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Beclin-1 1

丹参酮IIA 1

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凋亡 1

普列克底物蛋白同源物样结构域家族A成员1(PHLDA1) 1

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Targeting apoptosis to manage acquired resistance to third generation EGFR inhibitors

《医学前沿(英文)》 2022年 第16卷 第5期   页码 701-713 doi: 10.1007/s11684-022-0951-0

摘要: A significant clinical challenge in lung cancer treatment is management of the inevitable acquired resistance to third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors (EGFR-TKIs), such as osimertinib, which have shown remarkable success in the treatment of advanced NSCLC with EGFR activating mutations, in order to achieve maximal response duration or treatment remission. Apoptosis is a major type of programmed cell death tightly associated with cancer development and treatment. Evasion of apoptosis is considered a key hallmark of cancer and acquisition of apoptosis resistance is accordingly a key mechanism of drug acquired resistance in cancer therapy. It has been clearly shown that effective induction of apoptosis is a key mechanism for third generation EGFR-TKIs, particularly osimertinib, to exert their therapeutic efficacies and the development of resistance to apoptosis is tightly associated with the emergence of acquired resistance. Hence, restoration of cell sensitivity to undergo apoptosis using various means promises an effective strategy for the management of acquired resistance to third generation EGFR-TKIs.

关键词: acquired resistance     EGFR inhibitor     apoptosis     lung cancer    

Discovery of novel ursolic acid derivatives as effective antimicrobial agents through a ROS-mediated apoptosis

《化学科学与工程前沿(英文)》 2023年 第17卷 第12期   页码 2101-2113 doi: 10.1007/s11705-023-2361-5

摘要: In response to the reduction of food production and economic losses caused by plant bacterial diseases, it is necessary to develop new, efficient, and green pesticides. Natural products are rich and sustainable source for the development of new pesticides due to their low toxicity, easy degradation, and eco-friendliness. In this study, we prepared three series of ursolic acid derivatives and assessed their antibacterial ability. Most target compounds exhibited outstanding antibacterial activities. Among them, the relative optimal EC50 values of Xanthomonas oryzae pv. oryzae and Xanthomonas axonopodis pv. citri were 2.23 (A17) and 1.39 (A16) μg·mL–1, respectively. The antimicrobial mechanism showed that compound A17 induced an excessive accumulation and production of reactive oxygen species in bacteria and damaged the cell membrane integrity to kill bacteria. More interestingly, the addition of low concentrations of exogenous hydrogen peroxide enhanced the antibacterial efficacy of compound A17 against Xanthomonas oryzae pv. oryzae. These entertaining results suggested that compound A17 induced an apparent apoptotic behavior in the tested bacteria. Overall, we developed the promising antimicrobial agents that destroyed the redox system of phytopathogenic bacteria, further demonstrating the unprecedented potential of ursolic acid for agricultural applications.

关键词: ursolic acid     antibacterial activities     reactive oxygen species     apoptosis    

Relationship between expression of hepatocyte grow factor and apoptosis of trophoblasts in hypertensive

