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Associations of Perceived Stress, Resilience and Social Support with Sleep Disturbance Among Community-dwelling Adults
Liu, XH;Liu, CQ;Tian, XH;Zou, GY;Li, GP;Kong, LH;Li, P
STRESS AND HEALTH 2016年 32卷5期 页码:578-586
CONNOR-DAVIDSON RESILIENCE; CHINESE ADULTS; HEALTH-PROBLEMS; QUALITY INDEX; MENTAL-HEALTH; RISK-FACTORS; POOR SLEEP; HONG-KONG; INSOMNIA; POPULATION
Sleep disturbance is often described as sleeping poorly, difficulty falling asleep and maintaining sleep, and waking early. Currently, most studies examining sleep disturbance have focused on negative psychological variables; however, few studies have combined both negative and positive psychosocial factors to assess sleep. The aim of this study was to investigate the prevalence of sleep disturbance and psychosocial correlates in Chinese community-dwelling adults. A total of 1471 adults, between 18 and 60 years old, from eight selected community settings in Jinan, China, were surveyed using the Pittsburgh Sleep Quality Index, Perceived Stress Scale, 10-item Connor-Davidson Resilience Scale and Multidimensional Scale of Perceived Social Support and provided sociodemographic information. We found that the prevalence of sleep disturbance was 33.9%. After adjusting for age, employment status and physical co-morbidity, perceived stress was significantly associated with sleep disturbance [odds ratio (OR)=1.14, p<0.001], while resilience and social support were associated with a low likelihood of sleep disturbance (OR=0.90, p<0.001; OR=0.97, p<0.001). Furthermore, regression analysis showed that the interaction between perceived stress and resilience was significant (p<0.05). Resilience buffered the negative impact of perceived stress on sleep disturbance. Given the close relationship between sleep disturbance and psychosocial correlates, the development of effective intervention programmes to improve sleep quality in this population should be considered. Copyright (C) 2015 John Wiley & Sons, Ltd.
shRNA-mediated AMBRA1 knockdown reduces the cisplatin-induced autophagy and sensitizes ovarian cancer cells to cisplatin
Li, XY;Zhang, LJ;Yu, LL;Wei, W;Lin, XY;Hou, XM;Tian, YJ
JOURNAL OF TOXICOLOGICAL SCIENCES 2016年 41卷1期 页码:45-53
MOLECULAR-MECHANISMS; RESISTANCE; PROLIFERATION; CARCINOMA; THERAPY; BCL-2
Recent research has revealed a role for Ambra1, an autophagy-related gene-related (ATG) protein, in the autophagic pro-survival response, and Ambra1 has been shown to regulate Beclin1 and Beclin1-dependent autophagy in embryonic stem cells and cancer cells. However, whether Ambra1 plays an important role in the autophagy pathway in ovarian cancer cells is unknown. In this study, we hypothesized that Ambra1 is an important regulator of autophagy and apoptosis in ovarian cancer cells. We firstly confirmed autophagic activity in ovarian cancer OVCAR-3 cells which were treated with cisplatin by assessing endogenous microtubule-associated protein 1 light chain 3 (LC3) localization and the presence of autophagosomes and LC3 protein levels in OVCAR-3 cells. Cell apoptosis and viability were measured by annexin-V and PI staining and MTT assays. We then knocked down Ambra1 expression with transfection with the plasmid expressing the small hairpin RNA (shRNA) targeting AMBRA1, then re-evaluated autophagy in the OVCAR-3 cells subject to cisplatin treatment, and re-determined the sensitivity of OVCAR-3 cells to cisplatin. Results demonstrated that cisplatin treatment induced autophagy in OVCAR-3 cells in association with Ambra1 upregulation in the ovarian cancer cells. When Ambra1 expression was reduced by shRNA, the ovarian cancer cells were more sensitive to cisplatin. In conclusion, Ambra1 is a crucial regulator of autophagy and apoptosis in ovarian cancer cells subject to cisplatin to maintain the balance between autophagy and apoptosis. And the Ambra1-targeting inhibition might be an effective method to sensitize ovarian cancer cells to chemotherapy.
