subtype of ERalpha.

Breast Neoplasms ; chemistry ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Coumaric Acids ; pharmacology ; Estrogen Receptor alpha ; analysis ; Estrogen Receptor beta ; analysis ; Female ; Gene Expression Regulation, Neoplastic ; drug effects ; Humans ; RNA, Messenger ; analysis ; Trefoil Factor-1 ; Tumor Suppressor Proteins ; genetics

OBJECTIVETo study the molecular forms of TFF1 in normal gastric mucosa and its expression in normal, gastric carcinoma, atypical hyperplasia, and intestinalized gastric mucosa.

METHODSThe molecular forms of TFF1 in normal gastric mucosa was observed by western blotting. The expression of TFF1 in normal, gastric carcinoma, atypical hyperplasia, and intestinalization gastric mucosa was assayed immunohistochemically.

RESULTSTFF1 existed in normal gastric mucosa in forms of monomer, dimer and 21-kD TFF1 complex, with the last being the richest. TFF1 was expressed mainly in the epithelial cytoplasm of the mucosa in the gastric body and antrum, especially around the nucleus, and the closer to the lumen, the higher the expression. TFF1 expression in the tissues adjacent to gastric carcinoma was higher than that in normal gastric mucosa (P<0.001), and the expression in gastric adenocarcinoma was positively correlated to differentiation of adenocarcinoma. No TFF1 was expressed in poorly differentiated adenocarcinoma. The expression of TFF1 in moderate and well differentiated adenocarcinoma was a little lower than that in normal mucosa (P>0.05). The gastric mucosa with atypical hyperplasia had significantly higher TFF1 expression than normal gastric mucosa (P<0.001), and TFF1 was not detected in intestinalized gastric mucosa. There was no significant difference in TFF1 expression between gastric mucosa around the intestinalized tissues and normal gastric mucosa (P>0.05).

CONCLUSIONSTFF1 plays an important part in protection and restitution of the gastric mucosa, and TFF1 may be related to suppression and differentiation of carcinoma.

Adenocarcinoma ; metabolism ; pathology ; Adult ; Aged ; Blotting, Western ; Esophageal Neoplasms ; metabolism ; pathology ; Female ; Gastric Mucosa ; metabolism ; pathology ; Humans ; Immunohistochemistry ; Male ; Middle Aged ; Stomach Neoplasms ; metabolism ; pathology ; Trefoil Factor-1 ; Tumor Suppressor Proteins ; metabolism

OBJECTIVETo study the distribution and quantity of CD44+/CD24- cells in breast cancer tissue and the cell lines, and as well as its correlation with the expression of various breast cancer markers and molecular subtyping of breast carcinoma.

METHODSThe expression of CD44/CD24, estrogen receptor, progesterone receptor, HER2, human estrogen-induced protein PS2, bcl-2 and nm23 in 60 cases of invasive ductal carcinoma of breast were studied by either single or double immunohistochemical staining. The co-expression of CD44 and CD24 in 3 breast cancer cell lines (MCF-7, MDA-MB-468, and MDA-MB-231) was also examined.

RESULTSThe quantity and distribution of CD44+/CD24- cells varied greatly and no specific patterns were identified. The percentage of CD44+/CD24- in breast cancer was 65%. The amount of CD44+/CD24- cells did not correlate with the age of patients, lymph node metastasis, tumor size, molecular subtypes and expression of various breast cancer markers in breast carcinoma. The proportion of CD44+/CD24- cells in MCF-7, MDA-MB-468, and MDA-MB-231 cell lines was <1%, 5% and >80%, respectively.

CONCLUSIONSCD44+/CD24- cells are demonstrated in certain breast cancer tissues and cell lines. However, there is no relationship obtained between the quantity or the distribution of these cells and the molecular subtyping or the clinicopathologic parameters in breast cancer.

Adult ; Aged ; Biomarkers, Tumor ; Breast Neoplasms ; classification ; metabolism ; pathology ; CD24 Antigen ; metabolism ; Carcinoma, Ductal, Breast ; classification ; metabolism ; pathology ; Cell Line, Tumor ; Female ; Humans ; Hyaluronan Receptors ; metabolism ; Lymphatic Metastasis ; Middle Aged ; NM23 Nucleoside Diphosphate Kinases ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; metabolism ; Receptor, ErbB-2 ; metabolism ; Receptors, Progesterone ; metabolism ; Trefoil Factor-1 ; Tumor Suppressor Proteins ; metabolism

OBJECTIVETo study the expression and significance of interleukin-8 (IL-8), cyclooxygenase-2 (COX-2) and trefoil family factor 1 (TFF1) in the remnant stomach mucosa.

METHODSPatients after gastrectomy were examined by upper gastrointestinal endoscopy. Biopsy specimens were obtained from stoma and the greater curvature of the upper corpus to be assessed for Hp (by H.E. and Giemsa staining) and conduct real-time semi-quantitative PCR. mRNA was extracted from the biopsy specimens to determine the IL-8, COX-2 and TFF1 gene mRNA levels by real-time PCR method.

RESULTSIn the stoma, COX-2 level in Hp-positive patients was significantly higher than that in Hp-negative patients, but the difference of IL-8 levels between them was not significant. In the corpus, IL-8 and COX-2 levels in Hp-positive patients were significantly higher than those in Hp-negative patients. In Hp-negative patients, IL-8 and COX-2 levels in the stoma were significantly higher in B II anastomosis than in B I anastomosis cases; COX-2 level in the stoma was significantly higher in B II anastomosis than in B I anastomosis cases, but the difference of IL-8 levels between them was not significant. TFF1 level in the remnant stomach mucosa showed no significant difference between Hp-positive and Hp-negative patients.