OUYANG Shan, ZHANG Qinghua, QIAO Fuyuan

《医学前沿(英文)》 2007年 第1卷 第4期   页码 386-389 doi: 10.1007/s11684-007-0075-6

摘要: The aim of this study was to investigate the expression of hepatocyte growth factor (HGF) and Fas in placentas of uncomplicated pregnant women and those with hypertensive disorder complicating pregnancy (HDCP), and elucidate the possible relationship between HGF and apoptosis of trophoblasts. Reverse transcription-polymerase chain reaction (RT-PCR) was undertaken to examine the concentration of HGF mRNA and Fas mRNA obtained from 34 cases of HDCP and 30 cases of uncomplicated pregnancy. The expression of HGF mRNA in mild preeclampsia, severe preeclampsia and eclampsia cases was significantly lower than that in the uncomplicated cases (0.43±0.12, 0.38±0.09, 0.19±0.17 versus 0.67±0.19, <0.05), while the expression of Fas mRNA in mild preeclampsia, severe preeclampsia and eclampisa cases was significantly higher than that in the uncomplicated cases (1.58±0.26, 2.96±0.14, 5.98±1.17 versus 1.01±0.36, <0.05). For HGF mRNA and Fas mRNA, there was no difference between gestational hypertension cases and control cases. Decreased HGF mRNA or increased Fas mRNA was found along with the progress of HDCP. Negative correlation was found between the expressions of HGF and Fas. These results indicate that HGF inhibits the apoptosis mediated by Fas, and the reduced expression of HGF in HDCP may be responsible for the apoptosis of trophoblasts.

关键词: pregnancy     concentration     possible relationship     responsible     hepatocyte    

Effect on proliferation and apoptosis of T24 cell lines via silencing DNMT1 with RNA interference

ZHANG Shilong, ZENG Fuqing, PENG Shibo, WANG Liang

《医学前沿(英文)》 2008年 第2卷 第4期   页码 374-379 doi: 10.1007/s11684-008-0072-4

摘要: Expression of DNA methyltransferase 1 (DNMT1), which plays an important role on aberrantly methylated CpG in the promoter regions of tumor suppressor genes (TSGs), is higher in bladder cancer cells than in normal bladder cells. Therefore, its overexpression is closely related to tumor formation. In this study, the eukaryotic vector pshRNA-DNMT1 was constructed and transfected into T24 cells. Levels of DNMT1 mRNA and protein were detected by reverse transcription-polymerase chain reaction (RT-PCR) and western blot. Relative to the blank control at the 24th, 48th and 72nd hour after transfection of pshRNA-DNMT1, the inhibitory rates of DNMT1 mRNA levels in T24 cells were 28.44%, 52.48%, 70.91%, respectively. Those of DNMT1 proteins were 24.27%, 57.79%, and 77.74%, respectively. Proliferation and apoptosis were assayed by MTT and flow cytometry with Annexin-V-FITC/PI staining. The growth inhibition rates of pshRNA-DNMT1 at the 24th, 48th and 72nd hour after transfection of pshRNA-DNMT1 were (4.34 ± 0.76)%, (9.87 ± 1.54)% and (13.78 ± 1.93)%, respectively. There were statistically significant differences between pshRNA-DNMT1 and the control blank at each time points ( < 0.01); 24, 48 and 72 hours after T24 cells were transfected by pshRNA-DNMT1, the apoptosis rates of pshRNA-DNMT1 were (3.87 ± 0.81)%, (8.69 ± 1.23)% and (11.46 ± 1.24)%, respectively ( < 0.01 blank control). Based on this case, our conclusion is that the recombinant plasmid pshRNA-DNMT1 can silence the expression of gene DNMT1 mRNA and protein effectively, and to some extent, it also can inhibit the proliferation of bladder cancer cell and promote the cellular apoptosis.

Effect of arsenic trioxide on proliferation and apoptosis of U266 cells and its relationship with the

ZHAN Rong, YU Qinghong, HUANG Haobo

《医学前沿(英文)》 2008年 第2卷 第4期   页码 356-360 doi: 10.1007/s11684-008-0068-0

摘要: The aim of this article is to explore the effect of arsenic trioxide (AsO) on the proliferation and apoptosis of myeloma cell line U266 and its relationship with the expression variation of vascular endothelial growth factor (VEGF). The viability and apoptosis of U266 cells were observed by methylthiazolyl- tetrazolium (MTT) assay and terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL). The effect of AsO on the VEGF expression of U266 cells were tested by enzyme linked immunosorbent assay (ELISA) and reverse transcription-polymerase chain reaction (RT-PCR) analysis. We found that AsO could significantly inhibit the growth of U266 cells, and the concentration for 50% growth inhibition (IC) was 2 ?mol/L. After treatment with 2, 5, 10 ?mol/L AsO for 36 hours, dose-dependent apoptosis of U266 cells was observed. After treatment with 2, 5, 10 ?mol/L AsO for 72 hours, a dose-dependent reduction of VEGF in the supernatant of U266 cells culture was found. As far as single cells are concerned, nevertheless, the expression of VEGF mRNA did not vary. So we draw the conclusion that AsO could induce the apoptosis of U266 cells and inhibit their proliferation, decrease the tumor load, and lead to the reduction of VEGF in the culture supernatant, but not change the expression of VEGF in single U266 cells.

