الملخص
Objective @#To investigate the effects of C-type lectin domain family 5，member A( CLEC5A) on the pro- liferation，apoptosis，and cell cycle of leukemia cell lines THP-1 and K562，and the underlying mechanism．@*Methods @#The expression of CLEC5A in leukemia patients was investigated in the GEPIA database. Recombined plasmid containing CLEC5A was transfected into THP-1 and K562 cells for overexpression of CLEC5A．Small interfering RNA(siRNA) was used to knock down the endogenous CLEC5A in leukemia cells．CCK-8 and EdU assays were used to assess the leukemia cells proliferation．Flow cytometry was used to assess cell cycle．Flow cytometry was used to assess cell apoptosis under hydrogen peroxide( H2 O2 ) stress．The RNA sequencing( RNA-seq) and pathway enrichment analysis were used to analyze the signal pathways of significant enrichment of up-regulated or down-reg- ulated genes after knocking down CLEC5A gene．Protein expression levels of several members in AKT1 / mTOR and p53 signaling pathways were detected by Western blot assays. @*Results @#CLEC5A was significantly up-regulated in bone marrow tissues of leukemia patients compared to the matched non-tumor tissues of healthy individuals．Knock- down of CLEC5A significantly reduced the proliferation(all P＜0. 01) and S phase progression(all P＜0. 05) ，and increased the apoptosis(all P＜0. 001) under H2 O2 stress，in THP-1 and K562 cells．Conversely，overexpression of CLEC5A significantly increased the proliferation(all P ＜0. 001) and S phase progression ( all P ＜0. 01) ，and re- duced the apoptosis(all P＜0. 01) under H2 O2 stress，in THP-1 and K562 cells．The uregulated genes were sig- nificantly enriched in AKT1-mTOR and other signal pathways after knocking down CLEC5A，while the down-regula- ted genes were significantly enriched in cell cycle signal pathways．CLEC5A in leukemia cells significantly reduced the genes expression levels of BAX and p53，and significantly induced the gene expression levels of BCL-2 and phosphorylation levels of AKT1 and mTOR proteins．@*Conclusion @#CLEC5A increases the cell cycle and proliferation and inhibits cells apoptosis in THP-1 and K562 cells，and the mechanism may be related to activating the AKT / mTOR and p53 signaling pathways.
الملخص
Objective To investigate the effect of soybean isoflavone on histology and uhrastructure of benign prostatic hyperplasia in rats.Methods Male SD rats were injected subcutaneously testosterone propionate for 28 d to induce prostatic hyperplasia,and the rats were divided into 5 groups:control group,model group,and 3 test groups with SI in a dose of 60 mg/(kg·d),120 mg/(kg·d) and 240 mg/(kg·d),respectively.The wet prostate weight,prostatic index,morphological,uhrastmetural and morphometrie changes of the prostatic shndular and interstitial tissues were observed.Results The prostate wet weight,prostatic index and prostatic volumes in all dose groups were significantly lower than those in the models.In comparison with the model group,height of prostatic epithelial cells,glandular average diameters,volumes and surface areas in unit volume,as well as glandular circumferences,glandular relative total volumes and interstitial relative total volumes were all significantly decreased.Glandular counts,density,ratio of glandular surface area to volume,and glandular average curvature were all increased.Conclusions Soybean isoflavone can inhibit prostatic hyperplasia in rats.
الملخص
Objective To study the clinicopathological and immunohistochemical features, histogenesis and biological behavior of solid pseudopapillary tumor of the pancreas ( SPT ). Methods Routine HE and immunohistochemical ( SP) methods were used in 20 cases of SPT. Results There were 18 females and 2 males, age ranging from 13 to 48 years with mean age of 25. 3 years. Abdominal pain and palpable mass were among the main complains. Seventeen cases were followed-up from 9 to 120 monthes. Fourteen cases were alive. Tumors were encapsulated, mixed with solid and cystic tissues. Histological features were psudopapillary structure with a fibrovascular core. Immunohistogically, the tumors were positive for a-1-AT ( 17 cases) , vimentin ( 14 cases) , synaptophysin ( 10 cases) , CgA (5 cases) ,CK and insulin (2 cases) ,glucagon and S-100 (1 case) ,PR (14 cases) , ER (1 case) ,pS2 (6 cases) , but all were negative for CEA and gastrin. Conclusion SPT is of low-graded malignancy and a distinct clinicopathologic entity in young female patients with both exocrine as well as endocrine differentiation. The tumor is closely related with sex hormone receptors.
الملخص
Objective To investigate the effect of equol on ERK mediated signal transduction pathway and to clarify its mechanism of proliferation inhibition on human ovarian carcinoma cell line SKOV-3. Method SKOV-3 cells were treated with 10-8,10-7,10-6,10-5,5?10-5,10-4 mol/L equol for 24,48 and 72h. After pretreatment with 10 ?mol/L U0126 an ERK signaling pathway inhibitor or ICI182,780,estrogen receptor inhibitors for 1h,then treatment with 50 ?mol/L equol for 2h,the cell viability was examined and the expressions of ERK and p-ERK protein were determined using Western blotting. Results Equol was demonstrated to inhibit SKOV-3,proliferation time-and dose-dependently. The expression of p-ERK protein was decreased in dose-dependent manner,while the expression of total ERK was unchanged. Both the single use of U0126,or ICI182,780,and combined with equol could decrease the expression of p-ERK protein. Conclusion Equol could inhibit proliferation in ovarian carcinoma cell lines SKOV-3. Its inhibitory effect appears to be due to down-regulation of p-ERK protein.