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Effects of transferred NK4 gene on proliferation, migration, invasion and apoptosis of human prostate cancer DU145 cells

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Asian Journal of Andrology 2010年第3期12卷 381-389,I0010页

作者： Dan Yue Yong Wang Ping Ma Yin-Yan Li Hong Chen Ping Wang Chang-Shan Ren cancer Research Institute First Affiliated Hospital China Medical University Shenyang 110001 China Department of Urology Fourth Affiliated Hospital China Medical University Shenyang 110032 China Department of Ultrasound First Affihated Hospttal China Medical University Shenyang 110001 China

We investigated the ability of NK4, an antagonist of human hepatocyte growth factor （HGF）, to inhibit the influence of HGF on proliferation, migration, invasion and apoptosis of human prostate cancer cells. Expression vector pBudCE4.1-EGFP-NK4 containing NK4 cDNA was used to transfect human prostate cancer DU145 cells, and the effects of the autocrine NK4 on tumor cell proliferation, migration, invasion and apoptosis were assessed in vitro. in vivo, we subcutaneously implanted DU145 cells, mock-transfected clone （DU145/empty vector） cells and NK4- transfected clone （DU145/NK4） cells into nude mice, and then evaluated tumor growth, cell proliferation and cell apoptosis in vivo. We found that DU145/NK4 cells expressed NK4 protein. In the in vitro study, autocrine NK4 at- tenuated the HGF-induced tumor cell proliferation, migration and invasion, and stimulated apoptosis. Furthermore, autocrine NK4 effectively inhibited the HGF-induced phosphorylation of c-Met, extracellular signal-regulated kinase-1 （ERK1）. and protein kinase B 1/2 （Aktl/2）. Histological examination revealed that autocrine NK4 inhibited prolifera- tion and accelerated apoptosis of prostate cancer cells. These results show that genetic modification of DU145 cells with NK4 cDNA yields a significant effect on their proliferation, migration, invasion and apoptosis. Molecular targeting of HGF/c-Met by NK4 could be applied as a novel therapeutic approach to prostate cancer.

关键词： hepatocyte growth factor human prostate cancer NK4 DU 145 cells

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The role of TRPC6 in HGF-induced cell proliferation of human prostate cancer DU145 and PC3 cells

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Asian Journal of Andrology 2010年第6期12卷 841-852页

作者： Yong Wang Dan Yue Kai Li Yi-Li Liu Chang-Shah Ren Ping Wang Department of Urology Fourth Affiliated Hospital China Medical University Shenyang 110032 China College of Medical Laboratory Science Tianjin Medical University Tianjin 300070 China Department of Surgical Oncology First Affiliated Hospital China Medical University Shenyang 110001 China cancer Research Institute First Affiliated Hospital China Medical University Shenyang 110001 China

Hepatocyte growth factor （HGF） is a glycoprotein that induces prostate cancer cell proliferation, migration and invasion. The activation of transient receptor potential canonical 6 （TRPC6） channels is considered important in promoting prostate cancer cell proliferation. In this study, we assessed the role of endogenous TRPC6 channels in the HGF-induced cell proliferation of prostate cancer. Reverse transcription-PCR and Western blotting were used to investigate TRPC6 expression. Electrophysiological techniques （whole-cell patch clamp configuration） and Ca^2＋ imaging analysis were used to investigate the channel activity in cells. The effects of TRPC6 channels on cell cycle progression, cell apoptosis and cell growth were also examined. TRPC6 and c-MET were expressed in DU145 and PC3 cells. In addition, functional TRPC6 channels were present in DU145 and PC3 cells, and TRPC6 knockdown suppressed TRPC-Iike currents evoked by oleoyl-2-acetyl-sn-glycerol （OAG）. Inhibition of TRPC6 channels in DU145 and PC3 cells abolished OAG- and HGF-induced Ca^2＋ entry. Furthermore, inhibition of TRPC6 channels arrested DU145 and PC3 cells at the G2/M phase and suppressed HGF-induced cell proliferation. Collectively, our results indicate that TRPC6 has an important role in HGF-induced DU145 and PC3 cell proliferation.

