1.Mechanism of Cell Cycle G_2/M Arrest in Human Gastric Cancer BGC823 Cells Induced by Diallyl Disulfide
Hui LING ; Xiaoxia JI ; Ling WEN ; Hong XIA ; Hui TAN ; Jie HE ; Hailin TANG ; Lin DONG ; Qi SO
Chinese Journal of Clinical Oncology 2010;37(3):121-125
Objective: Cell cycle has recently become more appealing as a new target of anti-carcinogen-ic agent. Diallyl disulfide (DADS) inhibits growth and induces call cycle G_2/M arrest in human gastric cancer BGC823 cells. Cell division cycle protein 25C (Cdc25C) and CyclinB1 expression are involved in G_2/M arrest.However, mechanisms of G_2/M arrest are not yet fully understood. The aim of this study was to elucidate the mechanism of cell cycle G_2/M arrest in human gastric cancer BGC823 cells induced by DADS. Methods: The expression of chk1 and Chk2 mRNA associated with cell cycle arrest of BGC823 cells after the induction with DADS for 1 or 2 days was detected by RT-PCR. The protein expression of cycle-related proteins ATM-RAD3-related gene (ATR), checkpoint kinase1 (Chk1), checkpoint kinase 2 (Chk2), P-ATR, P-Chk1 and P-Chk2 was measured by Western blot. Interaction between Chk1/2 and Cdc25C was analyzed by immuno-precipitation. Results: After the cells were treated with 15 mg/L DADS for 1 or 2 days, the expression of Chk1 and Chk2 mRNA was not significantly different from that in untreated cells (P>0.05). Western blot analysis showed that the expression of total Chk1 and Chk2 treated with 15 mg/L DADS was not significantly different from that in untreated cells. But phospho-chk1 showed a significant increase after stimulation with 15 mg/L DADS for 2h to 12h and continued to increase gradually as time went on (P<0.05). Phospho-Chk2 showed a eak expression and a weaker expression after stimulation with DADS, but the changes were not statistically significant (P>0.05). Addition of 15 mg/L DADS to BGC823 cells for 15 rain to 120 min resulted in an increase in phospho-ATR expression, whereas no changes were found in ATR expression (P<0.05). The Chk1 Ab in-creasingly precipitated Cdc25C in BGC823 cells treated with DADS (P<0.05). In contrast, Chk2 Ab failed to change precipitation with Cdc25C by DADS (P>0.05). Conclusion: Activation of chk1 was involved in cell cy-cle G_2/M arrest in BGC823 cells treated with DADS. Cell cycle G_2/M arrest by DADS is associated with phos-phorylation of several cell cycle regulatory proteins including ATR and Chk1 which regulate expression of Cdc25C.
2.Inhibition of Cell Proliferation by siRNA Targeting PI3Kp85α in Breast Cancer MCF-7 Cell Line
Mei MEI ; Yu REN ; Xuan ZHOU ; Zheng SO ; Yanbin QI ; Hongmei WANG ; Hao ZHANG ; Zhi YAO ; Linghuo JIANG
Chinese Journal of Clinical Oncology 2009;36(23):1360-1364
Objective: To study the effect of and possible mechanism of knockinng down PI3Kp85α using siRNA in MCF-7 human breast cancer cell line. Methods: Oligofectamine was used to transfect PI3Kp85α siRNA to knock down the PI3Kp85α expression level in MCF-7 human breast cancer cell line in vitro. Real-time PCR was conducted to detect the expression of PI3Kp85α. The effect of PI3Kp85αsiRNA on the growth of MCF-7 cells was measured by MTT. The cell cycle distribution and cell apoptosis were detected by cell flow cytometry. Protein expression was evaluated by immunofluorescence staining and Western blot. Results: The expression of PI3Kp85 α was knocked down with PI3Kp85α siRNA in MCF-7 cells. Cell growth was delayed in PI3Kp85αsiRNA-treated group. Conclusion: The suppressive effect of PI3Kp85αsiRNA on the growth of MCF-7 human breast cancer cell line is significant and PI3Kp85α could be a candidate for gene therapy for breast cancer.
