ST6GALNAC4 promotes hepatocellular carcinogenesis by inducing abnormal glycosylation.

Hepatocellular carcinoma (HCC) is one of the most lethal tumor types worldwide. Glycosylation has shown promise in the study of tumor mechanisms and treatment. The glycosylation status of HCC and the underlying molecular mechanisms are still not fully elucidated. Using bioinformatic analysis we obtained a more comprehensive characterization of glycosylation of HCC. Our analysis presented that high glycosylation levels might correlate with tumor progression and poor prognosis. Subsequent Experiments identified key molecular mechanisms for ST6GALNAC4 promoting malignant progression by inducing abnormal glycosylation. We confirmed the contribution of ST6GALNAC4 to proliferation, migration, and invasion in vitro and in vivo. Mechanistic studies revealed that ST6GALNAC4 may be induced abnormal TGFBR2 glycosylation, resulting in the higher protein levels of TGFBR2 and TGF[Formula: see text] pathway increased activation. Our study also provided a further understand of immunosuppressive function of ST6GALNAC4 through T antigen-galectin3+ TAMs axis. This study has provided one such possibility that galectin3 inhibitors might be an acceptable treatment choice for HCC patients with high T antigen expression.

Determination of Organophosphorus Pesticides Using Solid-Phase Extraction Followed by Gas Chromatography-Mass Spectrometry.

In this study, a method was developed for determination of three organophosphorus pesticides (OPPs) using graphene aerogel solid-phase extraction (SPE) combined with gas chromatography-mass spectrometry (GC-MS). The experimental results showed that the target analytes could be extracted on packed SPE cartridges and then eluted with tetrahydrofuran. The final sample solution was analyzed by GC-MS, which demonstrated good linearity between 0.5 and 500 µg L-1 with a correlation coefficient (r) of 0.9991-0.9998. The limits of detection (S/N = 3) and the limits of quantification (S/N = 10) for the three OPPs ranged from 0.38 to 0.82 µg L-1 and 1.32 to 2.75 µg L-1, respectively. The accuracy of the proposed method was evaluated by measuring the recovery of the spiked samples, which ranged from 91.2 to 103.7%, with relative standard deviations of 2.1-7.2%. This method was successfully applied for the determination of the target analytes in water samples taken from tap, wetlands and canal water.

[The effect on apoptosis in anterior pituitary induced by cadmium chloride and its relations with caspase-9 pathway].

OBJECTIVE: To study the effects of cadmium chloride in anterior pituitary and the relation between apoptosis and expression of procaspase-9 mRNA. METHODS: In vivo studies:40 SD male rats were randomly distributed into four groups which were administered with CdCl2 at different doses by gavage for 6 weeks; IN VITRO STUDIES: the rats' anterior pituitary cells were primarily cultured for 120 hours, then treated with CdCl2 at the dose of 0, 1.56, 3.12, 6.25, 12.50, 25.00, 50.00, 100.00 micromol/L for 6 hours; The indices included: expression of procaspase-9 mRNA, detection of apoptosis with TUNEL assay. RESULTS: The results showed the excretion of ACTH, LH seemed to be decreased dramatically and the apoptosis inclined to enhance remarkably, and further more, the expression of procaspase-9 mRNA appeared to be increased significantly as compared with those of the control. It was show that a dose-effect relationship between the CdCl2 dosing and indices above with the regression analysis and a linear correlation between the mean gray value of apoptosis cell and the relative gray value of procaspase-9 mRNA positive cell. The results indicated that damnification, for example, apoptosis could be caused by certain dose of CdCl2 in anterior pituitary cells with dose dependent manner. Caspase-9 might play a role in the occurrence of apoptosis. CONCLUSION: It was suggested that cadmium could induce apoptosis of anterior pituitary both in vivo and in vitro in the manner of dose-dependent, and caspase-9 might play a role during above processes.