Objective To investigate the expression of programmed cell death 5 （PDCD5） in tissues of normal human prostate （NP）, benign prostatic hyperplasia （BPH）, and prostate cancer （PCa） in order to assess the clinica...Objective To investigate the expression of programmed cell death 5 （PDCD5） in tissues of normal human prostate （NP）, benign prostatic hyperplasia （BPH）, and prostate cancer （PCa） in order to assess the clinical role of PDCD5 in PCa. Methods PDCD5 expression was determined by EnVision immunohistochemical staining in forma-lin-fixed and paraffin-embedded specimens obtained from 12 subjects with NP, 22 with BPH, and 22 with PCa. In addition, PCa cases were classified as low/middle-risk （Gleason sumS7） and high-risk （Gleason sum〉7） on the basis of Gleason grade. Positive expression rates and intensity of PDCD5 protein were observed under light microscope and analyzed with computer imaging technique. Expression of PDCD5 was compared among different prostatic tissues. Results The expression of PDCD5 was significantly lower in tissue of PCa than in tissues of NP and BPH （P〈0.01）. However, there was no significant difference in PDCD5 expression between tissues of NP and BPH. In addition, the expression of PDCD5 was further downregulated with the increase of Gleason sum in PCa. Conclusions By downregulating apoptosis, low PDCD5 expression may play an important role in the occurrence and development of PCa. PDCD5 is supposed to have a potential clinical value to be a new predictor of progression and target of gene therapy in PCa.展开更多
This study examined the expression pattern of programmed cell death 5 (PDCD5) in co-chlear hair cells and spiral ganglion neurons (SGNs) and its association with age-related hearing loss in mice.Sixty C57BL/6J (C57) m...This study examined the expression pattern of programmed cell death 5 (PDCD5) in co-chlear hair cells and spiral ganglion neurons (SGNs) and its association with age-related hearing loss in mice.Sixty C57BL/6J (C57) mice at different ages were divided into four groups (3,6,9 or 12 months).PDCD5 expression was detected by using immunohistochemistry,real-time PCR and Western blot.Morphological change of the cochleae was also evaluated by using immunoassay.The results showed that the expression of PDCD5 had a gradual increase with ageing in both protein and RNA levels in C57 mice,as well as gradually increased apoptosis of cochlear hair cells and SGNs.In addition,we also found that caspase-3 activity was enhanced and its expression was enhanced with ageing.It is implied that overexpression of PDCD5 causes the increase in caspase-3 activity and the subsequent increase of apoptosis in cochlear hair cells and SGNs,and thereby plays a role in the pathogenesis of presbycusis.Thus,PDCD5 may be a new target site for the treatment and prevention of age-related hearing loss.展开更多
Polygonum cuspidatum is used as a traditional medicinal herb for the therapy of various diseases including several types of cancers. In the present study, we focused on addressing the anti-cancer activity and molecula...Polygonum cuspidatum is used as a traditional medicinal herb for the therapy of various diseases including several types of cancers. In the present study, we focused on addressing the anti-cancer activity and molecular mechanism of methanol extract of Polygonum cuspidatum (MEPC) in HSC-2 human oral cancer cells. The effect of MEPC on oral cancer cells was estimated by 3-(4,5-dimethylthiazol-20yl)-(3-carboxymethoxyphenyl)-2-(4-sulphophenyl)-2H-tetrazolium (MTS) assay, 4’-6-diamidino-2-phenylindole (DAPI) staining and Western blot analysis. MEPC inhibited the cell viability and induced apoptosis through the induction of death receptor (DR) 5. MEPC also increased the expression of C/EBP homologous protein/growth arrest and the DNA damage-inducible gene 153 (CHOP), a transcription factor induced by ER stress. Thus, we concluded that the induction of CHOP leading to DR5 up-regulation is required for the anti-cancer activity of MEPC in HSC-2 cells and MEPC may be a promising drug candidate for oral cancer.展开更多