Effects of PARP-1 inhibitor and ERK inhibitor on epithelial mesenchymal transitions of the ovarian cancer SKOV3 cells
Su, S;Lin, XY;Ding, N;Zhang, H;Zhang, QH;Ding, YM;Hou, XM;Tian, YJ
PHARMACOLOGICAL REPORTS 2016年 68卷6期 页码:1225-1229
KAPPA-B; POLY(ADP-RIBOSE) POLYMERASE-1; ACTIVATION; BINDING; KINASE; C-13-ASTERISK-CELLS; PROLIFERATION; DOMAINS
Background: To assess the effects of the poly (ADP-ribose) polymerase-1 (PARP-1) inhibitor PJ34 and ERK1/2 inhibitor U0126 on the proliferation and epithelial mesenchymal transitions (EMT) of cisplatin resistant ovarian cancer SKOV-3 cells.;-;Methods: Proliferation of SKOV-3 cells was evaluated using a 3-(4,5-dimethylthazol-2-yl)-2,5-diphenyl tetrazolium bromide assay with PJ34 and U0126 treatment. Expression changes of E-cadherin and vimentin with PJ34 and U0126 treatment was examined using Western blot and quantitative PCR. In addition, invasion assay was performed in cells treated with PJ34 and U0126.;-;Results: PJ34 and U0126 inhibited proliferation of SKOV-3 cells in a time dependent manner. PJ34 and U0126 suppressed the expression of vimentin and enhanced the expression of E-cadherin. PJ34 and U0126 reduced cell invasion. The inhibitory effects of PJ34 and U0126 were stronger than PJ34 alone. PJ34 inhibited the proliferation and invasion of SKOV-3 cells which can be enhanced by ERK1/2 inhibitor U0126.;-;Conclusions: These inhibitory effects are partially due to PARP-1 and ERK1/2 mediated attenuation of EMT activity. (C) 2016 Institute of Pharmacology, Polish Academy of Sciences. Published by Elsevier Sp. z o.o. All rights reserved.
PARP-1及EMT标志物在子宫腺肌病在位及异位内膜中的表达
林雪艳;李春艳;侯小满;田永杰
山东大学学报(医学版) 2017年 55卷9期
子宫腺肌病;;上皮-间质转化;;聚腺苷二磷酸核糖聚合酶-1;;E-钙黏蛋白;;波形蛋白;;Snail;;
目的 研究聚腺苷二磷酸核糖聚合酶-1(PARP-1)在子宫腺肌病在位内膜及异位内膜组织中的表达,讨论PARP-1与子宫腺肌病上皮间质转化(EMT)标志物在子宫腺肌病在位内膜及异位内膜中表达的相关关系.方法 采用免疫组织化学法检测PARP-1和EMT标志物包括E-钙黏蛋白(E-cadherin)、波形蛋白(vimentin)、转录调控因子Snail在子宫腺肌病在位、异位内膜和正常子宫在位内膜组织中的表达,并对PARP-1、E-cadherin、vimentin及Snail的表达水平进行Spearman等级相关性分析.结果 PARP-1、vimentin及Snail在子宫腺肌病在位及异位内膜中的表达比正常子宫在位内膜表达水平高(P均<0.05),E-cadherin在子宫腺肌病在位、异位内膜组织中的表达比正常子宫在位内膜组织表达水平低(P均<0.05).在子宫腺肌病在位、异位内膜组织中,PARP-1的表达水平均与E-cadherin的表达呈负相关,与vimentin及Snail的表达呈正相关.结论 PARP-1在子宫腺肌病在位、异位内膜组织中表达增高并与EMT标志物有相关关系,PARP-1可能参与了子宫腺肌病的EMT过程.
PARP-1及 EMT标志物在子宫腺肌病在位及异位内膜中的表达
林雪艳;李春艳;侯小满;田永杰
山东大学学报(医学版) 2017年9期 影响因子:0.482
子宫腺肌病;上皮 -间质转化;聚腺苷二磷酸核糖聚合酶-1;E-钙黏蛋白;波形蛋白;Snail;
目的 研究聚腺苷二磷酸核糖聚合酶-1(PARP-1)在子宫腺肌病在位内膜及异位内膜组织中的表达,讨论PARP-1与子宫腺肌病上皮间质转化(EMT)标志物在子宫腺肌病在位内膜及异位内膜中表达的相关关系。方法 采用免疫组织化学法检测 PARP-1和 EMT标志物包括 E-钙黏蛋白(E-cadherin)、波形蛋白(vimentin)、转录调控因子 Snail在子宫腺肌病在位、异位内膜和正常子宫在位内膜组织中的表达,并对 PARP-1、E-cadherin、vimentin及 Snail的表达水平进行 Spearman等级相关性分析。结果 PARP-1、vimentin及 Snail在子宫腺肌病在位及异位内膜中的表达比正常子宫在位内膜表达水平高(P均 <0.05),E-cadherin在子宫腺肌病在位、异位内膜组织中的表达比正常子宫在位内膜组织表达水平低(P均 <0.05)。在子宫腺肌病在位、异位内膜组织中,PARP-1的表达水平均与 Ecadherin的表达呈负相关,与 vimentin及 Snail的表达呈正相关。结论 PARP-1在子宫腺肌病在位、异位内膜组织中表达增高并与 EMT标志物有相关关系,PARP-1可能参与了子宫腺肌病的 EMT过程。
PARP-1及EMT标志物在子宫腺肌病在位及异位内膜中的表达
林雪艳;李春艳;侯小满;田永杰
山东大学学报(医学版) 2017年9期 页码:36-40 影响因子:0.482
子宫腺肌病;上皮-间质转化;聚腺苷二磷酸核糖聚合酶-1;E-钙黏蛋白;波形蛋白;Snail;