关键词: VEGF expression     expression variation     culture supernatant     labeling     concentration    

Absence of FHIT expression is associated with apoptosis inhibition in colorectal cancer

CAO Jie, LI Wanglin, XIA Jie, TANG Weibiao, WANG Hui, CHEN Xiwen, XIAO Huanqing, LI Yuyuan, CHEN Xiaoping, DU Hong, CHEN Shanming

《医学前沿(英文)》 2007年 第1卷 第2期   页码 147-156 doi: 10.1007/s11684-007-0028-0

摘要: The fragile histidine triad (FHIT) gene, a candidate tumor suppressor gene located at 3p14.2, has been shown to be involved in the carcinogenesis of many human tissues, including digestive tract tissues. However, the expression and the role of the FHIT in the initiation and the development of the colorectal cancer (CRC) are poorly understood. We have shown that the FHIT gene exhibits significantly decreased expression in human CRC compared to colorectal adenoma and normal colorectal tissue by tissue microarray (TMA). The positive rate of FHIT gene expression in normal colorectal tissue, adenoma and adenocarcinoma were 93.75%, 68.75% and 46.25%, respectively. We show this decreased expression to be significantly correlated with the progression of colorectal carcinoma (<0.05) as well as with differentiation and lymph node metastasis (<0.05). We detected two somatic alterations in the FHIT gene in human CRC. The presence of this mutation correlated significantly with decreased FHIT expression in the human CRC. In our present study we tested the hypothesis that the decreased FHIT expression resulted in apoptosis inhibition associated with abnormal expression of apoptosis related proteins. To test this hypothesis we did a series of experiments. In the first test, we assessed apoptosis status using a standard TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end-labeling) assay by comparing FHIT-positive CRC vs. FHIT-negative CRC. In the second experiment, the protein expression of the FHIT and other apoptosis related proteins (Bax, Bcl-2 and Survivin) were measured in human CRC by TMA. Our combined results demonstrate the mutation in the FHIT gene significantly reduced FHIT expression in human CRC. Both TUNEL and TMA experiments demonstrated significantly inhibited apoptosis by down-regulation of Bax and the up-regulation of Survivin and Bcl-2. Collectively, these studies identify the mechanism by which an important tumor suppressor gene, FHIT is inactivated specifically in human CRC contributing to our understanding of the mechanism of colorectal carcinogenesis.

-132) significantly suppresses tumor growth in mouse model by inhibiting angiogenesis and promoting apoptosis

《医学前沿(英文)》 2022年 第16卷 第6期   页码 873-882 doi: 10.1007/s11684-022-0925-2

摘要: Tumor growth is an angiogenesis-dependent process and accompanied by the formation of hypoxic areas. Tumstatin is a tumor-specific angiogenesis inhibitor that suppresses the proliferation and induces the apoptosis of tumorous vascular endothelial cells. VNP20009, an attenuated Salmonella typhimurium strain, preferentially accumulates in the hypoxic areas of solid tumors. In this study, a novel Salmonella-mediated targeted expression system of tumstatin (VNP-Tum5) was developed under the control of the hypoxia-induced J23100 promoter to obtain anti-tumor efficacy in mice. Treatment with VNP-Tum5 effectively suppressed tumor growth and prolonged survival in the mouse model of B16F10 melanoma. VNP-Tum5 exhibited a higher efficacy in inhibiting the proliferation and inducing the necrosis and apoptosis of B16F10 cells in vitro and in vivo compared with VNP (control). VNP-Tum5 significantly inhibited the proliferation and migration of mouse umbilical vascular endothelial cells to impede angiogenesis. VNP-Tum5 downregulated the expression of anti-vascular endothelial growth factor A, platelet endothelial cell adhesion molecule-1, phosphorylated phosphoinositide 3 kinase, and phosphorylated protein kinase B and upregulated the expression of cleaved-caspase 3 in tumor tissues. This study is the first to use tumstatin-transformed VNP20009 as a tumor-targeted system for treatment of melanoma by combining anti-tumor and anti-angiogenic effects.

