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  • Harvest of at Least 23 Lymph Nodes is Indispensable for Stage N3 Gastric Cancer Patients

    • 摘要:

      Background: The National Comprehensive Cancer Network (NCCN) recoMM.ends that at least 15 lymph nodes (LNs) be removed during radical gastrectomy. This study aims to investigate the optimal number of LNs resected for radical gastrectomy. Patients and Methods: From September 2008 to March 2015, a total of 1990 gastric cancer patients were enrolled in this study. Clinicopathological features and survivals were recorded, and the association between the number of LNs resected and the prognosis of gastric cancer were analyzed. Results: Overall, 1520 males (76.4%) and 470 females (23.6%) were included in the study, with a median age of 57 years (range 20–90). The median number of LNs resected was 24 (range 15–83) for stage N1, 25 (range 15–62) for stage N2, 25 (range 15–88) for stage N3a, and 28 (range 16–73) for stage N3b. The optimal cut-off value for the number of LNs resected was 22 for stage N3a (p = 0.000) and N3b (p = 0.003) patients, while no other cut-off value was significantly superior to 15 for stage N1–2 patients (both p > 0.05). Age, tumor size, tumor depth, and number of LNs resected were independent prognostic predictors for stage N3a patients, while resection type and number of LNs resected were independent prognostic predictors for stage N3b patients. Removing more than 22 LNs exhibited a significant survival benefit compared with removing 15–22 LNs for stage N3a and N3b patients (29.7 vs. 21.6%, p = 0.000; 12.9% vs. 0%, p = 0.003, respectively). Conclusion: Removing at least 23 LNs could yield better survival outcomes in stage N3 gastric cancer patients.

    • 作者:

      Gaozan Zheng;Fan Feng;Man Guo;Guanghui Xu;Shushang Liu;Zhen Liu;Li Sun;Liu Hong;Jianjun Yang;Xiao Lian;代明 樊;Hongwei Zhang

    • 刊名:

      Annals of Surgical Oncology

    • 在线出版时间:

      2017-4-1

  • Letter

    • 摘要:

    • 作者:

      X. Qi;代明 樊;G. Han

    • 刊名:

      Alimentary Pharmacology and Therapeutics

    • 在线出版时间:

      2014-6

  • Restoration of tumor suppressor miR-34 inhibits human p53-mutant gastric cancer tumorspheres

    • 摘要:

      Background: MicroRNAs (miRNAs), some of which function as oncogenes or tumor suppressor genes, are involved in carcinogenesis via regulating cell proliferation and/or cell death. MicroRNA miR-34 was recently found to be a direct target of p53, functioning downstream of the p53 pathway as a tumor suppressor. miR-34 targets Notch, HMGA2, and Bcl-2, genes involved in the self-renewal and survival of cancer stem cells. The role of miR-34 in gastric cancer has not been reported previously. In this study, we examined the effects of miR-34 restoration on p53-mutant human gastric cancer cells and potential target gene expression. Methods: Human gastric cancer cells were transfected with miR-34 mimics or infected with the lentiviral miR-34-MIF expression system, and validated by miR-34 reporter assay using Bcl-2 3'UTR reporter. Potential target gene expression was assessed by Western blot for proteins, and by quantitative real-time RT-PCR for mRNAs. The effects of miR-34 restoration were assessed by cell growth assay, cell cycle analysis, caspase-3 activation, and cytotoxicity assay, as well as by tumorsphere formation and growth. Results: Human gastric cancer Kato III cells with miR-34 restoration reduced the expression of target genes Bcl-2, Notch, and HMGA2. Bcl-2 3'UTR reporter assay showed that the transfected miR-34s were functional and confirmed that Bcl-2 is a direct target of miR-34. Restoration of miR-34 chemosensitized Kato III cells with a high level of Bcl-2, but not MKN-45 cells with a low level of Bcl-2. miR-34 impaired cell growth, accumulated the cells in G1 phase, increased caspase-3 activation, and, more significantly, inhibited tumorsphere formation and growth. Conclusion: Our results demonstrate that in p53-deficient human gastric cancer cells, restoration of functional miR-34 inhibits cell growth and induces chemosensitization and apoptosis, indicating that miR-34 may restore p53 function. Restoration of miR-34 inhibits tumorsphere formation and growth, which is reported to be correlated to the self-renewal of cancer stem cells. The mechanism of miR-34-mediated suppression of self-renewal appears to be related to the direct modulation of downstream targets Bcl-2, Notch, and HMGA2, indicating that miR-34 may be involved in gastric cancer stem cell self-renewal/ differentiation decision-making. Our study suggests that restoration of the tumor suppressor miR-34 may provide a novel molecular therapy for p53-mutant gastric cancer.