目的研究聚腺苷二磷酸核糖聚合酶-1(PARP-1)在子宫腺肌病在位内膜及异位内膜组织中的表达,讨论PARP-1与子宫腺肌病上皮间质转化(EM T)标志物在子宫腺肌病在位内膜及异位内膜中表达的相关关系。方法采用免疫组织化学法检测PARP-1和EMT标志物包括E-钙黏蛋白(E-cadherin)、波形蛋白(vimentin)、转录调控因子Snail在子宫腺肌病在位、异位内膜和正常子宫在位内膜组织中的表达,并对PARP-1、E-cadherin、vimentin及Snail的表达水平进行Spearman等级相关性分析。结果 PARP-1、vimentin及Snail在子宫腺肌病在位及异位内膜中的表达比正常子宫在位内膜表达水平高(P均<0.05),E-cadherin在子宫腺肌病在位、异位内膜组织中的表达比正常子宫在位内膜组织表达水平低(P均<0.05)。在子宫腺肌病在位、异位内膜组织中,PARP-1的表达水平均与E-cadherin的表达呈负相关,与vimentin及Snail的表达呈正相关。结论 PARP-1在子宫腺肌病在位、异位内膜组织中表达增高并与EMT标志物有相关关系,PARP-1可能参与了子宫腺肌病的EMT过程。
PARP-1及EMT标志物在子宫腺肌病在位及异位内膜中的表达
林雪艳;李春艳;侯小满;田永杰
山东大学学报:医学版 2017年9期 页码:36-40,共5页
子宫腺肌病;上皮-间质转化;聚腺苷二磷酸核糖聚合酶-1;E-钙黏蛋白;波形蛋白;SNAIL
目的研究聚腺苷二磷酸核糖聚合酶-1(PARP-1)在子宫腺肌病在位内膜及异位内膜组织中的表达,讨论PARP-1与子宫腺肌病上皮间质转化(EM T)标志物在子宫腺肌病在位内膜及异位内膜中表达的相关关系。方法采用免疫组织化学法检测PARP-1和EMT标志物包括E-钙黏蛋白(E-cadherin)、波形蛋白(vimentin)、转录调控因子Snail在子宫腺肌病在位、异位内膜和正常子宫在位内膜组织中的表达,并对PARP-1、E-cadherin、vimentin及Snail的表达水平进行Spearman等级相关性分析。结果 PARP-1、vimentin及Snail在子宫腺肌病在位及异位内膜中的表达比正常子宫在位内膜表达水平高(P均〈0.05),E-cadherin在子宫腺肌病在位、异位内膜组织中的表达比正常子宫在位内膜组织表达水平低(P均〈0.05)。在子宫腺肌病在位、异位内膜组织中,PARP-1的表达水平均与E-cadherin的表达呈负相关,与vimentin及Snail的表达呈正相关。结论 PARP-1在子宫腺肌病在位、异位内膜组织中表达增高并与EMT标志物有相关关系,PARP-1可能参与了子宫腺肌病的EMT过程。
The Drug Combination of SB202190 and SP600125 Significantly Inhibit the Growth and Metastasis of Olaparib-resistant Ovarian Cancer Cell
Chen, XY;Chen, YM;Lin, XY;Su, S;Hou, XM;Zhang, Q;Tian, YJ
CURRENT PHARMACEUTICAL BIOTECHNOLOGY 2018年 19卷6期 页码:506-513
ACTIVATED PROTEIN-KINASE; P38 MAP KINASE; INTRINSIC RESISTANCE; COLORECTAL-CANCER; INDUCED APOPTOSIS; PATHWAY; INDUCTION; SB203580; RISK; LINE
Background & Objective: Many targeted ovarian cancer patients are resistant to olaparib treatment. Here we seek to understand the underlying molecular events and search for potential combinational therapeutics to surmount the intrinsic olaparib resistance in human ovarian cancer.;-;Methods: The cytotoxicity was determined by the MTT assay and cell viability was measured using Cell Counting Kit-8 (CCK-8). Protein expressions of ERK, P38, JNK, ERK5, LC3, N-CADHERIN, alpha-SMA were determined by western blotting. The invasion capacity was evaluated by the transwell chamber. Autophagy flux was monitored by the LC3 puncta formation. The epithelial-mesenchymal transition (EMT) markers were profiled by immunoblotting detection. The in vivo tumor progression was determined by xenograft mice model.;-;Results: The olaparib-resistant cell lines were successfully generated in both SKOV3 and A2780 cells. The proliferative index was significantly higher in resistant cells in comparison with sensitive counterparts in the presence of olaparib. Both P38 and JNK were up-regulated in olaparib-resistant cells. The combinational treatment with P38-specific inhibitor SB202190 and JUN-specific inhibitor SP600125 significantly suppressed cell growth and migration, which was further attributed to the induction of autophagy flux and inhibition of EMT processing. We further consolidated the anti-tumor activities of SB202190 and SP600125 in xenograft mice.;-;Conclusion: Our data suggested that aberrant over-expression of P38 and JNK is causally linked to the olaparib resistance in ovarian cancer. Combination of P38 and JUN inhibitors demonstrated significant anti-tumor activity both in vitro and in vivo. Our study highlighted the potential therapeutic value of Mitogen-Activated Protein Kinase (MAPK) inhibitors in olaparib-resistant human ovarian cancer.
