• Title/Summary/Keyword: Zhu Zhen

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Prognostic Value of T Cell Immunoglobulin Mucin-3 in Prostate Cancer

  • Piao, Yong-Rui;Piao, Long-Zhen;Zhu, Lian-Hua;Jin, Zhe-Hu;Dong, Xiu-Zhe
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.6
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    • pp.3897-3901
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    • 2013
  • Background: Optimal treatment for prostate cancer remains a challenge worldwide. Recently, T cell immunoglobulin mucin-3 (TIM-3) has been implicated in tumor biology but its contribution prostate cancer remains unclear. The aim of this study was to investigate the role of TIM-3 as a prognostic marker in patients with prostate cancer. Methods: TIM-3 protein expression was determined by immunohistochemistry and Western blotting in 137 prostate cancer tumor samples and paired adjacent benign tissue. We also performed cell proliferation assays using 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl- 2H tetrazolium bromide (MTT) and cell invasion assays. The effects of small interfering RNA (siRNA)-mediated knockdown of TIM-3 (TIM-3 siRNA) in two human prostate cancer cell lines were also evaluated. Results: TIM-3 expression was higher in prostate cancer tissue than in the adjacent benign tissue (P<0.001). High TIM-3 expression was an independent predictor of both recurrence-free survival and progression-free survival. TIM-3 protein was expressed in both prostate cancer cell lines and knockdown suppressed their proliferation and invasion capacity. Conclusions: TIM-3 expression is associated with a poor prognosis in prostate cancer. Taken together, our resutlts indicate that TIM-3 is a potential prognostic marker in prostate cancer.

Diversity and Antifungal Activity of Endophytic Fungi Associated with Camellia oleifera

  • Yu, Jinxiu;Wu, Ying;He, Zhen;Li, Mi;Zhu, Kaiming;Gao, Bida
    • Mycobiology
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    • v.46 no.2
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    • pp.85-91
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    • 2018
  • Endophytic fungi strains (n = 81) were isolated from the leaves, barks, and fruits of Camellia oleifera from Hunan province (China) to delineate their species composition and potential as biological control agents of C. oleifera anthracnose. The fungi were identified by morphological and phylogenetic analyses. Fungal colonization rates of the leaves, barks, and fruits were 58.02, 27.16, and 14.81%, respectively. The isolates were identified as 14 genera, belonging to two subdivisions, Deuteromycotina and Ascomycotina; 87.65% of all isolates belonged to Deuteromycotina. The dominant species, occurring with a high relative frequency, were Pestalotiopsis sp. (14.81%), Penicillium sp. (14.81%), and Fusarium sp. (12.35%). The Simpson's and Shannon's diversity indices revealed the highest species diversity in the leaves, followed by the barks and fruits. The similarity index for the leaves versus barks comparison was the highest, indicating that the number of endophytic fungal species shared by the leaves and barks was higher than barks and fruits or leaves and fruits. Based on the results of dual culture experiments, only five strains exhibited antifungal activity against C. oleifera anthracnose pathogen, with isolate ty-64 (Oidium sp.) generating the broadest inhibition zones. Our results indicate that the endophytes associated with C. oleifera could be employed as natural agents controlling C. oleifera anthracnose.

Expression of bcl-2 and p53 in Induction of Esophageal Cancer Cell Apoptosis by ECRG2 in Combination with Cisplatin

  • Song, Hai-Yan;Deng, Xiao-Hui;Yuan, Guo-Yan;Hou, Xin-Fang;Zhu, Zhen-Dong;Zhou, Li;Ren, Ming-Xin
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.3
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    • pp.1397-1401
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    • 2014
  • Aim: To investigate the mechanisms of induction of apoptosis of esophageal cancer cells by esophageal cancer-related gene 2 (ECRG2) in combination with cisplatin (DDP). Methods: Hoechest staining was performed to analyze the effects of single ECRG2 and ECRG2 in combination with DDP on apoptosis of EC9706 cells. The expression levels of p53 and bcl-2 mRNA and protein were determined by RT-PCR and Western blotting, respectively. Results: The number of apoptotic cells after the treatment with ECRG2 in combination with DDP for 24 hours was more than that after the treatment with single ECRG2. RT-PCR and Western blotting showed that the expression levels of bcl-2 mRNA and protein were both down-regulated, while p53 mRNA and protein were both up-regulated in the cells treated with ECRG2 in combination with DDP compared with those given ECRG2 alone. Conclusion: ECRG2 in combination with DDP can enhance the apoptosis of EC9706 cells, possibly by down-regulating bcl-2 expression and up-regulating p53.