    • 作者:

      Qing Ji;Xinbao Hao;Yang Meng;Min Zhang;Jeffrey DeSano;代明 樊;Liang Xu

    • 刊名:

      BMC Cancer

    • 在线出版时间:

      2008-9-21

  • Cloning and identification of an angiostatic molecule IP-10/crg-2

    • 摘要:

      AIM: To obtain human and murine cDNAs encoding IFN-γ inducible protein 10 (IP-10) and cytokine responsive gene-2 (Crg-2). METHODS: The encoding genes of IP-10 and Crg-2 were amplified by RT-PCR from cultured human fibroblast cells and Balb/ c mouse liver treated by IFN-γ and TNF-α, respectively, and cloned into plasmids of pUC19 and pGEMSZf (+). RESULTS: The nucleotide sequences of the amplified DNA were confirmed by endonucleases digestion and sequencing. CONCLUSION: Recombinant IP-10/ crg-2 gene clones with 306 bp and 314 bp inserts were established for further research on biological activities and ligands of hIP-10/mCrg-2. Copyright

    • 作者:

      Zhi Guo Liu;Jing Hua Yang;Hua Zhang An;Hai Yan Wang;Feng Tian He;Zhe Yi Han;Ying Han;Han Ping Wu;Bing Xiao;代明 樊

    • 刊名:

      World Journal of Gastroenterology

    • 在线出版时间:

      1999-6

  • Safety, tolerability and satisfaction with tegaserod therapy in Asia-Pacific patients with irritable bowel syndrome with constipation

    • 摘要:

      Background and Aim: The 5-HT4receptor agonist tegaserod (6 mg b.i.d.) provides significantly better overall multiple symptom relief compared with placebo in patients with irritable bowel syndrome with constipation (IBS-C). The clinical benefit and safety of tegaserod in IBS-C patients has been demonstrated worldwide in several studies. The aim of this study was to obtain further safety and tolerability data in patients with IBS in the Asia-Pacific region, and to assess patients' satisfaction and compliance with treatment and willingness to re-use tegaserod in a post-marketing setting. Methods: A multicenter, single-arm, open-label trial was conducted at 869 outpatient centers in 10 countries. Men and women with IBS, whose predominant bowel symptom was not diarrhea (non-D-IBS), received tegaserod for 4-12 weeks. Safety and tolerability were assessed by recording adverse events (AE). Patients were questioned about compliance, satisfaction with treatment and willingness to use tegaserod in future. Results: Data were available from 14 537 patients (18% men, 82% women). Four percent of patients reported at least one AE. The most common AE were diarrhea (2%) and abdominal pain (1%), and most treatment-related AE occurred in the first week of treatment. Serious AE (SAE) were observed in eight patients, and no deaths were reported. Most patients (79%) reported to be satisfied or very satisfied with treatment, and 76% stated they would use tegaserod in the future. Compliance was 97%. Conclusions: Tegaserod has a favorable safety and tolerability profile for treating non-D-IBS and IBS-C in men and women in the Asia-Pacific region. Satisfaction with tegaserod treatment can be expected in the majority of patients.

    • 作者:

