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Long non-coding RNAs (lncRNAs) are members of RNA that are structurally similar to mRNA. They cannot encode proteins because they do not have a conserved open reading frame. LncRNAs were once regarded as abnormalities or noises or without any biological function after gene transcription. With the further development of research, it has been found that it can participate in normal or abnormal biological processes as an important regulator. LncRNAs are closely related to the development of nervous system function, metabolic disorders and tumors. LncRNAs abnormally expressed in cervical cancer participate in the regulation of various biological processes of cervical cancer by inhibiting or promoting tumors. This article reviews the recent reports on the abnormal regulation, molecular regulation mechanism and potential clinical application of lncRNAs in cervical cancer.
Subject(s)
Female , Humans , RNA, Long Noncoding , RNA, Messenger , Uterine Cervical Neoplasms , GeneticsABSTRACT
This paper is aimed to present a research on fusion protein of human tumor necrosis factor-alpha (hTNF-alpha), matrix metalloproteinase 1 (MMP1), and foldon sequence using the methord of gene engineering. We transformed the recombinant plasmid, which contains the DNA sequences of hTNF-alpha, MMP1, and foldon sequence, into Rosetta2, and successfully induced the fusion protein to express under given conditions by isopropyl beta-D-1-Thiogalactopyranoside (IPTG). Then we purified the expression product through a glutathione S-transferase (GST) resin and collected the interested protein. This research may lay the groundwork for scientific research and clinical application.
Subject(s)
Humans , Base Sequence , Escherichia coli , Genetics , Metabolism , Matrix Metalloproteinase 1 , Genetics , Molecular Sequence Data , Recombinant Fusion Proteins , Genetics , Tumor Necrosis Factor-alpha , GeneticsABSTRACT
OBJECTIVE: To study the mechanisms of the antitumor and immunoregulation functions of polyporus polysaccharide (PPS). METHODS: The production of nitric oxide (NO), the activity and mRNA expression of inducible nitric oxide synthase (iNOS) in peritoneal macrophages of mice administered with different dose of PPS were observed by Griess reaction, fluorimetry assay and RT-PCR, respectively. RESULTS: PPS could elevate the iNOS activity with dose-dependence and stimulate the iNOS mRNA expression of peritoneal macrophages in mice. CONCLUSION: The regulation of PPS on the production of NO in peritoneal macrophages of mice may occur at transcriptional level of iNOS. This indicates that the mechanism of PPS's antitumor and immunoregulation functions may be related to increasing NO output of macrophages through stimulating iNOS's denovo synthesis.
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Medical biochemistry is a frontal science, esp. molecular biology. The bilingual teaching in medical biochemistry has not only advantages but also disadvantages. By making use of its advantages and correcting its shortcomings, we should try our best to be close to international level in the teaching of medical biochemistry.
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Purpose:The objective of the study is to investigate the pattern of apoptosis and to explore the effect of Fas/FasL on the process of apoptosis induced by daunorubicin (DNR) on human myeloid leukemia cell line HL 60.Methods:The effect on apoptosis and the expression of Fas and FasL antigen induced by DNR on cell line HL 60 were measured by fluorescence microscope ,DNA electrophoresis and flow cytometry analysis.Results:DNR could induce typical apoptosis of HL 60 cells with the DNR plating concentration at 0.1,1 ?g/ml after 6 hours. Morphological changes such as apoptosis bodies, chromatic condensation and cytoplasm budding were observed by fluorescence microscope. Sub G 1 peaks was found by flow cytometry. HL 60 cell apoptosis rate reached a peak at 24 hours. Sub G 1 peaks were not found by flow cytometry with the DNR plating concentration at 10 ?g/ml after 6 hours. DNR could upregulate the expression of Fas and FasL of HL 60 cells.Conclusions:Apoptosis induced by DNR is one of the primary mechanisms in chemotherapy. Fas/FasL system participate in the apoptosis induced by DNR .
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Object To investigate the mechanisms of action of lentinan (LTN) activated mouse peritoneal macrophages to produce nitric oxide (NO). Methods The effects of LTN on NO output and intracellular glutathione (GSH) in mouse peritoneal macrophages and the correlation of them were studied. Results (1) LTN can significantly increase production of NO in mouse peritoneal macrophages, decrease level of intracellular GSH followed increase of NO production. (2) The above effect can be blocked efficiently by the NO production inhibitors. (3) NO production can be inhibited by GSH lowering drugs. Conclusion LTN increase NO production with depletion of intracellular GSH in the activated mouse peritoneal macrophages. It suggested that intracellular GSH plays an important role in regulation of NO production and protection of host cells from cytotoxic attack induced by NO.
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Objective To investigate the effects of procyanidin on apoptosis and caspase-8 activation in HeLa cell induced by TNF-?. Methods Flow cytometry was used to analyze the apoptosis. The caspase-8 fluorescent kits were used to detect the activity of caspase-8. And the expression of caspase-8 enzymogen was examined by Western blot. Results Procyanidin (5, 10, and 20 mg/L) significantly inhibited the apoptosis of HeLa cells induced by rhTNF-? (100 ?g/L) (P
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Aim To inhibit the expression of human protection of telomere gene hPOT1 in HeLa cells using vector based on RNA interference(RNAi) technique and to investigate its effects on the activation of Caspase-3 in HeLa cell.Methods Three recombinant plasmids(our group constructed before) containing different hPOT1 target sequences(pmU6-shRNA1,pmU6-shRNA2 and pmU6-shRNA3)were transfected into HeLa cells by liposomal.The expression inhibition of hPOT1 was detected by RT-PCR and EMSA.The expression and activation of Caspase-3 were inspected by RT-PCR,Western blot analysis and Caspase-3 kit.Results After 48 hour′s transfecting,hPOT1 mRNA and protein level in HeLa cells reduced and the expression of Caspase-3 mRNA had no change.Caspase-3 zymogen decreased but its activity increased.Conclusions hPOT1 expression in HeLa cells can be significantly inhibited by using siRNAvectored RNAi and the down-regulation of hPOT1 expression can activate Caspase-3.