1.Early nutritional support in brain operation patients
Wenxin YANG ; Zhengjiang ZHONG ; Hong SHEN ; Huaiyi ZHAN ; Xiaomei CHENG ; Xingxin HU
Parenteral & Enteral Nutrition 2004;0(06):-
0.05) between two groups. Abdominal distention and diarrhea occurred in 6 patients in observed group. Nitrogen balance, PA, TFN, IgA, IgG and IgM after nutritional support were better than those before nutritional support in two groups. Nitrogen balance, PA, TFN, IgA, IgG and IgM were better in observed group than those in the control group. Conclusions:Early nutritional support can improve metabolic status,the immune function and the nitrogen balance in brain operation patients.
2.Stable inhibition of human prion protein through a retrovirus-based RNAi system.
Wenjing XU ; Di WANG ; Juan WANG ; Huaiyi YANG
Chinese Journal of Biotechnology 2009;25(7):1022-1027
Prion leads to fatal transmissible spongiform encephalopathies. Cellular prion protein (PrPc) is necessary in prion disease. At present, it is demonstrated that PrPc plays a protective role in several carcinomas, such as gastric and breast cancer. We designed four 19-nt siRNAs according to cDNA sequence of human PrPc and constructed retrovirus-based RNAi vectors. We evaluated the inhibitive effect of these sequences on HuPrPc (human PrPc) and selected out three sequences with stable and efficient inhibition. And the efficiency of si626 reached more than 85%, which effect was significant. Next, we performed cell invasion assays of PC3M-si292 and PC3M-si626 in which PrPc was inhibited. And it showed that the cell invasive ability decreased in PrPc knock-down cell lines. This will make preparations for the further research on gene therapy of prion diseases and PrPc related carcinoma treatment and PrPc could be considered as a potential therapeutic target molecule in prostate cancer treatment.
Base Sequence
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Cell Line, Tumor
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DNA, Complementary
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genetics
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Genetic Therapy
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Humans
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Male
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Molecular Sequence Data
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PrPC Proteins
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biosynthesis
;
genetics
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Prostatic Neoplasms
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drug therapy
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RNA Interference
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RNA, Small Interfering
;
genetics
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Retroviridae
;
genetics
3.11'-Deoxyverticillin A induces caspase-dependent cell apoptosis in PC3M cells.
Yingdi SHI ; Yingqiu ZHANG ; Yangxiao NI ; Guoli SHI ; Huaiyi YANG
Chinese Journal of Biotechnology 2012;28(1):96-103
Recent years, the incidence and mortality of prostate cancer have increased dramatically in China. At earlier stages, most diagnosed prostate cancers are responsive to androgen depletion treatment, yet, nearly all patients will eventually progress to metastatic androgen-independent prostate cancer (AIPC), which still has no effective therapeutic method or drug to deal with. 11'-Deoxyverticillin A (C42) belongs to the family of epipolythiodioxopiperazines (ETPs), an interesting class of fungal toxins that inhibit farnesyl transferase. Compounds holding such a property have been explored as putative anticancer agents. In this study, using PC3M cells, an AIPC cell line, we investigated the effect of the compound on apoptosis and explored the underlying mechanism. It revealed that C42 markedly enhanced the activity of caspase-3/7 and increased the accumulation of the cleaved PARP, all of which are the markers of apoptosis. It also revealed that C42 either decreased cell viability or inhibited the growth of PC3M cells. Moreover, we observed that the loss of cell viability and cell growth inhibition induced by C42 were both time- and dosage dependent. Taken together, we indicated that C42 can induce caspase-dependent apoptosis in AIPC cells, and the results presented here will broaden our knowledge about the molecular mechanisms by which C42 exerts its anticancer activity, and future work in this direction may provide valuable information in the development of these compounds into effective cancer therapeutic strategies against androgen-independent prostate cancer.
Apoptosis
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drug effects
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Caspase 3
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metabolism
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Caspase 7
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metabolism
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Cell Line, Tumor
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Disulfides
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pharmacology
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Farnesyltranstransferase
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antagonists & inhibitors
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Humans
;
Male
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Mycotoxins
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pharmacology
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Piperazines
;
pharmacology
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Prostatic Neoplasms
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pathology