关键词: Salmonella VNP20009     tumstatin     B16F10     melanoma     apoptosis     angiogenesis    

Effects of 3-aminobenzamide on poly (ADP-ribose) polymerase expression, apoptosis and cell cycle progression

DU Xiang, ZHAO Hongguang, GUO Wei, GONG Shouliang, WANG Wen

《医学前沿(英文)》 2008年 第2卷 第2期   页码 204-206 doi: 10.1007/s11684-008-0039-5

摘要: The aim of this paper is to study the changes of apoptosis and cell cycle progression in HeLa cells after the poly (ADP-ribose) polymerase (PARP) was inhibited by its inhibitor 3-aminobenzamide (3-AB) and the mechanisms of PARP action on HeLa cells damaged by irradiation. Flow cytometry (FCM) was used to examine the PARP expression and the percentage of apoptotic cells and cell cycle progression. The percentage of HeLa cells with positive expression of PARP protein 2, 4, 8 and 12 h after administrated with 3-AB was significantly lower than that of the control ( < 0.01). The percentages of apoptotic cells in the 3-AB plus irradiation group at the time points of 2, 8, 12 and 24 h after 2 Gy irradiation were higher than that in the irradiation group ( < 0.01 or < 0.05) and the percentage of G cells decreased significantly ( < 0.01 or < 0.05). It indicates that 3-AB can rapidly inhibit PARP expression of HeLa cells, promote cell apoptosis and block G arrest induced by irradiation.

关键词: control     irradiation     apoptotic     progression     3-AB    

Inhibition of NF-kappa B can enhance Fas-mediated apoptosis in leukemia cell line HL-60

Li WANG, Shi ZHAO, Hong-Xiang WANG, Ping ZOU

《医学前沿(英文)》 2010年 第4卷 第3期   页码 323-328 doi: 10.1007/s11684-010-0026-5

摘要: This study explored the effects of nuclear factor-kappa B (NF-κB) inhibitor Bay 11-7082 on Fas/FasL system and Fas-mediated apoptosis in cell line HL-60 cells. The mRNA and protein levels of Fas, FasL, and X-linked inhibitor of apoptosis protein (XIAP) were detected by reverse transcription-polymerase chain reaction (RT-PCR) and flow cytometry (FCM); the level of sFasL was evaluated by enzyme-linked immunosorbent assay (ELISA); and apoptosis was determined by FCM. After treatment with Bay 11-7082, the mRNA and protein levels of FasL and XIAP in HL-60 cells were significantly lower than in the controls ( <0.05), but the mRNA and protein levels of Fas and sFasL did not change significantly ( >0.05). Apoptotic rate of HL-60 cells treated with Bay 11-7082 was significantly higher than in the controls ( <0.05). Therefore, we conclude that Bay 11-7082 can enhance Fas-mediated apoptosis in HL-60 cells by downregulating FasL and XIAP levels.