3.The Effect of Preinfarction Angina as Ischemic Preconditioning on Myocardial Protection.
Tae Young CHOI ; Seung Jae TAHK ; Myeong Ho YOON ; So Yeon CHOI ; Min Cheol KIM ; Heung Mo YANG ; Jung Hyun CHOI ; Zhen Guo ZHENG ; Long QI ; Hyuk Jae CHANG ; Gyo Seung HWANG ; Joon Han SHIN
Korean Circulation Journal 2004;34(5):451-458
BACKGROUND AND OBJECTIVES: By measuring the coronary flow reserve (CFR) and echocardiographic left ventricular function, the purpose of this study was to evaluate the effect of pre-infarction angina (PA) on myocardial protection in patients with acute myocardial infarction (AMI). SUBJECTS AND METHODS: Sixty-two patients (mean 54+/-10 years, 51 males) with first anterior AMI were studied. CFR, defined as the ratio of hyperemic (hAPV) to baseline APV (bAPV), was measured at least 24 hours after the onset of AMI at the left anterior descending artery (mean 7+/-4 days) with a Doppler wire. Echocardiography was performed at admission (baseline) and during follow-up periods (mean 9+/-7 month). All patients were divided into two groups according to the presence of PA within 72 hours prior to AMI:group A (with PA, n=27) and group B (without PA, n=35). RESULTS: Between the two groups, CFR were higher in group A (2.1+/-0.5 vs.1.6+/-0.5, p<0.001). The baseline left ventricular ejection fraction (LVEF, %) and wall motion score index (WMSI) were better in group A than in B (53.4+/-9.7 vs. 45.1+/-8.8, p=0.001;1.42+/-0.23 vs. 1.72+/-0.28, p<0.001, respectively). LVEF (%) and WMSI during follow-up periods were better in group A than in B (61.3+/-10.2 vs. 54.4+/-13.3, p=0.03;1.24+/-0.21 vs. 1.47+/-0.37, p=0.004, respectively). CONCLUSION: Patients with PA had a significantly higher CFR and better LVF at the baseline and during follow-up periods. This study suggests that brief and repeated myocardial ischemia prior to AMI as ischemic pre-conditioning might have the effect of myocardial protection.
Angina, Unstable*
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Arteries
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Blood Flow Velocity
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Echocardiography
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Follow-Up Studies
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Humans
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Ischemic Preconditioning*
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Myocardial Infarction
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Myocardial Ischemia
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Stroke Volume
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Ventricular Function, Left
4. Neuromodulation-Based Stem Cell Therapy in Brain Repair: Recent Advances and Future Perspectives
Ti-Fei YUAN ; Ti-Fei YUAN ; Kwok-Fai SO ; Ti-Fei YUAN ; Chun YAO ; Yongjun WANG ; Renjie CHAI ; Yan LIU ; Yi DONG ; Li ZHANG ; Kwok-Fai SO ; Li ZHANG ; Kwok-Fai SO ; Jieyu QI ; Renjie CHAI ; Chun YAO ; Yongjun WANG ; Yan LIU
Neuroscience Bulletin 2021;37(5):735-745
Stem cell transplantation holds a promising future for central nervous system repair. Current challenges, however, include spatially and temporally defined cell differentiation and maturation, plus the integration of transplanted neural cells into host circuits. Here we discuss the potential advantages of neuromodulation-based stem cell therapy, which can improve the viability and proliferation of stem cells, guide migration to the repair site, orchestrate the differentiation process, and promote the integration of neural circuitry for functional rehabilitation. All these advantages of neuromodulation make it one potentially valuable tool for further improving the efficiency of stem cell transplantation.