Objective: To study the relationship of PDCD5 expression with apoptosis, inflammatory factors and MMPs/TIMPs expression in degenerated intervertebral disc tissue. Methods:Patients with lumbar disc herniation who were ...Objective: To study the relationship of PDCD5 expression with apoptosis, inflammatory factors and MMPs/TIMPs expression in degenerated intervertebral disc tissue. Methods:Patients with lumbar disc herniation who were treated in the Seventh People's Hospital of Shanghai between March 2015 and February 2017 were selected as the LDH group and patients with violent thoracolumbar vertebral fracture were selected as the control group. The intervertebral disc tissue was collected to determine the mRNA expression of PDCD5 as well as the protein levels of apoptosis molecules, inflammatory factors and MMPs/TIMPs molecules. Results: PDCD5 mRNA expression in intervertebral disc tissue of LDH group was significantly higher than that of control group;Caspase-3, Caspase-8, Fas, Caspase-9, Bax, SDF-1, CXCR-4, TNF-α, PGE2, MMP1, MMP2, MMP8 and MMP9 protein levels in intervertebral disc tissue of LDH group were significantly higher than those of control group and positively correlated with PDCD5 mRNA expression while TIMP1 and TIMP2 protein levels were significantly lower than those of control group and negatively correlated with PDCD5 mRNA expression. Conclusion: The high expression of PDCD5 in degenerated intervertebral disc tissue can activate apoptosis and inflammatory response and cause MMPs/TIMPs imbalance.展开更多
目的:分析新凋亡促进因子-程序化细胞死亡分子5(programmed cell death 5,PDCD5)在肝细胞癌(hepatocellular carcinoma,HCC)发生发展中的作用.方法:用免疫组织化学法(immunohisto-chemistry,IHC)检测40例HCC及其癌旁组织(包括24例肝硬化...目的:分析新凋亡促进因子-程序化细胞死亡分子5(programmed cell death 5,PDCD5)在肝细胞癌(hepatocellular carcinoma,HCC)发生发展中的作用.方法:用免疫组织化学法(immunohisto-chemistry,IHC)检测40例HCC及其癌旁组织(包括24例肝硬化和16例慢性肝炎)中的PDCD5和Fas蛋白表达.用等级资料Kruskal-WallisH检验方法进行统计学分析,并用Spearman's等级资料的相关分析比较PDCD5和Fas的表达差异.结果:PDCD5在肝癌组织中多呈阴性表达,在癌旁肝组织中表达增加.肝癌及其癌旁肝硬化肝炎各组间PDCD5表达具有显著性差异(χ2=46.03,P=0.000).Fas在肝癌组织及其癌旁肝硬化或慢性肝炎组织中的表达分布与PDCD5相似,各组间Fas表达有显著性差异(χ2=24.45P=0.000).PDCD5与Fas的相关性分析结果显示,两者呈正相关(r=0.839,P=0.001).结论:PDCD5是HCC发生、发展过程中的一个重要凋亡调控因子.展开更多
目的:探讨在子宫内膜癌细胞中重组人程序性细胞死亡蛋白5(recombinant human programmed cell death protein 5,rhPDCD5)对紫杉醇化疗的促进作用。方法:子宫内膜癌KLE细胞培养完成后,通过重组人rh PDCD5(20μg/ml)处理KLE细胞,再分别以0...目的:探讨在子宫内膜癌细胞中重组人程序性细胞死亡蛋白5(recombinant human programmed cell death protein 5,rhPDCD5)对紫杉醇化疗的促进作用。方法:子宫内膜癌KLE细胞培养完成后,通过重组人rh PDCD5(20μg/ml)处理KLE细胞,再分别以0、1.0、5.0、10.0、50μmol/L紫杉醇(paclitaxel,PTX)处理24 h或以10μmol/L PTX处理0、12、24、48 h,提取细胞总RNA及蛋白后,CCK法检测KLE细胞的增殖情况,流式细胞术检测KLE细胞凋亡情况,实时定量PCR检测KLE细胞中PDCD5mRNA的表达量,实时定量PCR或Western blotting测定凋亡相关基因的Bax、Bcl2、caspase-3 mRNA或蛋白水平的变化。结果:PTX对PDCD5表达的促进作用具有剂量依赖性和时间依赖性;PTX的最佳作用浓度为10μmol/L,最佳作用时间为24 h。rh PDCD5明显增强紫杉醇对KLE细胞的抑制作用。CCK实验、流式细胞术及Western blotting检测显示:PTX+rhPDCD5联合处理组KLE细胞的增殖抑制率和凋亡率均较PTX组明显增加、pro-caspase 3的表达量明显增加(均P<0.01)。促进凋亡蛋白Bax和抑制凋亡蛋白Bcl2的比值亦较明显增加(P<0.01)。结论:rhPDCD5可协同PTX抑制子宫内膜癌KLE细胞的增殖、促进细胞的凋亡,可明显增强KLE细胞对PTX的药物敏感性。展开更多
文摘Objective To investigate the expression of programmed cell death 5 （PDCD5） in tissues of normal human prostate （NP）, benign prostatic hyperplasia （BPH）, and prostate cancer （PCa） in order to assess the clinical role of PDCD5 in PCa. Methods PDCD5 expression was determined by EnVision immunohistochemical staining in forma-lin-fixed and paraffin-embedded specimens obtained from 12 subjects with NP, 22 with BPH, and 22 with PCa. In addition, PCa cases were classified as low/middle-risk （Gleason sumS7） and high-risk （Gleason sum〉7） on the basis of Gleason grade. Positive expression rates and intensity of PDCD5 protein were observed under light microscope and analyzed with computer imaging technique. Expression of PDCD5 was compared among different prostatic tissues. Results The expression of PDCD5 was significantly lower in tissue of PCa than in tissues of NP and BPH （P〈0.01）. However, there was no significant difference in PDCD5 expression between tissues of NP and BPH. In addition, the expression of PDCD5 was further downregulated with the increase of Gleason sum in PCa. Conclusions By downregulating apoptosis, low PDCD5 expression may play an important role in the occurrence and development of PCa. PDCD5 is supposed to have a potential clinical value to be a new predictor of progression and target of gene therapy in PCa.