      Kwong M. Fock;Amy Wagner;M. A. Ahad;D. S. Ahmed;F. Ahmed;M. M. Ahmed;M. S. Ali;M. R. Bhuiyan;D. Chowdhury;M. Hasan;S. M. Ishaqe;A. Kabir;M. R. Khan;H. Masud;M. A. Masud;M. A. Rab Sarkar;M. A. Rahim Mia;M. H. Rahman;A. S.M.A. Raihan;A. H.M. Rowsan;P. K. Roy;S. K. Saha;W. Y. Bai;J. T. Cai;B. Cao;X. M. Chang;J. F. Chen;J. X. Chen;J. Y. Chen;L. D. Chen;L. J. Chen;M. X. Chen;W. C. Chen;W. X. Chen;X. M. Chen;Y. Chen;Y. L. Chen;Y. S. Chen;J. X. Cheng;X. Y. Cui;M. M. Deng;Y. J. Ding;J. D. Dong;L. Dong;S. X. Dong;G. P. Du;L. P. Duan;代明 樊;Z. J. Fan;D. C. Fang;H. Feng;K. Feng;Y. K. Feng;Z. T. Feng;B. Y. Fu;J. Fu;A. H. Gan;X. Y. Gao;X. Z. Gao;F. L. Gong;F. Y. Gong;L. Gong;G. M. Gu;X. H. Gu;H. X. Guo;X. Z. Guo;Y. M. Guo;L. Q.M. Hai;R. G. Han;S. X. Han;Z. Han;Y. Hong;J. R. Hou;X. H. Hou;Y. Hu;Z. K. Hu;D. W. Hua;G. M. Huang;H. Huang;J. F. Huang;K. M. Huang;L. Y. Huang;S. P. Huang;X. F. Huang;Y. M. Huang;Z. J. Huang;L. J. Huo;F. Ji;Z. Z. Ji;L. P. Jia;F. H. Jian;Y. B. Jiang;Z. C. Kan;B. Li;B. J. Li;D. G. Li;F. K. Li;F. R. Li;J. J. Li;J. S. Li;N. Li;R. Z. Li;S. D. Li;S. L. Li;Y. Li;Y. M. Li;Y. Q. Li;P. X. Liang;M. Lin;W. Lin;F. Liu;H. L. Liu;J. Y. Liu;N. Z. Liu;Q. Liu;Q. Y. Liu;S. Y. Liu;W. Z. Liu;X. G. Liu;X. H. Liu;X. M. Liu;Y. L. Liu;Z. W. Liu;J. Y. Lu;Q. Lu;S. Y. Lu;X. P. Lu;Z. P. Lu;H. S. Luo;Z. J. Luo;B. Lu;N. H. Lu;J. Ma;X. D. Ma;X. Z. Meng;Y. Q. Nie;Y. Q. Ou;X. B. Peng;Y. F. Piao;S. M. Qi;C. H. Qiao;J. L. Ren;X. Ren;B. B. Shen;S. R. Shen;W. Shen;W. Z. Shen;Y. Z. Shen;S. H. Shi;F. Shu;Y. L. Si;S. H. Song;J. C. Sui;C. Sun;G. H. Sun;S. Q. Sun;Z. B. Tian;B. Wang;B. J. Wang;B. M. Wang;C. D. Wang;F. Y. Wang;G. S. Wang;J. B. Wang;J. G. Wang;M. Wang;M. Y. Wang;Q. Wang;Q. Wang;Q. M. Wang;Q. Y. Wang;S. F. Wang;S. X. Wang;X. Q. Wang;X. Z. Wang;Y. D. Wang;Z. F. Wang;L. Wei;L. Wei;Z. F. Wen;G. Wu;H. Wu;J. Wu;P. Wu;Q. Wu;Q. M. Wu;W. Wu;W. D. Wu;H. Z. Xia;M. Xie;W. F. Xie;C. H. Xu;H. L. Xu;J. M. Xu;L. Xu;L. G. Xu;Y. G. Xu;Z. Xu;H. J. Yan;G. M. Yang;N. Yang;Y. L. Yang;Y. S. Yang;Y. X. Yang;H. C. Yao;H. J. Ye;Y. A. Ye;C. M. Yu;J. J. Yu;J. X. Yu;X. M. Yu;Y. Z. Yuan;X. Z. Zeng;B. X. Zhang;C. Q. Zhang;C. Y. Zhang;G. Y. Zhang;L. Zhang;R. H. Zhang;R. X. Zhang;S. S. Zhang;S. T. Zhang;T. C. Zhang;W. Q. Zhang;X. Zhang;X. P. Zhang;Z. G. Zhang;Z. J. Zhang;B. Zhao;C. X. Zhao;H. C. Zhao;Y. H. Zhao;Y. X. Zhao;Z. Q. Zhao;J. H. Zhen;J. J. Zheng;J. W. Zheng;L. Zheng;S. H. Zheng;W. H. Zheng;C. L. Zhou;H. X. Zhou;L. Zhou;L. Y. Zhou;M. Z. Zhou;N. F. Zhou;P. Z. Zhou;S. D. Zhou;Z. L. Zhou;F. L. Zhu;H. H. Zhu;H. M. Zhu;L. M. Zhu;R. M. Zhu;W. Zhu;X. L. Zhu;Y. Q. Zhu;Z. H. Zhu;Z. Y. Zhu;E. T. Chan;K. C. Chan;K. D.K. Chan;C. C. Chang;P. K. Cheng;C. S. Cheung;K. P. Fung;R. B. Heath;L. S.C. Hooi;W. J. Hu;W. L. Hui;P. S. Ip;K. C. Lam;D. K.K. Leung;Y. K. Leung;C. H. Lo;R. Lo;M. T. Lui;S. W.L. Luk;A. C.W. Mui;K. K. Ng;W. C. Ng;C. O. Pong;O. S. Poon;R. K.W. Tang;C. A. Tsang;K. H. Tsang;C. G. Tsui;C. S. Wong;J. Wong;T. C. Wong;R. K.H. Yau;W. H. Yau;F. Y.K. Yu;K. C. Yu;W. H. Yu;G. K. Abadi;B. Y. Anwar;H. F. Arifin;G. Arsyadi;S. Ashar;A. F. Bakry;H. Basri;Y. Chandra;L. Choandry;T. R. Damanik;T. Daryatmo;T. S. Denny;A. Dharmawan;G. Dibjojuwono;L. K. Djimesha;I. Effendi; Indriyanto; Komariatun;A. Kristanto;S. Leonardi;S. Makmun;S. Marpaung;A. Masidin;E. Merentek;K. Nazar;T. Ongko;W. Permadi;M. S. Pranantyo;H. Purbayu;A. Rahimi;A. Rasjid;Q. Rijono;Z. Said;P. B. Santoso;A. Setiadarma;S. Setiadji;H. Setiady;I. Setyopranantyo;H. Sidhojoyo;C. Sjah;R. Sitompul;J. Soedjono;N. Soemargo;F. X.T. Soetjahjo;L. Soetjipto;H. R. Surasmo;F. Suriadi;H. Suryadi;H. Susatyo;A. F. Syam;L. S. Tanudjaja;A. Taslam;L. Taufik;N. Tjahjo;W. Tjandra;G. Tjora;E. W. Walujan;U. Wibowo;I. Wijaya;A. Wirawan;G. Wirotomo;A. Yudiono;W. Zaenudin; Zainab;H. Y. A;J. K. Ahn;K. H. Ahn;T. W. Ahn;H. C. An;L. S. An;S. S. Bae;Y. G. Bae;J. C. Baek;J. G. Baek;K. R. Chae;S. D. Chai;D. H. Chang;H. W. Chang;W. K. Chang;S. R. Cheon;J. K. Cho;J. S. Cho;K. S. Cho;M. N. Choe;B. C. Choi;H. S. Choi;J. Choi;J. P. Choi;J. S. Choi;K. H. Choi;K. S. Choi;M. S. Choi;W. S. Choi;Y. S. Choi;C. W. Chun;W. S. Chung;H. Y. Eo;J. H. Eun;W. K. Go;H. Y. Ha;B. S. Han;K. I. Han;S. H. Han;S. T. Han;S. W. Han;S. C. Hong;S. M. Hong;E. W. Hwang;J. H. Hwang;J. Y. Hwang;K. K. Hwang;S. H. Hwang;C. H. Jang;D. I. Jang;J. Jang;S. J. Jang;M. H. Jeon;S. K. Jeon;S. D. Jeong;S. B. Jin;Y. J. Jin;Y. H. Joo;E. G. Journ;H. J. Ju;J. S. Ju;B. Y. Jung;D. W. Jung;H. J. Jung;H. S. Jung;K. H. Jung;Y. H. Jung;Y. S. Jung;Y. C. Jyeong;H. A. Kang;J. S. Kang;J. W. Kang;M. S. Kang;P. J. Kang;S. W. Kang;S. M. Keum;A. K. Kim;B. R. Kim;B. S. Kim;C. S. Kim;D. H. Kim;D. H. Kim;D. S. Kim;D. Y. Kim;E. C. Kim;G. H. Kim;G. H. Kim;G. W. Kim;H. B. Kim;H. H. Kim;H. W. Kim;J. B. Kim;J. C. Kim;J. H. Kim;J. H. Kim;J. H. Kim;J. H. Kim;J. I. Kim;J. M. Kim;J. S. Kim;J. S. Kim;J. W. Kim;J. Y. Kim;J. Y. Kim;J. Y. Kim;K. J. Kim;K. W. Kim;M. R. Kim;S. E. Kim;S. S. Kim;S. T. Kim;T. Y. Kim;W. D. Kim;W. S. Kim;Y. G. Kim;Y. H. Kim;Y. J. Kim;Y. S. Kim;Y. T. Kim;Y. W. Kim;B. G. Ko;S. P. Kook;O. S. Kwon;N. K. Kwun;B. D. Lee;B. G. Lee;B. J. Lee;B. W. Lee;C. W. Lee;G. J. Lee;G. T. Lee;H. Lee;H. J. Lee;H. M. Lee;H. Y. Lee;J. I. Lee;J. N. Lee;J. W. Lee;J. Y. Lee;K. R. Lee;K. S. Lee;M. B. Lee;M. S. Lee;P. K. Lee;S. B. Lee;S. C. Lee;S. H. Lee;S. J. Lee;S. M. Lee;S. W. Lee;S. W. Lee;W. S. Lee;Y. B. Lee;Y. W. Lee;H. K. Lim;J. H. Lim;W. S. Lim;D. K. Lo;C. S. Moon;D. S. Moon;S. I. Moon;S. H. Na;B. H. Nam;G. H. Nam;L. H. Nam;S. Y. O;H. S. Oh;H. S. Oh;S. H. Oh;S. H. Oh;S. H. Oh;G. T. Park;H. C. Park;H. J. Park;J. H. Park;J. J. Park;J. N. Park;J. Y. Park;K. H. Park;K. T. Park;S. G. Park;S. H. Park;T. R. Park;Y. H. Park;Y. I. Park;Y. J. Park;Y. S. Park;H. S. Rhim;Y. H. Rho;S. K. Ro;S. K. Roh;T. S. Roh;S. K. Ryu;J. S. Ryue;J. H. Shim;H. W. Shin;J. C. Shin;J. H. Shin;K. S. Shin;K. S. Shin;N. C. Shin;S. T. Shin;Y. Shin;D. H. Shon;J. H. Sohn;K. S. Sohn;S. H. Sohn;H. B. Son;T. Y. Son;C. W. Song;H. Y. Song;I. K. Song;J. S. Song;K. H. Song;K. H. Song;K. J. Song;H. R. Suh;D. J. Sung;M. S. Sung;J. Y. Tack;W. H. Won;K. E. Woo;J. Y. Woo;D. H. Yang;H. H. Yang;J. S. Yang;J. Y. Yang;S. W. Yang;S. W. Yang;J. Y. Yeo;K. Y. Yeom;H. S. Yim;K. B. Yim;J. S. Yoo;Y. K. Yoo;C. K. Yoon;D. H. Yoon;J. G. Yoon;J. Y. Yoon;Y. K. Yoon;Y. S. Yoon;C. M. Youk;Y. H. Youn;B. J. Yu;K. H. Yu;S. J. Yun;U. D. Yun;A. Ahmad; Bahari.S;K. Chandran;W. S. Chen;Y. C. Chia; Davaraj;S. Doshi;P. S. Gill;A. Gunn;M. R.A. Hassan;S. Huang;S. Jacob;H. M. Liau;P. Y. Lu; Manohari;J. Menon;K. T. Ong;E. K. Ooi;R. Ponnudurai;G. Salleho;A. Shukri;L. K. Tan;I. Acusar;M. Adraneda;B. Agbay;F. Aguas;W. Alba;A. Aldon;S. Alegarbes;L. Alves;V. Ang;M. Aquino;M. Arguillas;M. Atienza;Q. Babaran;R. Babaran;R. Bagsic;R. Balmaceda;D. Banayo;A. Bansil;I. Baquiran Masa;M. Basco;J. Bautista;B. Benitez;J. Bocobo;E. Bondoc;C. Bruel;M. Bunyi;R. Caballero;J. Caluag;J. Campos;L. Carandang;R. Carpio;A. Ceniza;J. Cervantes;C. Chan;M. Chan;A. Chua;A. M. Chua;F. Chua;A. Co;A. Comia;J. CoSoriano;O. Cruz;C. Dado-Dalupang;L. Daez;C. De Castro;J. Demyttenaere;N. Dizon;F. Domingo;G. Duque;E. Dy;M. Einanloo;A. Elevazo;D. Encarnacion;P. Eng