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An indoor exposure experiment with juvenile Babylonia areolata was conducted to study its survival, growth, cadmium (Cd) accumulation, metallothionein (MT) induction, and glycogen content as well as the DNA integrity of hepatopancreas tissue. The juveniles were starved or fed with mussel (Perna viridis) or clamworm (Perinereis aibuhitensis), and exposed to 50 μg·L-1 of Cd2+ for 10 weeks. Prolonged starvation and simultaneous exposure to Cd reduced the survival rate of B. areolata, and its glycogen was mobilized in great extent. Feeding with P. viridis or P. aibuhitensis helped the B. areolata to combat Cd toxicity and lessen mortality. After exposed to Cd, the damage of the DNA integrity of hepatopancreas tissue for the B. areolata fed with P. viridis or P. aibuhitensis could be recovered with time, but not for the starved B. areolata. Prolonged starvation caused tissue atrophy and led to Cd accumulation and MT increase, while feeding with P. viridis or P. aibuhitensis increased the B. areolata mass and lowered the Cd accumulation and MT level because of the tissue dilution effect. The B. areolata fed with P. viridis had better growth and lower Cd content than that fed with P. aibuhitensis. This study indicated that starvation intensified the toxicity of Cd to B. areolata, while prey type had significant effects on the growth rate of the B. areolata and indirectly affected its Cd accumulation, MT induction, and glycogen consumption. It was suggested that when using gastropods such as B. areolata as the indicator species to monitor marine environmental pollution, it would be necessary to consider the effects of habitat ecological data including food richness and prey type. Moreover, in the high-density cultivation of B. areolata in factory, rational feeding and periodic measurement of Cd concentration in seawater should be made. [ABSTRACT FROM AUTHOR]

Objective: To investigate the role of long non-coding RNA growth arrest-specific transcript 5 (lncRNA-GAS5) in breast cancer progression and epithelial-mesenchymal transition (EMT) of the cancer cells., Methods: Real-time quantitative PCR (qRT-PCR) was used to detect the expression of lncRNA-GAS5 in 37 pairs of breast cancer and adjacent non-tumor tissues and in parental MCF-7 cells and paclitaxel-resistant MCF-7 (MCF-7/PR) cells, and the correlation of lncRNA-GAS5 expression with the clinical stage and lymph node metastasis of breast cancer was investigated. The expressions of the genes related with cell cycle and EMT at both the mRNA and protein levels were detected using qRT-PCR, Western blotting and immunohistochemistry. The changes in the biological behaviors and morphology of breast cancer cells with either lncRNA-GAS5 knockdown or overexpression were observed. Nude mouse models were established bearing breast cancer xenografts derived from MCF-7/PR cells or MCF-7/PR cells over-expressing lncRNA-GAS5, and the inhibitory effect of paclitaxel on tumor growth was evaluated., Results: The transcriptional levels of lncRNA-GAS5 were significantly lower in breast cancer tissues than in the adjacent non-tumor tissues (P<0.05), and decreased lncRNA-GAS5 expression was significantly correlated with TNM stage and lymph node metastasis of breast cancer (P<0.05). lncRNA-GAS5 expression was also significantly lowered in paclitaxel-resistant breast cancer cells and showed a positive correlation with P21 expression and a negative correlation with CDK6. MCF-7 cells during EMT presented with a lowered expression of lncRNA-GAS5, whereas lncRNA-GAS5 over-expression strongly suppressed MCF-7/PR cell migration and invasion, and increased the susceptibility of the cells to paclitaxel. In the tumor-bearing nude mouse models, lncRNA-GAS5 overexpression in the tumor cells obviously enhanced the inhibitory effect of paclitaxel on tumor growth and lung metastasis by reversing the EMT marker proteins., Conclusion: A decreased expression of lncRNA-GAS5 promotes lung metastasis of breast cancer by inducing EMT, suggesting the potential of lncRNA-GAS5 as a therapeutic target in breast cancer.