关键词: nuclear factor-kappa B     Fas/FasL system     HL-60     Bay 11-7082    

Non-genetic mechanisms of diabetic nephropathy

null

《医学前沿(英文)》 2017年 第11卷 第3期   页码 319-332 doi: 10.1007/s11684-017-0569-9

摘要:

Diabetic nephropathy (DN) is one of the most common microvascular complications in diabetes mellitus patients and is characterized by thickened glomerular basement membrane, increased extracellular matrix formation, and podocyte loss. These phenomena lead to proteinuria and altered glomerular filtration rate, that is, the rate initially increases but progressively decreases. DN has become the leading cause of end-stage renal disease. Its prevalence shows a rapid growth trend and causes heavy social and economic burden in many countries. However, this disease is multifactorial, and its mechanism is poorly understood due to the complex pathogenesis of DN. In this review, we highlight the new molecular insights about the pathogenesis of DN from the aspects of immune inflammation response, epithelial–mesenchymal transition, apoptosis and mitochondrial damage, epigenetics, and podocyte–endothelial communication. This work offers groundwork for understanding the initiation and progression of DN, as well as provides ideas for developing new prevention and treatment measures.

关键词: diabetic nephropathy     immune inflammatory response     epithelial–mesenchymal transition     apoptosis     mitochondrial damage     epigenetics     podocyte–endothelial communication    

Effect of pirfenidone on renal tubulointerstitial fibrosis

Dixin LI MM , Hongbing ZENG MD , Chunyang JI MM ,

《医学前沿(英文)》 2009年 第3卷 第3期   页码 316-322 doi: 10.1007/s11684-009-0045-2

摘要: Renal tubulointerstitial fibrosis (TIF) is the common end stage of various chronic renal diseases, and pirfenidone (PFD) is a novel, broad-spectrum anti-fibrotic compound but little is known about its effect and mechanism of action on renal TIF. In this work, we employed a unilateral ureteral obstruction (UUO) rat model to investigate the apoptosis of renal tubular epithelial cells (RTC) after PFD treatment. Thirty-five Sprague Dawley (SD) rats were randomized into three groups: sham-operated group (=7), UUO group (=14) and PFD group (=14). All rats were sacrificed at day 7 or 14 after operation. Renal histology was studied by using periodic acid schiff reagent (PAS) and Masson trichromic stain (MASSON); apoptosis was detected by terminal deoxynucleotide transferase-mediated dUTP-biotin nick end-labeling (TUNEL); tubular caspase-3 expression was assessed by immunohistochemistry. The content of malondialdehyde (MDA) and total activity of superoxide dismutase (T-SOD) in the renal cortex was determined by chemical colorimetry method. TIF, apoptosis of RTC, tubular expression of caspase-3 and the content of MDA were increased in the UUO group compared with those in the sham-operated group, and were ameliorated significantly by PFD treatment (<0.05). The activity of SOD was decreased in the UUO group, but was improved by PFD treatment (<0.05). Our results showed that PFD could ameliorate TIF in the UUO group, and the possible mechanism was by reducing the apoptosis of RTC, which involved oxidative stress and caspase-3.

关键词: pirfenidone     apoptosis     caspase 3     oxidative stress    

hydrophobic environment triggering reactive fluorescence probe to real-time monitor mitochondrial DNA damage

《化学科学与工程前沿(英文)》 2022年 第16卷 第1期   页码 92-102 doi: 10.1007/s11705-021-2063-9

摘要: Mitochondrial DNA has a special structure that is prone to damage resulting in many serious diseases, such as genetic diseases and cancers. Therefore, the rapid and specific monitoring of mitochondrial DNA damage is urgently needed for biological recognition. Herein, we constructed an in situ hydrophobic environment-triggering reactive fluorescence probe named MBI-CN. The fluorophore was 2-styrene-1H-benzo[d]imidazole, and malononitrile was introduced as a core into a molecule to initiate the hydrolysis reaction in the specific environment containing damaged mitochondrial DNA. In this design, MBI-CN conjugates to mitochondrial DNA without causing additional damages. Thus, MBI-CN can be hydrolyzed to generate MBI-CHO in an in situ hydrophobic environment with mitochondrial DNA damage. Meanwhile, MBI-CHO immediately emitted a significative fluorescence signal changes at 437 and 553 nm within 25 s for the damaged mitochondria DNA. Give that the specific and rapid response of MBI-CN does not cause additional damages to mitochondrial DNA, it is a potentially effective detection tool for the real-time monitoring of mitochondrial DNA damage during cell apoptosis and initial assessment of cell apoptosis.