Resibufogenin suppresses tumor growth and Warburg effect through regulating miR-143-3p/HK2 axis in breast cancer
Guo, Y; Liang, F; Zhao, FL; Zhao, J
MOLECULAR AND CELLULAR BIOCHEMISTRY 2020年 466卷1-2期 页码:103-115
POOR-PROGNOSIS; NONCODING RNAS; METASTASIS; METABOLISM; PROLIFERATION; LDHA
Increasing evidence confirmed that the Warburg effect plays an important role involved in the progression of malignant tumors. Resibufogenin (RES) has been proved to have a therapeutic effect in multiple malignant tumors. However, the mechanism of whether RES exerted an antitumor effect on breast cancer through regulating the Warburg effect is largely unknown. The effect of RES on glycolysis was determined by glucose consumption, lactate production, ATP generation, extracellular acidification rate and oxygen consumption rate in breast cancer cells. The total RNA and protein levels were respectively measured by RT-qPCR and western blot. Cell proliferation and apoptosis were examined using the CCK-8 assay, colony formation assay, and flow cytometry, respectively. The interaction between miR-143-3p and HK2 was verified by dual-luciferase reporter gene assay. We also evaluated the influence of RES on the tumor growth and Warburg effect in vivo. RES treatment significantly decreased glycolysis, cell proliferation and induced apoptosis of both MDA-MB-453 and MCF-7 cells. Simultaneously, the expression of HK2 was decreased in breast cancer cells treated with RES, which was positively associated with tumor size and glycolysis. Moreover, HK2 was a direct target gene of miR-143-3p. Mechanistically, upregulation of miR-143-3p by RES treatment inhibited tumor growth by downregulating HK2-mediated Warburg effect in breast cancer. Our findings suggested that RES exerted anti-tumorigenesis and anti-glycolysis activities in breast cancer through upregulating the inhibitory effect of miR-143-3p on HK2 expression, which provided a new potential strategy for breast cancer clinical treatment.
MicroRNA-324-5p affects the radiotherapy response of cervical cancer via targeting ELAV-like RNA binding protein 1
Fan, MJ; He, PJ; Lin, XY; Yang, CR; Li, CZ; Xing, LG
KAOHSIUNG JOURNAL OF MEDICAL SCIENCES 2020年 36卷12期 页码:965-972
METASTASIS; EXPRESSION; GROWTH
Cervical cancer (CC) seriously threatens the health of women. Radiation therapy (RT) is the major treatment for CC. However, the recurrent CC can acquire resistance to RT. Thus, it is necessary to find a new method for reversing RT resistance in CC. It has been reported that microRNA-324-5p (miR-324-5p) can suppress the progression of multiple cancers. However, whether it can reverse resistance to RT in CC remains unclear. qRT-PCR and Western blotting were used to detect gene and protein expression in CC cells, respectively. Cell proliferation was tested by CCK-8 assay and colony formation assay. In addition, cell apoptosis was detected by flow cytometry. Transwell assays were performed to detect cell migration. Dual luciferase reporter assay and TargetScan were used to explore the targets of miR-324-5p. MiR-324-5p was downregulated in CC cells. Overexpression of miR-324-5p sensitized CC cells to RT. In addition, miR-324-5p mimics significantly induced apoptosis and inhibits the migration of CC cells in the presence of(137)Cs ionizing radiation. Furthermore, miR-324-5p sensitized CC cells to ionizing radiation by targeting ELAV-like RNA binding protein 1 (ELAVL1). MiR-324-5p overexpression affects the radiotherapy response of CC by targeting ELAVL1, which may serve as a new target for the treatment of CC.
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