Intragastric administration of interferon-α-transformed Bifidobacterium promotes lymphocyte proliferation and maturation in mice / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effects of intragastric administration of human interferon-α (hIFN-α)-transformed Bifidobacterium on immune functions of mice.</p><p><b>METHODS</b>The E.coli-Bifidobacterium shuttle expression vector containing hIFN-α gene was constructed and transformed into Bifidobacterium. The hIFN-α-transformed Bifidobacterium suspension (1010 /ml) was prepared after induction with 0.2% L-arabinose for hIFN-α expression and administered intragastrically in male Balb/C mice at the dose of 0.1 ml every other day for 2 weeks, with the mice receiving empty vector-transformed Bifidobacteria as the negative control and those having an equal volume of saline as the blank control. The percentages of mononuclear cell subsets in the thymus, spleen and blood were detected in the mice by flow cytometry, and the serum levels of IL-4, IL-12, IFN-γ and TNF-α were assayed using mouse cytokine FlowCytomix Kit.</p><p><b>RESULTS</b>The percentages of CD3⁺CD8⁺ and CD4⁺CD8⁺ cells in the thymus, CD3⁺CD4⁺, CD3⁺CD8⁺ and CD4⁺CD8⁺ cells in the spleen, and CD3⁺CD8⁺ cells in the blood all increased significantly in IFN group as compared with those in the negative and blank control groups (P<0.01 or 0.05). The serum level of IFN-γ also increased significantly (P<0.05) while IL-4 level remained unchanged in IFN group compared with those in the two groups.</p><p><b>CONCLUSION</b>Intragastric administration of hIFN-α-transformed Bifidobacterium promotes lymphocyte proliferation and maturation and increases the serum levels of Th1 cytokines in mice.</p>

BRCA1 inhibits progesterone-induced proliferation and migration of breast cancer cells / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the effect of BRCA1 in regulating the proliferation and migration of breast cancer cells stimulated by progesterone.</p><p><b>METHODS</b>Breast cancer MCF-7 and T-47D cell were transfected with a vector containing the coding sequence of BRCA1 (pFlag-CMV2-BRCA1 wt) to induce BRCA1 overexpression or with the empty vector (control). The cells were then stimulated with progesterone, and the cell proliferation and migration were observed using MTT assay and wound healing assay, respectively. The proliferation and migration of MCF-7 cells were also observed following transfection with a small interfering RNA (siRNA) for BRCA1 knockdown or with a scrambled siRNA prior to progesterone stimulation.</p><p><b>RESULTS</b>Transfection with the empty vector and with pFlag-CMV2-BRCA1 wt prior to progesterone stimulation caused significantly different proliferation rates in MCF-7 cells [(114.4∓6.0)% vs (82.1∓3.2)%, P<0.05] and in T-47D cells [(111.3∓4.3)% vs (84.2∓3.5)%, P<0.05], resulting also in significantly different cell migration rates (55.9% vs 15.8% in MCF-7 cells and 44.83% vs 10.43% in T-47D cells). Compared to the scrambled siRNA, BRCA1 siRNA transfection prior to progesterone stimulation significantly increased the proliferation rates [(114.4∓3.05)% vs (125.3∓4.0)%, P<0.05] and migration rate (39.2% vs 69.08%) of MCF-7 cells. The progesterone antagonist RU468 could antagonize the effects of BRCA1 knockdown in enhancing progesterone-stimulated MCF-7 cell proliferation and migration.</p><p><b>CONCLUSION</b>A decreased BRCA1 expression can enhance progesterone-stimulated tumor cell proliferation and migration in sporadic breast cancer.</p>

Correlation between the axillary lymph node metastasis of patients with breast cancer and the expression of estrogen receptor,progesterone receptor and Her-2 in tumor tissue / 解放军医学杂志

0.05). The positive rate of ER expression was lower in young age-group than in the other two groups,the differences among the three groups was statistically significant (P0.05). The rate of Her-2 expression was higher in young age-group than in both middle age-and elderly-group (P

Study on the apoptosis of gastric cancer cells SGC-7901 induced by DHA and its mechanism / 中国海洋药物

Objective To investigate the inhibitory effect of DHA and its mechanism of apoptosis induced by DHA on human gastric cancer cell SGC-7901.Methods The survival rate of tumor cells was evaluated by MTT assay,cell morphology of apoptotic cell was observed with Hoechest 33258 staining.The contents of MDA and GSH were measured respectively by TBA and DTNB assay.Flow cytometry was used to detect the rate of apoptotic cell and intracellular variation of ROS level.Results After being treated with different concentrations of DHA,the survival rate of tumor cells was decreased in a dose-dependent manner and apoptosis was induced.The morphological characterizes of apoptotic cells were chromatin condensation and formation of apoptotic bodies.Intracellular MDA content was increased in the treated cells compared with control group,whereas GSH was decreased.After treated with 80 ?mol?L-1 DHA 5 h,flow cytometic analysis showed ROS peak and NAC could block the generation of ROS.Conclusion DHA can inhibit the growth of human gastric cancer cell SGC-7901 via inducing apoptosis.The increase of lipid peroxidation production and ROS may play an important role in apoptosis of the cells.