Efficacy and Safety of Bevacizumab in Chinese Patients with Metastatic Colorectal Cancer

  • Zhu, Li-Ming;Zhao, Ya-Zhen;Ju, Hai-Xing;Liu, Lu-Ying;Chen, Lei;Liu, Bi-Xia;Xu, Qi;Luo, Cong;Ying, Jie-Er;Yang, Yun-Shan;Zhong, Hai-Jun
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.16
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    • pp.6559-6564
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    • 2014
  • Objective: To evaluate the efficacy and safety of bevacizumab in the treatment of patients with metastatic colorectal cancer (mCRC). Methods: In a single-center, observational study of 91 Chinese patients with mCRC who received bevacizumab in combination with chemotherapy was conducted. Objective response rates (ORRs), progression-free survival (PFS), overall survival (OS) and adverse events were recorded, and the relationships between various clinical factors and PFS or OS were evaluated by Cox proportional hazards models. Results: Treatment with bevacizumab and chemotherapy was effective and tolerable. Univariate analysis showed that PFS and OS were significantly associated with the Eastern Cooperative Oncology Group performance status (ECOG-PS) score, duration of bevacizumab exposure, and whether chemotherapy was continued after discontinuation of bevacizumab treatment. A multivariate analysis showed that the duration of bevacizumab exposure and whether chemotherapy was continued after discontinuation of bevacizumab were independent prognostic factors for PFS and OS. Conclusion: In Chinese mCRC population, the shorter the duration of exposure to bevacizumab and chemotherapy, the worse the prognosis is.

Cryptotanshinone Induces Inhibition of Breast Tumor Growth by Cytotoxic CD4+ T Cells through the JAK2/STAT4/ Perforin Pathway

  • Zhou, Jun;Xu, Xiao-Zhen;Hu, Yao-Ren;Hu, Ai-Rong;Zhu, Cheng-Liang;Gao, Guo-Sheng
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.6
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    • pp.2439-2445
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    • 2014
  • Cryptotanshinone (CPT), is a quinoid diterpene isolated from the root of the Asian medicinal plant, Salvia miotiorrhiza bunge. Numerous researchers have found that it could work as a potent antitumor agent to inhibit tumor growth in vitro, buith there has been much less emphasis on its in vivo role against breast tumors. Using a mouse tumor model of MCF7 cells, we showed that CPT strongly inhibited MCF7 cell growth in vivo with polarization of immune reactions toward Th1-type responses, stimulation of naive CD4+ T cell proliferation, and also increased IFN-${\gamma}$ and perforin production of CD4+ T cells in response to tumor-activated splenocytes. Furthermore, data revealed that the cytotoxic activity of CD4+ T cells induced by CPT was markedly abrogated by concanamycin A(CMA), a perforin inhibitor, but not IFN-${\gamma}$ Ab. On the other hand, after depletion of CD4+ T cells or blocked perforin with CMA in a tumor-bearing model, CPT could not effectively suppress tumor growth, but this phenomenon could be reversed by injecting naive CD4+ T cells. Thus, our results suggested that CPT mainly inhibited breast tumor growth through inducing cytotoxic CD4+ T cells to secrete perforin. We further found that CPT enhanced perforin production of CD4+ T cells by up-regulating JAK2 and STAT4 phosphorylation. These findings suggest a novel potential therapeutic role for CPT in tumor therapy, and demonstrate that CPT performs its antitumor functions through cytotoxic CD4+ T cells.