关键词： hepatocyte growth factor human prostate cancer proliferation TRPC6

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Effects of bortezomib in sensitizing human prostate ：ancer cell lines to NK-mediated cytotoxicity

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Asian Journal of Andrology 2012年第5期14卷 695-702页

作者： Wei Hu Rui-Rui Zheng Hui-Xia Cui Dan Yue Yong Wang You-Hong Jiang cancer Research Institute First Affiliated HospitalChina Medical UniversityShenyang 110001China Department of Laboratory Medicine Tianjin Medical University Tianjin 300192China Tianjin Institute of Urology Tianjin Medical UniversityTianjin 300192China

The proteasome inhibitor, bortezomib, has been demonstrated to sensitize tumor cells to tumor necrosis factor-related apoptosis-inducing ligand （TRAIL）-mediated apoptosis. Natural killer （NK） cells represent potent antitumor effector cells. They also express TRAIL. Therefore, we investigated whether bortezomib could sensitize tumor cells to NK cell-mediated killing, and have the same effect in human prostate cancer cell lines （LNCaP and DU145）. We found that bortezomib strongly inhibits proliferation in both cell lines. Furthermore, compared with LNCaP cells, DU145 cells are more sensitive to bortezomib-induced apoptosis. However, bortezomib is unable to sensitize these two cell lines to NK cell-mediated killing in short-term assays. In long-term assays, we found that killing mediated by activated NK cells following bortezomib treatment leads to greater antitumor effects than either treatment alone. In addition, treatment with bortezomib causes these cells to upregulate apoptosis-related mRNA as well as death receptors and downregulate the major histocompatibility class （MHC）-I molecule on the cell surface of DU145 cells. In contrast, LNCaP cells are not sensitized by this treatment. Death receptors and the MHC-I molecule did not change in this cell line. These data suggest that bortezomib can be used to sensitize prostate cancer cells to NK cell-mediated killing and improve current cancer therapies. This theral）eutic stratelzv may be more effective in I）atients with androeen-insensitive orostate cancer.

关键词： bortezomib DU145 cells human prostate cancer LNCaP ceils NK cells

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Elucidation of regulatory interaction networks underlying human prostate adenocarcinoma

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Journal of Chinese Pharmaceutical Sciences 2015年第1期24卷 12-27页

作者： Sujit Nair Celine Liew Tin-Oo Khor Li Cai Ah-Ng Tony Kong Amrita cancer Discovery Biology Laboratory and Amrita School of Pharmacy Amrita Vishwa Vidyapeetham University Ponekkara P.O. Kochi-682041 Kerala India Department of Pharmaceutics Rutgers The State University of New Jersey Piscataway NJ-08854 USA Department of Pharmacy National University of Singapore 18 Science Drive 4 Singapore--117543 Department of Biomedical Engineering Rutgers the State University of New Jersey Piscataway NJ-08854 USA

The incidence of prostate cancer is rising in the Asia-Pacific region as well as other countries. Androgen-ablation therapy is clinically useful in the androgen-dependent phenotype however, many patients progress to hormone refractory prostate cancer that is difficult to treat and needs newer interventions that are more effective. The objective of this study was to determine functionally-relevant biological networks, to appreciate the potential crosstalk between signaling members, and to identify biomarker signatures in prostate cancer. We used microarray analyses to identify key genes that were upregulated or down regulated at least five-fold in human prostate cancer and constructed canonical interaction networks that are important in prostate cancer through metabolomics analyses. Our prostate cancer network architecture revealed several key biomarkers including ERK1/2, JNK, p38, MEK, PI3 K, NFκB, AP-1, 14-3-3, VEGF, PDGF, Rb, WNT8 A, WNT10 A, CD44, ESR2, FSH and LH. Furthermore, the top ten transcription factors identified by TFBS-association signature analysis in the regulatory elements of co-regulated biomarkers were delineated, which may crosstalk with upstream or downstream genes elicited in our network architecture. Taken together, our results demonstrate that the regulatory interaction networks in prostate cancer provide a universal view of crosstalk between important biomarkers, i.e., key players in the pathogenesis of this disease. This will facilitate more rapid screening of functional biomarkers in early/intermediate drug discovery.

关键词： human prostate cancer Microarray Biological network Biomarker

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