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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.
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.
Microwave ablation versus radiofrequency ablation for subcapsular hepatocellular carcinoma: a propensity score-matched study
Zheng, H; Liu, KW; Yang, Y; Liu, B; Zhao, XY; Chen, Y; Feng, YM; Meng, M; Tan, X; Zhu, Q
EUROPEAN RADIOLOGY 2022年 页码:-null
无关键词信息
Objectives Thermal ablation is now accepted as one of the curative treatments for patients with early-stage hepatocellular carcinoma (HCC), but the efficacy of this treatment for subcapsular HCC is not well characterized. Therefore, we aimed to compare the outcomes of microwave ablation (MWA) and radiofrequency ablation (RFA) for patients with subcapsular HCC. Methods In total, 195 patients with subcapsular HCC who met the Milan criteria and underwent MWA or RFA were included. Local tumor progression (LTP), overall survival (OS), recurrence beyond the Milan criteria (RBM), and complications of these patients were compared. Results After propensity score matching, the 1-, 3-, and 5-year cumulative LTP rates were 6.7%, 9.6%, and 11.4% in the MWA group, and 13.4%, 24.6%, and 29.1% in the RFA group, respectively (p = 0.006). The cumulative rates of RBM were lower in patients treated with MWA than in those treated with RFA (4.4% versus 12% at 1 year; 14.5% versus 23.0% at 3 years; and 37.4% versus 53.9% at 5 years; p = 0.03). The OS rates at 1, 3, and 5 years were 97.1%, 85.9%, and 73.4% in the MWA group, and 95.6%, 80.4%, and 61.4% in the RFA group, respectively (p = 0.36). The rate of major complications showed no significant difference between the MWA group and the RFA group (17.4% vs. 11.6%, p = 0.33). Conclusion Compared to RFA, MWA showed better tumor control for subcapsular HCC within the Milan criteria. There was no difference in the incidence of major complications between the two groups.
Liver resection versus radiofrequency ablation for recurrent hepatocellular carcinoma: a systematic review and meta-analysis
Yang, Y; Yu, HL; Tan, X; You, YJ; Liu, FY; Zhao, T; Qi, JN; Li, J; Feng, YM; Zhu, Q
INTERNATIONAL JOURNAL OF HYPERTHERMIA 2021年 38卷1期 页码:875-
INTRAHEPATIC RECURRENCE; HEPATIC RESECTION; MILAN CRITERIA; RE-RESECTION; SURGICAL RESECTION; HEPATECTOMY; SURVIVAL; RISK; THERAPY; SINGLE
Background & aims Liver resection (LR) and radiofrequency ablation (RFA) are commonly used for the treatment of recurrent hepatocellular carcinoma (HCC), but the optimal treatment modality remains unclear. We aimed to compare the efficacy and safety of LR vs RFA for recurrent HCC. Methods We searched PubMed, Embase, Web of Science, and the Cochrane Library for relevant studies. The primary outcomes were overall survival (OS) and disease-free survival (DFS). The secondary outcomes were major complications and hospital stay. Results Eighteen studies with 1991 patients with recurrent HCC were included. The pooled hazard ratio (HR) for OS demonstrated that LR had significantly better OS than RFA in recurrent HCC (HR, 0.81; 95% confidence interval [CI], 0.68-0.95). Specifically, LR was associated with higher 2-, 3- and 4-year OS rates compared with RFA. The pooled HR for DFS showed no significant difference between LR and RFA during the whole follow-up period (HR, 0.90; 95% CI, 0.76-1.07). However, LR was associated with significantly higher 2- to 5-year DFS rates compared to RFA. LR was also associated with more major complications (p < .001) and longer hospital stay (p < .001). Subgroup analyses demonstrated that LR and RFA had similar efficacy in patients with recurrent tumors less than 3 cm or patients presenting three or fewer recurrent nodules. Conclusion LR could provide better long-term survival outcomes than RFA for recurrent HCC patients, while RFA has a higher safety profile. RFA can be a good alternative to LR for patients with small-sized recurrence or patients with a limited number of recurrent nodules. However, as tumor size increases, LR tends to be more efficacious.
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