关键词: hydrolysis reaction     mitochondrial DNA damage     in situ hydrophobic environment trigger     fluorescence probe     apoptosis    

Combined gemcitabine and CHK1 inhibitor treatment induces apoptosis resistance in cancer stem cell-like

null

《医学前沿(英文)》 2013年 第7卷 第4期   页码 462-476 doi: 10.1007/s11684-013-0270-6

摘要:

Evaluating the effects of novel drugs on appropriate tumor models has become crucial for developing more effective therapies that target highly tumorigenic and drug-resistant cancer stem cell (CSC) populations. In this study, we demonstrate that a subset of cancer cells with CSC properties may be enriched into tumor spheroids under stem cell conditions from a non-small cell lung cancer cell line. Treating these CSC-like cells with gemcitabine alone and a combination of gemcitabine and the novel CHK1 inhibitor PF-00477736 revealed that PF-00477736 enhances the anti-proliferative effect of gemcitabine against both the parental and the CSC-like cell populations. However, the CSC-like cells exhibited resistance to gemcitabine-induced apoptosis. Collectively, the spheroid-forming CSC-like cells may serve as a model system for understanding the mechanism underlying the drug resistance of CSCs and for guiding the development of better therapies that can inhibit tumor growth and eradicate CSCs.

关键词: drug resistance     cancer stem cell     checkpoint kinase 1 (CHK1)     PF-00477736     lung cancer     tumorigenicity    

丹参酮IIA通过Beclin-1介导的自噬性凋亡抑制非小细胞肺癌 Article

白莎莎, 崔赛男, 温文浩, 梁丽娴, 白静, 林慧媛, 崔永飞, 杨蕾, 刘中秋, 郑远, 张荣

《工程(英文)》 2022年 第19卷 第12期   页码 128-138 doi: 10.1016/j.eng.2021.07.014

摘要:

肺癌是癌症死亡的主要原因,因此有必要制定一种新的治疗策略。丹参酮IIA(Tan IIA)是常用中药丹参的一种有效成分,为开发治疗肺癌的新策略提供了新方向。Tan IIA 在体外和体内均可通过诱导自噬性细胞凋亡从而抑制肺癌。Tan IIA 在人类非小细胞肺癌(NSCLC)细胞系中增加凋亡细胞以及剪切型-半
胱氨酸天冬氨酸蛋白水解酶(cleaved caspase)3 和cleaved caspase 9 的表达,降低B淋巴细胞瘤(Bcl-2)与Bcl-2 相关X蛋白(Bax)的比值;自噬激活剂雷帕霉素可促进此过程,而自噬抑制剂3-甲基腺嘌呤(3-MA)减弱此作用。Tan IIA 诱导更多的自噬体,上调轻链3β(LC-3B)I 和LC-3B II,减少螯合体1(SQSTM1/p62)的表达,caspase 3 拮抗剂未能减弱此作用。此外,LC-3B基因(LC3B)过表达和白噬基因5(ATG-5)下调细胞株的实验结果进一步证实Tan IIA 诱导NSCLC细胞发生了自噬相关调亡。过表达和沉默Beclin-1都明显减弱Tan IIA 的作用,提示Tan IIA 诱导的自噬相关调亡依赖于Beclin-1。总之,研究证明Tan IIA是一种潜在的新的抗癌治疗选择。

关键词: 丹参酮IIA     自噬     细胞凋亡     Beclin-1    

Human menstrual blood-derived stem cells alleviate autoimmune hepatitis via JNK/MAPK signaling pathway and