Efficacy and Safety of Trastuzumab Added to Standard Treatments for HER2-positive Metastatic Breast Cancer Patients

  • Zhu, Zhen-Li;Zhang, Jun;Chen, Mei-Lan;Li, Ke
    • Asian Pacific Journal of Cancer Prevention
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    • v.14 no.12
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    • pp.7111-7116
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    • 2013
  • Introduction: Trastuzumab, an HER2-targeting agents, has shown efficacy in metastatic HER2-positive breast cancer patients. Single-agent clinical trials have evaluated therapeutic regimens using trastuzumab for metastatic breast cancer patients. The aim of our study is to evaluate the efficacy and safety of trastuzumab in combination with chemotherapy or hormone therapy in HER2-positive metastatic breast cancer patients. Methods: A literature research was conducted in PubMed and to identify appropriate studies from relevant reviews. Randomized controlled trials comparing chemotherapy or hormone therapy regimens in combination with trastuzumab were eligible. Dadta on clinical outcomes, including safety, efficacy, and patient characteristics were collected. Results: Seven articles describing five trials were included in our systematic review and meta-analysis. Partners of trastuzumab included in trials were anthracycline, paclitaxel, docetaxel, anastrozole and letrozole. The addition of trastuzumab to chemotherapy improved the overall survival (HR=0.79, 95%CI 0.65-0.96), while to hormone therapy did not (HR=0.85 95%CI 0.56-1.30). All trastuzumab-containing regimens increased cardiac toxicity (RR=3.37, 95%CI 1.26-9.02) and grade III-IV adverse events. Conclusions: Our study supports the addition of trastuzumab to chemotherapy which is effective and tolerated for metastatic breast cancer with HER2+ patients. Of note, more adverse events will occur followed the use of trastuzumab, especially cardiac toxicity, with two treatment regimens.

Isolation and Characterization of a cDNA Encoding Two Novel Heat-shock Factor OsHSF6 and OsHSF12 in Oryza Sativa L.

  • Liu, Jin-Ge;Yao, Quan-Hong;Zhang, Zhen;Peng, Ri-He;Xiong, Ai-Sheng;Xu, Fang;Zhu, Hong
    • BMB Reports
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    • v.38 no.5
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    • pp.602-608
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    • 2005
  • As a crucial transcription factor family, heat-shock factors were mainly analyzed and characterized in tomato and Arabidopsis. In this study, we isolated two putative heat shock factors OsHSF6 and OsHSF12 that interact specifically with heat-shock element (HSE) from Oryza sativa L by yeast one-hybrid method. The full-length cDNA of OsHSF6 and OsHSF12 have 1074bp and 920bp open reading frame (ORF), respectively. Analysis of the deduced amino acid sequences revealed that OsHSF6 was a class A heat shock factor (HSF) with all the conserved sequence elements characteristic of heat stress transcription factor, while OsHSF12 was a class B HSF with C-terminal domain (CTD) lacking of AHA motif. Bioinformatic analysis showed that the sequences and structures of two HSFs' DNA binding domain (DBD) had a high similarity with LpHSF24. The results of RT-PCR indicated OsHSF6 gene was expressed immediately after rice plants exposure to heat stress, and the transcription of OsHSF6 gene accumulated primarily in immature seeds, roots and leaves. However, we did not find the transcription of OsHSF12 gene in different organs and growth periods. Our results implied that OsHSF6 might be function as a HSF regulating early expression of stress genes in response to heat shock, and OsHSF12 might be act as a synergistic factor to regulate the expression of down-stream genes.

XRCC1 Arg399Gln Gene Polymorphism and Hepatocellular Carcinoma Risk in the Chinese Han Population: A Meta-analysis

  • Duan, Wei-Hong;Zhu, Zhen-Yu;Liu, Jun-Gui;Dong, Mao-Sheng;Chen, Jun-Zhou;Liu, Quan-Dda;Xie, Yu;Sun, Ti-Ye;Gao, Ze-Feng;Zhou, Ning-Xin
    • Asian Pacific Journal of Cancer Prevention
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    • v.13 no.8
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    • pp.3601-3604
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    • 2012
  • Purpose: Numerous studies have evaluated the association between XRCC1 Arg399Gln gene polymorphism and hepatocellular carcinoma risk in the Chinese Han population. However, the results have been inconsistent. We therefore here examined whether the XRCC1 Arg399Gln gene polymorphism confers hepatocellular carcinoma risk by conducting a meta-analysis. Methods: PubMed, Google scholar and China National Knowledge Infrastructure databases were searched for eligible articles in English and Chinese that were published before April 2012. Results: 6 studies involving 1,246 patients with hepatocellular carcinoma and 1,953 controls were included. The association between XRCC1 Arg399Gln gene polymorphism and hepatocellular carcinoma in the Chinese Han population was significant under GG vs AA (OR = 1.48, 95% CI = 1.13 to 1.94). Limiting the analysis to the studies with controls in the Hardy-Weinberg equilibrium, the results were persistent and robust. Conclusions: In the Chinese Han population, the XRCC1 Arg399Gln gene polymorphism is associated with an increased hepatocellular carcinoma risk.