CONCLUSIONHp infection and bile reflux are important risk factors for the secondary stomach carcinogenesis. Expression of IL-8 and COX-2 in the remnant stomach mucosa is related to the risk of secondary stomach carcinogenesis. The relationship between the TFF1 expression and secondary stomach carcinogenesis in the remnant stomach mucosa is still unclear and should further be studied.

Adult ; Aged ; Aged, 80 and over ; Cyclooxygenase 2 ; biosynthesis ; genetics ; Female ; Gastrectomy ; Gastric Mucosa ; metabolism ; Gastric Stump ; Helicobacter Infections ; metabolism ; Helicobacter pylori ; Humans ; Interleukin-8 ; biosynthesis ; genetics ; Male ; Middle Aged ; RNA, Messenger ; biosynthesis ; genetics ; Risk Factors ; Stomach Neoplasms ; metabolism ; microbiology ; surgery ; Trefoil Factor-1 ; Tumor Suppressor Proteins ; biosynthesis ; genetics

OBJECTIVETo explore the estrogenic activity and its mechanism of ethanol extract from black soybean (BSE).

METHODThe modified MCF-7 cell proliferation assay was used to evaluate the estrogenic activity of BSE. And the possible mechanisms were addressed using RT-PCR measurements in which pure estrogen receptor antagonist ICI182,780 was employed as a tool.

RESULTThe estrogenic activity of BSE at various concentrations (1-1000 microg x mL(-1)), expressed as proliferative effect (PE) relative to that of solvent control, was examined. The results indicated that, at low concentration range (10-200 microg x mL(-1)), BSE was able to induce MCF-7 cell growth with a maximum at 100 microg x mL(-1). The results of RT-PCR showed that pS2 and PR mRNA could be significantly induced by BSE in MCF-7 cells, which was relative to the concentration of BSE. Moreover, the specific estrogen receptor antagonist, ICI182,780 could block these reactions.

CONCLUSIONEthanol extract of black soybean can stimulate the growth of MCF-7 cells and increase the expression of estrogen receptor-responsive gene, suggesting that the estrogenic effects of BSE are mediated by the estrogen receptor.

Breast Neoplasms ; metabolism ; pathology ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; isolation & purification ; pharmacology ; Estradiol ; analogs & derivatives ; pharmacology ; Estrogen Receptor Modulators ; pharmacology ; Female ; Humans ; Plants, Medicinal ; chemistry ; RNA, Messenger ; biosynthesis ; genetics ; Receptors, Progesterone ; biosynthesis ; genetics ; Seeds ; chemistry ; Soybeans ; chemistry ; Trefoil Factor-1 ; Tumor Suppressor Proteins ; biosynthesis ; genetics

OBJECTIVETo investigate the expression of ER alpha in chemically induced, ER alpha-negative human breast cancer MDA-MB-435 cells and its restoration of the responsiveness to endocrine therapy.

METHODSMDA-MB-435 cells were treated with HDAC inhibitor trichostatin A(TSA)and DNMT1 inhibitor 5-AZA-CdR (AZA). The mRNA level of ER alpha, PR and PS2 in treated MDA-MB-435 cells was detected by RT-PCR. The WST-8 (water-soluble tetrazolium salt-8) method was used to analyze the proliferation rate of the cells. Xenograft in female nude mice was used to further explore the change of proliferation rate of treated MDA-MB-435 cells in vivo.

RESULTSAfter treatment with AZA and TSA, mRNA expression of ER alpha, PR and pS2 was up-regulated in MDA-MB-435 cells. The mRNA level of ER alpha was the hightest when MDA-MB-435 cells were treated with 2.5 micromol/L AZA and 100 ng/ml TSA. The treated MDA-MB-435 cells showed different proliferation rate in various media containing different concentration of estrodial. The MDA-MB-435 cells showed down-regulated proliferation rate after treatment with the combination of 2.5 micromol/L AZA and 100 ng/ml TSA, and 4-OH tamoxifen could suppress the growth rate of the induced MD-MBA-435 cells but not the untreated cells. The treated MDA-MB-435 cells showed slower proliferation rate than that of untreated cells in vivo (P <0. 01), and the proliferation rate of the treated MDA-MB-435 cells became lower when the nude mice were deprived of estrogen by castration (P <0. 01).

CONCLUSIONAfter treatment with TSA and AZA, ER alpha-negative MDA-MB-435 cells can express functional ER alpha and regain responsiveness to estrogen both in vitro and in vivo. HDAC inhibitor and DNMT1 inhibitor may play an important role in restoration of sensitivity of ER alpha-negative breast cancers to endocrine therapy.

Animals ; Azacitidine ; analogs & derivatives ; pharmacology ; Breast Neoplasms ; genetics ; pathology ; prevention & control ; Cell Line, Tumor ; Cell Proliferation ; drug effects ; DNA Modification Methylases ; antagonists & inhibitors ; Enzyme Inhibitors ; pharmacology ; Estrogen Receptor alpha ; genetics ; Female ; Gene Expression Regulation, Neoplastic ; drug effects ; Histone Deacetylase Inhibitors ; Humans ; Hydroxamic Acids ; pharmacology ; Mammary Neoplasms, Experimental ; genetics ; pathology ; prevention & control ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Ovariectomy ; RNA, Messenger ; biosynthesis ; genetics ; Receptors, Progesterone ; genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Trefoil Factor-1 ; Tumor Suppressor Proteins ; genetics ; Xenograft Model Antitumor Assays