Lim;D. Entera;A. Espiritu;A. Esteras;E. Flores;A. Frias;E. Gabriel;A. Galang;C. Gallinera;E. Gambe;T. Gamutan;J. Gapasin;G. Gaw;B. Gonzales;D. Gonzales;R. Gonzales;J. M. Guzman;J. Ignacio;A. Ismael;A. Jimenez;R. Kiok Go;A. Kuan;R. Lacson;R. Lacuesta;J. Lao-Tan;J. Ledesma;C. P. Lim;E. Lim;V. Lim;V. Lo;R. Lobaton;R. Lopez;J. R. Lubag;N. Lucido;M. Lustre;J. Macaraeg;R. Magdaong;L. Manabat;W. Manuela;G. Marquez;R. Mercado;R. Miranda;J. Moreno;B. Moscoso;T. Nadala;R. Naval;D. Ngo;E. Olympia;D. Ona;E. Ong;H. Ong;L. Ong;M. Ortiz;V. Paez;R. Palaganas;M. Pamaylaon;J. Pangilinan;D. Parungao;D. Payawal;D. Peña;G. Perlas;J. Pio Reyes;A. Policarpio;E. Portigo;S. Querubin-De Ocampo;J. L. Ramos;P. Retusto;V. Revelo;A. Reyes;C. Reyes;E. Ricarte;N. Rico;A. Ruiz;C. Salazar-Tady;L. Salvador;R. Santi;J. Sollano;M. Sotomil;A. Sta. Ana;C. Sy;R. Tambuyat;J. Tan;G. Tecson;A. M. Tolentino;C. Torio;R. Umil;A. Uy;D. Valencia;V. Valencia;R. Vallar;R. Venezuela;L. C. Vicerra;T. Villa;G. Villanueva;A. Vitug;R. Yap;R. Ycong;G. Ypil;A. Zablan;F. Zaño;P. K. Ang;S. H. Cheng;D. Eu;P. Goh;K. A. Gwee;S. M. Heah;L. Ho;P. Ho;W. W. Hu;S. M. Kong;P. L. Kwak;G. Kwan;C. G. Leow;C. C. Lim;G. L. Lim;C. Loo;H. F. Lui;M. H. Ng;D. Nyam;K. B. Siah;H. H. Tan;S. T. Tan;Y. T. Tan;M. L. Wong;C. C. Chang;C. S. Chang;P. C. Chen;C. H. Chu;S. K. Chuah;W. C. Ho;C. Y. Huang;A. W. Kao;C. H. Kuo;C. H. Kuo;C. C. Lin;J. H. Liu;C. C. Lo;G. H. Lo;M. Y. Su;Y. C. Su;K. M. Tam;H. H. Wang;W. M. Wang;D. C. Wu;F. J. Yu;J. Amornrattanakosol;K. Angkananupong;V. Ariyawongsopon;R. Boonsirichan;V. Cahmchuklin;W. Chaiphornphothana;V. Chantarasuntinkul;C. Chaoprasong;B. Chareonsil;P. Charuscharoenwitt-haya;D. Chokmongkolkij;V. Chomsaksakul;P. Chualwiwat;Y. Dhapasita;S. Gonlachanvit;N. Issariyakullkran;K. Jankiatfoo;D. Janthayanont;P. Kengchon;U. Kiatpanabrikul;P. Kobklachaiyapong;A. Konchome;C. Koosirirat;V. Kositsakulchai;S. Kuslasiyanon;B. Lecksiwlai;S. Lee;K. Mahapol;P. Manosithisak;K. Memonkolkulldilok;S. Mungkorn;D. Noothongkam;T. Noungkunsan;Y. Osothtanakorn;W. Pasurapanya;E. Pethplook;A. Ploodi;T. Pongnakine;S. Prasertsuk;C. Saengborisuit;T. Sanchai;W. Sanpanich;K. Sarakune;E. Singhatiraj;S. Sirinthornpunya;W. Srisukchalarn;P. Sueyunyongsiri;J. Sukchai;P. Tansenee;K. Thhikul;T. Tongbai;P. Trongritthichaikan;W. Uthaisaengsook;A. Vasuwat;R. Vilaichom;V. Vimolchalao;P. Virajsilp;P. Wongtagual;N. Wuttidechkamjorn;C. Yamcharoen;P. Yimchalarn;J. Yossombat