基金supported by a grant from the National Natural Science Foundation of China (No. 30672307)
文摘This study examined the expression pattern of programmed cell death 5 (PDCD5) in co-chlear hair cells and spiral ganglion neurons (SGNs) and its association with age-related hearing loss in mice.Sixty C57BL/6J (C57) mice at different ages were divided into four groups (3,6,9 or 12 months).PDCD5 expression was detected by using immunohistochemistry,real-time PCR and Western blot.Morphological change of the cochleae was also evaluated by using immunoassay.The results showed that the expression of PDCD5 had a gradual increase with ageing in both protein and RNA levels in C57 mice,as well as gradually increased apoptosis of cochlear hair cells and SGNs.In addition,we also found that caspase-3 activity was enhanced and its expression was enhanced with ageing.It is implied that overexpression of PDCD5 causes the increase in caspase-3 activity and the subsequent increase of apoptosis in cochlear hair cells and SGNs,and thereby plays a role in the pathogenesis of presbycusis.Thus,PDCD5 may be a new target site for the treatment and prevention of age-related hearing loss.
文摘Polygonum cuspidatum is used as a traditional medicinal herb for the therapy of various diseases including several types of cancers. In the present study, we focused on addressing the anti-cancer activity and molecular mechanism of methanol extract of Polygonum cuspidatum (MEPC) in HSC-2 human oral cancer cells. The effect of MEPC on oral cancer cells was estimated by 3-(4,5-dimethylthiazol-20yl)-(3-carboxymethoxyphenyl)-2-(4-sulphophenyl)-2H-tetrazolium (MTS) assay, 4’-6-diamidino-2-phenylindole (DAPI) staining and Western blot analysis. MEPC inhibited the cell viability and induced apoptosis through the induction of death receptor (DR) 5. MEPC also increased the expression of C/EBP homologous protein/growth arrest and the DNA damage-inducible gene 153 (CHOP), a transcription factor induced by ER stress. Thus, we concluded that the induction of CHOP leading to DR5 up-regulation is required for the anti-cancer activity of MEPC in HSC-2 cells and MEPC may be a promising drug candidate for oral cancer.
文摘Objective: To study the relationship of PDCD5 expression with apoptosis, inflammatory factors and MMPs/TIMPs expression in degenerated intervertebral disc tissue. Methods:Patients with lumbar disc herniation who were treated in the Seventh People's Hospital of Shanghai between March 2015 and February 2017 were selected as the LDH group and patients with violent thoracolumbar vertebral fracture were selected as the control group. The intervertebral disc tissue was collected to determine the mRNA expression of PDCD5 as well as the protein levels of apoptosis molecules, inflammatory factors and MMPs/TIMPs molecules. Results: PDCD5 mRNA expression in intervertebral disc tissue of LDH group was significantly higher than that of control group;Caspase-3, Caspase-8, Fas, Caspase-9, Bax, SDF-1, CXCR-4, TNF-α, PGE2, MMP1, MMP2, MMP8 and MMP9 protein levels in intervertebral disc tissue of LDH group were significantly higher than those of control group and positively correlated with PDCD5 mRNA expression while TIMP1 and TIMP2 protein levels were significantly lower than those of control group and negatively correlated with PDCD5 mRNA expression. Conclusion: The high expression of PDCD5 in degenerated intervertebral disc tissue can activate apoptosis and inflammatory response and cause MMPs/TIMPs imbalance.
文摘目的:分析新凋亡促进因子-程序化细胞死亡分子5(programmed cell death 5,PDCD5)在肝细胞癌(hepatocellular carcinoma,HCC)发生发展中的作用.方法:用免疫组织化学法(immunohisto-chemistry,IHC)检测40例HCC及其癌旁组织(包括24例肝硬化和16例慢性肝炎)中的PDCD5和Fas蛋白表达.用等级资料Kruskal-WallisH检验方法进行统计学分析,并用Spearman's等级资料的相关分析比较PDCD5和Fas的表达差异.结果:PDCD5在肝癌组织中多呈阴性表达,在癌旁肝组织中表达增加.肝癌及其癌旁肝硬化肝炎各组间PDCD5表达具有显著性差异(χ2=46.03,P=0.000).Fas在肝癌组织及其癌旁肝硬化或慢性肝炎组织中的表达分布与PDCD5相似,各组间Fas表达有显著性差异(χ2=24.45P=0.000).PDCD5与Fas的相关性分析结果显示,两者呈正相关(r=0.839,P=0.001).结论:PDCD5是HCC发生、发展过程中的一个重要凋亡调控因子.
