Tumour budding is a novel marker in breast cancer: the clinical application and future prospects.

Breast cancer (BC) is a group of markedly heterogeneous tumours. There are many subtypes with different biological behaviours and clinicopathological characteristics, leading to significantly different prognosis. Despite significant advances in the treatment of BC, early metastatic is a critical factor for poor prognosis in BC patients. Tumour budding (TB) is considered as the first step process of tumour metastasis and is related to the epithelial-mesenchymal transition (EMT). TB has been observed in a variety of cancers, such as colorectal and gastric cancer, and had been considered as a distinct clinicopathological characteristics for early metastasis. However, TB evaluation standards and clinical application are not uniform in BC, as well as its molecular mechanism is not fully understood. Here, we reviewed the interpretation criteria, mechanism, clinicopathological characteristics and clinical application prospects of TB in BC. Key messagesCurrently, tumour budding is a poor prognosis for various solid tumours, also in breast cancer.Tumour budding is based on epithelial-mesenchymal transition and tumour microenvironment factors and is presumed to be an early step in the metastatic process.Breast cancer tumour budding still needs multi-centre experiments. We summarize the current research on breast cancer tumour budding, analyse the method of discriminating breast cancer tumour budding and explore the prognostic role and mechanism in breast cancer.

Cadmium induces ovarian granulosa cell damage by activating PERK-eIF2α-ATF4 through endoplasmic reticulum stress.

This study aimed to investigate whether cadmium induces ovarian granulosa cell damage by activating protein kinase R-like endoplasmic reticulum kinase (PERK)-eIF2α-ATF4 through endoplasmic reticulum (ER) stress and to elucidate the underlying regulation mechanism. Two models of cadmium exposure were established. In one model, ovarian granulosa cells isolated from 21-day-old female Sprague Dawley rats were cultured in vitro for 36 h and exposed to CdCl2 (0, 5, 10, and 20 µM), and in another model, a human ovarian granulosa tumor cell line (COV434) was used to construct the binding immunoglobulin protein (BIP)-knockdown cell line sh-BIP and exposed to 0 and 20 µM CdCl2. After exposure to cadmium for 12 h, the expression mRNA and protein levels of BIP, p-PERK, and p-eIF2α were determined in the two models. miRNAs related to BIP were also detected in granulosa cells after cadmium exposure. We found that mRNA and protein levels of all factors were upregulated in each cadmium-dose group, except for BIP mRNA expression in the 5 µM Cd group. The BIP gene was knocked down in COV434 cells before exposure to cadmium. All factors were upregulated in COV434 cells exposed to Cd, and the expression of the p-eIF2α protein was downregulated in sh-BIP cells exposed to Cd. In addition, no differences in BIP-related miRNAs were detected in cadmium-exposed rat ovarian granulosa cells versus the control group. Cadmium induces ovarian granulosa cell damage by inducing ER stress.

N-hexane alters the maturation of oocytes and induces apoptosis in mice.

OBJECTIVE: This study was aimed to determine the effects of n-hexane on the maturation of mouse oocytes. METHODS: Cell culture was used to observe the maturation of mouse oocytes and CLSM was employed to determine their apoptosis. RESULTS: Germinal vesicle breakdown (GVBD) and extrusion of the first polar body in mouse oocytes were significantly inhibited by n-hexane. After fertilization, the number of eggs in the mouse was significantly reduced by n-hexane. Mitochondrial membrane potentials (ΔΨm) were altered in mouse oocytes that were leading to apoptosis of the oocytes. CONCLUSION: N-hexane might have affected the maturation of oocytes, causing alteration of ΔΨm and leading to apoptosis which maybe one of the most important mechanisms.

[Efficiency and yeast community structure of oil-containing treatment system inoculated by different yeast strains complex wastewater].

Ten yeast stains were grouped and applied in pilot-scale sequencing batch reactors to treat oil-containing wastewater. The efficiency and stability of different reactors were discussed and yeast community structure was investigated by PCR-DGGE method. The results show: the group consisting of O2, G1 and W1 is markedly superior to others in efficiency and stability respects; the group absence of these 3 stains fails to form a system with high efficiency and good stability; O4 and G2 strains lead to turbid supernatant fluid and are eliminated from system step by step; the distribution of yeast cells in settlement sludge varies with different stains. When aeration is stopped, G1 deposits into lower layer but O2 or W1 distributes evenly.

[Effects of nitrogen on performance and yeast morphology of yeast-SBR system].

Effects of nitrogen on yeast cell morphology, settleability and performance of wastewater treatment were investigated in treating oil-containing wastewater by yeast-SBR system. The results show that: nitrogen supply affects directly yeast biomass, settleability, pH and treatment efficiency of system; the absence of nitrogen induces the transformation of certain yeast cells from single cell to hypha morphology. Based on an overall consideration of efficiency and stability of yeast-SBR system, the optimum BOD/N ratio of influent is 20/1. The optimum nitrogen supply can improve wastewater treatment efficiency of systems with different degrees of nitrogen absence and make yeast morphology become the predominant morphology for slightly mycelial system over a short time, but for severe mycelial system, the hypha morphology still keeps dominant.

[Effects of selenium on benzo[a] pyrene-induce DNA damage in mouse lung cells].

OBJECTIVE: To explore the effects of selenium on DNA damage induced by benzo[a] pyrene (BaP) in mouse lung cells. METHODS: Sodium selenite was given to Kunming male mice by i.p. and BaP was given by oral gavage. The control group was given solvent only with the same method. DNA damage was detected by single cell gel electrophoresis (or comet assay). RESULTS: The damage degrees in mice treated with 125, 250 and 500 mg/kg of BaP were more severe than that of control (P < 0.01). The rates of comet cells in the BaP-treated groups (43.50%, 84.00%, 95.63%) were significantly higher than that of control (9.75%, P < 0.01), and there was obvious dose-response relationship. 0.75, 1.50 and 3.00 mg/kg of sodium selenite presented antagonistic effects against DNA damage induced by 250 mg/kg of BaP in mouse's lung cells. The antagonistic effect of sodium selenite at the dose of 1.50 mg/kg was better than those of sodium selenite at the doses of 0.75, 3.00 mg/kg. CONCLUSION: BaP at the doses of 125 approximately 500 mg/kg could significantly induce DNA damage of lung cells in mice. 0.75 approximately 3.00 mg/kg of sodium selenite could inhibit DNA damage of lung cells in mice induced by 250 mg/kg of BaP.

[Effect of soybean isoflavone on the cognitive function in ovariectomized mice].

OBJECTIVE: To explore the effect of soybean isoflavone on the cognitive function in ovariectomized mice and to study the cognitive function mechanism of soybean isoflavone. METHODS: Forty-five Kunming female mice were randomly assigned into 5 groups: A (sham operated); B (ovariectomized, OVX); C (OVX + low dose soybean isoflavone); D (OVX + moderate dose soybean isoflavone); and E (OVX + high dose soybean isoflavone). The experiment lasted 60 days. RESULTS: Ovariectomy significantly elongated the destination time of water maze, shortened the latent time of step-down test, decreased SOD of serum and Na+ K+ -ATPase and Ca2+ Mg2+ -ATPase of brain, and increased malonaldehyde of serum and monoamine oxidase of brain, which-could be inhibited by soybean isoflavone consumption. CONCLUSION: The continuous oral administration of soybean isoflavone can improve the cognitive function of ovariectomized mice.