《医学前沿(英文)》 2023年 第17卷 第3期   页码 534-548 doi: 10.1007/s11684-022-0953-y

摘要: Autoimmune hepatitis (AIH) is a severe globally distributed liver disease that could occur at any age. Human menstrual blood-derived stem cells (MenSCs) have shown therapeutic effect in acute lung injury and liver failure. However, their role in the curative effect of AIH remains unclear. Here, a classic AIH mouse model was constructed through intravenous injection with concanavalin A (Con A). MenSCs were intravenously injected while Con A injection in the treatment groups. The results showed that the mortality by Con A injection was significantly decreased by MenSCs treatment and liver function tests and histological analysis were also ameliorated. The results of phosphoproteomic analysis and RNA-seq revealed that MenSCs improved AIH, mainly by apoptosis and c-Jun N-terminal kinase/mitogen-activated protein signaling pathways. Apoptosis analysis demonstrated that the protein expression of cleaved caspase 3 was increased by Con A injection and reduced by MenSCs transplantation, consistent with the TUNEL staining results. An AML12 co-culture system and JNK inhibitor (SP600125) were used to verify the JNK/MAPK and apoptosis signaling pathways. These findings suggested that MenSCs could be a promising strategy for AIH.

关键词: autoimmune hepatitis (AIH)     concanavalin A (Con A)     human menstrual blood-derived stem cells (MenSCs)     apoptosis     mitogen-activated protein kinase (MAPK)    

标题 作者 时间 类型 操作

Targeting apoptosis to manage acquired resistance to third generation EGFR inhibitors

期刊论文

Discovery of novel ursolic acid derivatives as effective antimicrobial agents through a ROS-mediated apoptosis

期刊论文

Relationship between expression of hepatocyte grow factor and apoptosis of trophoblasts in hypertensive

OUYANG Shan, ZHANG Qinghua, QIAO Fuyuan

期刊论文

Effect on proliferation and apoptosis of T24 cell lines via silencing DNMT1 with RNA interference

ZHANG Shilong, ZENG Fuqing, PENG Shibo, WANG Liang

期刊论文

Effect of arsenic trioxide on proliferation and apoptosis of U266 cells and its relationship with the

ZHAN Rong, YU Qinghong, HUANG Haobo

期刊论文

Absence of FHIT expression is associated with apoptosis inhibition in colorectal cancer

CAO Jie, LI Wanglin, XIA Jie, TANG Weibiao, WANG Hui, CHEN Xiwen, XIAO Huanqing, LI Yuyuan, CHEN Xiaoping, DU Hong, CHEN Shanming

期刊论文

-132) significantly suppresses tumor growth in mouse model by inhibiting angiogenesis and promoting apoptosis

期刊论文

Effects of 3-aminobenzamide on poly (ADP-ribose) polymerase expression, apoptosis and cell cycle progression

DU Xiang, ZHAO Hongguang, GUO Wei, GONG Shouliang, WANG Wen

期刊论文

Inhibition of NF-kappa B can enhance Fas-mediated apoptosis in leukemia cell line HL-60

Li WANG, Shi ZHAO, Hong-Xiang WANG, Ping ZOU

期刊论文

Non-genetic mechanisms of diabetic nephropathy

null

期刊论文

Effect of pirfenidone on renal tubulointerstitial fibrosis

Dixin LI MM , Hongbing ZENG MD , Chunyang JI MM ,

期刊论文

hydrophobic environment triggering reactive fluorescence probe to real-time monitor mitochondrial DNA damage

期刊论文

Combined gemcitabine and CHK1 inhibitor treatment induces apoptosis resistance in cancer stem cell-like

null

期刊论文

丹参酮IIA通过Beclin-1介导的自噬性凋亡抑制非小细胞肺癌

白莎莎, 崔赛男, 温文浩, 梁丽娴, 白静, 林慧媛, 崔永飞, 杨蕾, 刘中秋, 郑远, 张荣

期刊论文

Human menstrual blood-derived stem cells alleviate autoimmune hepatitis via JNK/MAPK signaling pathway and

期刊论文