An indoor exposure experiment with juvenile Babylonia areolata was conducted to study its survival, growth, cadmium (Cd) accumulation, metallothionein (MT) induction, and glycogen content as well as the DNA integrity of hepatopancreas tissue. The juveniles were starved or fed with mussel (Perna viridis) or clamworm (Perinereis aibuhitensis), and exposed to 50 microg x L(-1) of Cd2+ for 10 weeks. Prolonged starvation and simultaneous exposure to Cd reduced the survival rate of B. areolata, and its glycogen was mobilized in great extent. Feeding with P. viridis or P. aibuhitensis helped the B. areolata to combat Cd toxicity and lessen mortality. After exposed to Cd, the damage of the DNA integrity of hepatopancreas tissue for the B. areolata fed with P. viridis or P. aibuhitensis could be recovered with time, but not for the starved B. areolata. Prolonged starvation caused tissue atrophy and led to Cd accumulation and MT increase, while feeding with P. viridis or P. aibuhitensis increased the B. areolata mass and lowered the Cd accumulation and MT level because of the tissue dilution effect. The B. areolata fed with P. viridis had better growth and lower Cd content than that fed with P. aibuhitensis. This study indicated that starvation intensified the toxicity of Cd to B. areolata, while prey type had significant effects on the growth rate of the B. areolata and indirectly affected its Cd accumulation, MT induction, and glycogen consumption. It was suggested that when using gastropods such as B. areolata as the indicator species to monitor marine environmental pollution, it would be necessary to consider the effects of habitat ecological data including food richness and prey type. Moreover, in the high-density cultivation of B. areolata in factory, rational feeding and periodic measurement of Cd concentration in seawater should be made.

Objective: To study the expression of aquaporin-1 (AQP-1) in pleural mesothelial cells (PMCs) and the influence of hypertonic medium thereupon., Methods: Rat PMCs were isolated, cultured, and divided into 2 groups: hypertonic group, cultured in hypertonic media with NaCl of different concentrations for 24 h and control group, cultured in D-MEM/F-12 medium. The 100 mmol/L NaCI group was examined at the time points 6, 12, 18, and 24 h respectively. RT-PCR and Western blotting were used to analyze the mRNA and protein expression of AQP-1., Results: The A values of AQP-1 protein expression were 24.0 +/- 1.8, 27.8 +/- 2.4, 31.7 +/- 2.5, 89.7 +/- 6.2, and 107.7 +/- 9.3 respectively in the PMCs treated with hypertonic media with NaCl of the concentrations of 25, 50, 75, 100, and 150 mmol/L, all significantly higher than that in the control group (10.8 +/- 1.5, all P < 0.01). The A values of AQP-1 protein expression were 42.1 +/- 2.6, 78.9 +/- 3.6, 109.6 +/- 7.6, and 123.4 +/- 8.7 in the PMCs treated with hypertonic media with NaCl of the concentration of 100 mmol/L after 6 h, 12 h, 18 h, and 24 h, all significantly higher than that in the control group (12.9 +/- 1.9, P < 0. 01). The a values of AQP-1 mRNA expression were 62.6 +/- 6.4, 75.3 +/- 5.5, 122.3 +/- 11.4, 196.2 +/- 18.1, and 223.0 +/- 19.3 respectively in the PMCs treated with hypertonic media with NaCl of the concentrations of 25, 50, 75, 100, and 150 mmol/L, all significantly higher than that in the control group (23.5 +/- 2.7, all P < 0.01). The A values of AQP-1 protein expression were 83.6 +/- 6.1, 159.3 +/- 6.9, 266.2 +/- 24.1, and 196.2 +/- 15.7 in the PMCs treated with hypertonic media with NaCl of the concentration of 100 mmol/L after 6 h, 12 h, 18 h, and 24 h, all significantly higher than that in the control group (26.5 +/- 2.8, P < 0.01)., Conclusion: Hypertonic medium increases the expression of AQP-1 mRNA and protein. AQP-1 participates in the pleural fluid formation.