Efficacy and Safety of Laser Surgery and Transurethral Resection of the Prostate for Treating Benign Prostate Hyperplasia: a Network Meta-analysis

  • Wang, Li;Yu, Qiu-Yan;Liu, Yan;Zhu, Zhen-Li;Huang, Yuan-Wei;Li, Ke
    • Asian Pacific Journal of Cancer Prevention
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    • v.17 no.9
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    • pp.4281-4288
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    • 2016
  • Background: Traditional meta-analyses or systematic reviews of randomized controlled trials (RCTs) have been used to compare laser surgeries and transurethral resection of the prostate (TURP) for benign prostate hyperplasia (BHP), but they cannot provide a hierarchy regarding efficacy and safety of treatment. Objective: We therefore performed a network meta-analysis (NMA) to compare and create hierarchies for efficacy and safety of TUPR and laser surgeries for BPH. Materials and Methods: We searched for reports of RCTs published up to April 25, 2015. After methodological quality assessment and data extraction, we performed an NMA to compare TURP and laser surgeries for BPH. Results: We ranked the treatments of TURP and laser surgeries for BPH. For IPSS at 6 months, holmium laser resection of the prostate (HoLRP) ranked the first-best and at 12 months, holmium laser enucleation of the prostate (HoLEP). For Qmax at 6 and 12 months, HoLEP ranked the first-best; for operative time it was TURP; for cathedral removal time, diode laser enucleation of the prostate (DiLEP) ranked the first-best. Conclusions: Although TURP is considered the gold standard for treating BPH, it is not better in terms of efficacy and safety compared with the laser surgery. Our NMA created hierarchies for the 9 types of surgery in terms of efficacy and safety, which should help clinicians choose the best approach for the individual patient.

A Functional SNP in the MDM2 Promoter Mediates E2F1 Affinity to Modulate Cyclin D1 Expression in Tumor Cell Proliferation

  • Yang, Zhen-Hai;Zhou, Chun-Lin;Zhu, Hong;Li, Jiu-Hong;He, Chun-Di
    • Asian Pacific Journal of Cancer Prevention
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    • v.15 no.8
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    • pp.3817-3823
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    • 2014
  • Background: The MDM2 oncogene, a negative regulator of p53, has a functional polymorphism in the promoter region (SNP309) that is associated with multiple kinds of cancers including non-melanoma skin cancer. SNP309 has been shown to associate with accelerated tumor formation by increasing the affinity of the transcriptional activator Sp1. It remains unknown whether there are other factors involved in the regulation of MDM2 transcription through a trans-regulatory mechanism. Methods: In this study, SNP309 was verified to be associated with overexpression of MDM2 in tumor cells. Bioinformatics predicts that the T to G substitution at SNP309 generates a stronger E2F1 binding site, which was confirmed by ChIP and luciferase assays. Results: E2F1 knockdown downregulates the expression of MDM2, which confirms that E2F1 is a functional upstream regulator. Furthermore, tumor cells with the GG genotype exhibited a higher proliferation rate than TT, correlating with cyclin D1 expression. E2F1 depletion significantly inhibits the proliferation capacity and downregulates cyclin D1 expression, especially in GG genotype skin fibroblasts. Notably, E2F1 siRNA effects could be rescued by cyclin D1 overexpression. Conclusion: Taken together, a novel modulator E2F1 was identified as regulating MDM2 expression dependent on SNP309 and further mediates cyclin D1 expression and tumor cell proliferation. E2F1 might act as an important factor for SNP309 serving as a rate-limiting event in carcinogenesis.