In vivo observations and electron microscopy showed that topical use of anti-HSV monoclonal glycoprotein antibodies produced marked antiviral effects in inhibiting the development of experimental herpetic keratitis in rabbits and in protecting the susceptible corneal cells. As a new biological product, the anti-HSV monoclonal antibodies may provide a new approach to the treatment of HSV keratitis.
Objective To investigate the effects of the Bcl-XL antisense oligodeoxynucleotides （ASODN） in suppressing the Bel-XL expression and increasing the sensitivity of esophageal cancer cell line EC9706 to 5-fluorouracil （ 5-Fu ）, Methods The proliferation inhibitory rate of EC9706 was assessed by MTT, the expression of Bel-XL was detected by RT-PCR and Western blot, and the apoptotic changes were examined by acridine orange （AO） fluorescent staining and flow eytometry, respectively, Results In the group of ASODN combined with 5-Fu, the proliferation inhibitory rate of esophageal cancer cells was 71.58%, the expression inhibitory rate of Bel-XL mRNA was 81.25%, the expression of Bcl-XL protein was decreased significantly. The apoptosis rates detected by AO fluorescent staining and flow eytometry were 69.5% and （63.32±9.23 ）%, respectively. There were significant differences as compared with the cell control group, the vacuity control group, the N-ODN group, the ASODN group and the 5-Fu group, respectively （P 〈 0. 05 ）. Conclusion Bel-XL ASODN combined with 5-Fu can effectively inhibit the proliferation of esophageal cancer cells in vitro. Bel-XL ASODN can significantly increase the sensitivity of esophageal cancer cells to 5-Fu through suppressing the expression of Bel-XL.
Key words:
Esophageal neoplasms; 5-fluorouracil; BcI-XL; Antisense oligodeoxynueleotide
The mass spectral behaviour of 15 new type of organic phosphorus compounds with a considerable insecticidal activity, 1, 3,2-oxazaphospholidine 2-sulfides derivatives, under 70 eV electron impact has been studied by means of high and low resolution mass spectrometry as well as by B/E linked scan and MIKES/CID analysis. Discussion is focused into the isomerization between oxygen and sulphur in molecules and some rearrangement reactions.
Recent results and progress of mass measurements of neutron-rich nuclei utilizing Isochronous Mass Spectrometry (IMS) based on the HIRFL-CSR complex at Lanzhou are reported. The nuclei of interest were produced through projectile fragmentation of primary 86Kr ions at a realistic energy of 460.65 MeV/u. After in-flight separation by the fragment separator RIBLL2, the fragments were injected and stored in the experimental storage ring CSRe, and their masses were determined from measurements of their revolution times. The re-determined masses were compared and evaluated with other mass measurements, and the impact of these evaluated masses on the shell evolution study is discussed.
We aimed at investigating the effects of rapamycin on apoptosis and autophagy of human acute promyelocytic leukemia cell line HL-60, and to preliminarily explore the mechanism of extra medullary infiltration of leukemia cells with human acute promyelocytic leukemia cell line HL-60 as the object of study, providing a theoretical basis for the clinical treatment of leukemia.After HL-60 cells were cultured in vitro, the effect of rapamycin on proliferation ability of HL-60 cells was determined by methyl thiazolyl tetrazolium (MTT) method, the cell apoptosis ratio was detected by flow cytometer, the change of autophagy after HL-60 cells acted by rapamycin was tested by monodansylcadaverine (MDC) fluorescence staining, the mRNA expression of autophagy-related molecule was detected by polymerase chain reaction (PCR), and the expressions of apoptosis-related protein and autophagy-related protein were determined by Western blotting (WB).HL-60 cell proliferation could be significantly inhibited by rapamycin (80 μg/mL-640 μg/mL), which was in a dose-dependent manner. HL-60 cell apoptosis ratio and apoptosis-related protein expression were distinctly improved by rapamycin. Cell autophagy level, mRNA expression of autophagy-related molecule and autophagy-related protein expression were remarkably induced by rapamycin.Rapamycin can induce HL-60 cell apoptosis, which is produced mainly by inducing cell autophagy.
MicroRNAs (miRNAs) are small and highly conserved non-coding RNAs that regulate gene expression of target mRNAs through posttranscriptional inhibition involved in the tumorigenesis and progression of multiple malignancies. Although miR-133a has been shown to function as a tumor suppressor in some cancers, the clinical significance and function of miR-133a in gastric cancer remain unclear. Hence, we were focused on the expression and mechanisms of miR-133a in the development of gastric cancer in this study. It was found that the expression of miR-133a was downregulated (P<0.001), while transgelin-2 (TAGLN2) was upregulated (P<0.05) in primary gastric cancer tissues, compared to the adjacent non-cancerous tissues (ANCT). Furthermore, decreased expression of miR-133a and increased expression of TAGLN2 were both associated with lymph node metastases in patients with gastric cancer (P<0.001; P=0.011). Functional analysis studies revealed that ectopic expression of miR-133a reduced cell proliferation and invasion, and induced cell apoptosis and cycle arrest via suppressing the level of TAGLN2 from transcriptional and translational levels and downregulated the expression of proliferating cell nuclear antigen (PCNA) and matrix metalloproteinase-2 (MMP-2) in gastric cancer cells. In conclusion, these results demonstrate that decreased expression of miR-133a is associated with the lymph node metastases of patients with gastric cancer. Overexpression of miR-133a inhibits cell growth and invasion and induces cell apoptosis and cycle arrest through repressing TAGLN2 gene, suggesting that miR-133a might be used as a biomarker or therapeutic target for the treatment of gastric cancer.
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