[Prostatic cystadenoma: a case report and review of the literature].

OBJECTIVE: To study the clinicopathological characteristics of prostatic cystadenoma (PC). METHODS: A sample from surgically removed tissues of a PC patient was examined by conventional pathology and immunohistochemistry. The clinical data and clinicopathological features were analyzed, and the related literature reviewed. RESULTS: The patient was a male aged 55 years, treated by TUVP for dysuria a year before. The tumor was a grey mass, with lots of different sized capsular spaces full of clear white liquid in the cross section. Histologically, the tumor cells were arranged in a sieve-like, microcapsule-shaped or adenoid pattern, lined with cuboidal and columnar epithelial cells, the nuclei located in the base with neither cellular atypia nor mitosis. Concerning the immunophenotype, PSA, PAP and CK7 were positively expressed in the columnar epithelial cells and 34betaE12 in the basal cells, while CK20, P504S, CEA and villin were negatively expressed, with Ki67 + < 2%. CONCLUSION: Prostatic cystadenoma is a rare benign tumor originating in the prostate, with a unique morphological structure, and mostly with the expressions of PSA and PAP.

[Effects of Ginsenoside RB1 on neural cell apoptosis and expressions of Bcl-2 and Bax in rats following subjected to cerebral ischemia-reperfusion].

OBJECTIVE: To observe the effects of Ginsenoside Rb1 (GRb1) on neuronal cell apoptosis and the expressions of Bcl-2 and Bax in rats after cerebral ischemia-reperfusion so as to investigate the neuroprotective mechanism of GRb1. METHDOS: The model of cerebral ischemia-reperfusion was established by occluding rat middle cerebral artery for 2 h. The rats were randomly divided into two groups: ischemia-reperfusion group (I/R group) and GRb1 treat group (GRb1 group). GRb1 (40 mg/kg, i.p.) was administered immediately to rats after the onset of reperfusion. Two groups were further subdivided 7 subgroups according to various reperfusion time (3 h, 12 h, 1 d, 2 d, 3 d, 5 d and 10 d, n=4 per time point). HE staining was used to observe histological features. TUNEL and immunohistochemical method were used to analyze the cell apoptosis and expressions of Bcl-2 and Bax, respectively. RESULTS: Compared with I/R group, GRb1 reduced pathological changes, and decreased the number of apoptotic neural cells (P<0.05 on 12 h, 1 d, 2 d and 3 d) and up-regulated the number of Bcl-2 positive cells (P<0.05 on 12 h, 1 d, 3 d, 5 d and 10 d), and meanwhile down-regulated the number of Bax positive cells (P<0.05 on 3 h, 12 h, 1 d, 2 d, 3 d, 5 d and 10 d) in the ipsilateral hemisphere. CONCLUSION: The neuroprotective effect of GRb1 on cerebral ischemia-reperfusion injury is related to inhibit neuronal apoptosis and to up-regulate the expression of Bcl-2 with down-regulating the expression of Bax.

Juglanin induces apoptosis and autophagy in human breast cancer progression via ROS/JNK promotion.

Breast cancer is one of the most common primary malignant tumors of among women, the long-term survival of which has stagnated in the past decades. Juglanin as a natural production mainly extracted from green walnut husks of Juglans mandshurica has been defined as the functional composition among a series of compounds. It showed powerful protective effect in various diseases by inhibiting inflammation and tumor cells growth. However, the effect of juglanin on human breast cancer and the underlying mechanisms remains to be elucidated. We reported here that juglanin could inhibit cell proliferation by leading to G2/M phase arrest. Exposure to juglanin resulted in the activation of cleaved caspase -3, -8, and -9, indicating that juglanin induced apoptosis. Autophagy occurred in juglanin-treated cells as evidenced by formation of autophagosome and up-regulation of LC3B-II. The juglanin-induced cell death was significantly restored by the combination of autophagy and apoptosis. Further, juglanin also induced JNK activation and ROS production. The JNK inhibitor attenuated juglanin-caused apoptosis and autophagy significantly while ROS scavenger could reverse them. In addition, the ROS scavenger also inhibited G2/M phase arrest and phosphorylated JNK. Of note, we found that juglanin had the similar effects on breast cancer cells. Finally, juglanin inhibited tumor growth in the mouse xenograft model in vivo. Together, our results suggested that juglanin led to G2/M phase arrest, induced apoptosis as well as autophagy through the ROS/JNK signaling pathway in human breast cancer cells. Hence, juglanin might be a promising candidate for development of anti-tumor drugs targeting breast cancer.

MiR-886-5p inhibition inhibits growth and induces apoptosis of MCF7 cells.

BACKGROUND AND AIMS: To explore the molecular mechanisms of miR-886-5p in breast cancer., we examined roles in inhibiting growth and migration of MCF-7 cells. METHODS: MiR-886-5p mimics and inhibitors were used to express or inhibit MiR-886-5p, respectively, and MTT and clone formation assays were used to determine the survival and proliferation. Hoechst 33342/ PI double staining was applied to detect apoptosis. The expression of caspase-3, caspase-8, caspase-9, MT1-MMP, VEGF-C and VEGF-D was detected by Western blotting, and the levels of MMP2 and MMP9 secreted from MCF-7 cells were assessed by ELISA. MCF-7 cell migration was determined by wound healing and Transwell assays. RESULTS: We found that the growth of MCF-7 cells was inhibited upon decreasing miR-886-5p levels. Inhibiting miR-866-5p also significantly induced apoptosis and decreased the migratory capacity of these cells. The expression of VEGF-C, VEGF-D, MT1-MMP, MMP2, and MMP9 was also found to be decreased as compared to controls. CONCLUSIONS: Our data show that downregulation of miR-886-5p expression in MCF-7 cells could significantly inhibit cell growth and migration. This might imply that inhibiting miR-886-5p could be a therapeutic strategy in breast cancer.