    • 刊名:

      Journal of Gastroenterology and Hepatology (Australia)

    • 在线出版时间:

      2007-8-1

  • Macroautophagy and ERK phosphorylation counteract the antiproliferative effect of proteasome inhibitor in gastric cancer cells

    • 摘要:

      The ubiquitin-proteasome system and macroautophagy are two complementary pathways for protein degradation. Emerging evidence suggests that proteasome inhibition might be a promising approach for the treatment of cancer. In this study, we show that proteasome inhibitor MG-132 suppressed gastric cancer cell proliferation and induced macroautophagy. The induction of macroautophagy was evidenced by the formation of LC3+ autophagosomes and the accumulation of acidic vesicular organelles and autolysosomes and was accompanied by the suppression of mammalian target of rapamycin complex 1 activity. Abolition of macroautophagy by knockdown of class iii phosphatidylinositol-3 kinase Vps34 or ATG5/7 sensitized gastric cancer cells to the antiproliferative effect of MG-132 by promoting G2/M cell cycle arrest. in addition, MG-132 increased ERK phosphorylation whose inhibition by MEK inhibitor significantly enhanced the antiproliferative effect of proteasome inhibition. To conclude, this study demonstrates that macroautophagy and ERK phosphorylation serve as protective mechanisms to counteract the antiproliferative effect of proteasome inhibition. This discovery may have implication in the application of proteasome-directed therapy for the treatment of cancer.

    • 作者:

      William Ka Kei Wu;Chi Hin Cho;Chung Wa Lee;Ya Chun Wu;Le Yu;Zhi Jie Li;Clover Ching Man Wong;Hai Tao Li;Lin Zhang;Shun Xiang Ren;Chun Tao Che;Kaichun Wu;代明 樊;Jun Yu;Joseph Jao Yiu Sung

    • 刊名:

      Autophagy

    • 在线出版时间:

      2010-2-16

  • Screening and identification of phage-displayed polypeptides specifically binding to human gastric cancer with high metastatic potential to peritoneum

    • 摘要:

      OBJECTIVE: By means of phage-display technique, to screen polypeptides that specifically bind to human gastric cancer with high metastatic potential to peritoneum. METHODS: Two human gastric cancer cell lines were used: GC9811-P with high metastatic potential to peritoneum and its wild type parental GC9811, to carry out subtractive screening with a phage display-12 peptide library. RESULTS: After three rounds of screening, 40 phage clones bond to GC9811-P cells were randomly selected. When injected into the peritoneal cavity of nude mice, 6 of the 40 clones did not bind to mouse peritoneum as examined by immunohistochemical staining. They were considered to be capable of binding specifically to GC9811-P cells. Sequence analysis revealed two different exogenous peptides: TLNINRLILPRT and SMSI(X)SPYI(XXX). CONCLUSION: Two peptides have been obtained that specifically bind to a gastric cancer cell variant GC9811-P, which easily disseminates to the peritoneum. Whether or not they could block GC9811-P metastasis to peritoneum in vivo remains to be determined.

    • 作者:

      Ke dong Zhang;Xin ning Guo;L. Yang;Dong tao Zhang;Fei hu Bai;Hai ping Jiang;Hui hong Zhai;Yong zhan Nie;Kai chun Wu;代明 樊

    • 刊名:

      Chinese Journal of Oncology

    • 在线出版时间:

      2005-7

  • Single-step method to prepare native angiostatin from human plasma

    • 摘要:

      As a specific angiogenesis inhibitor, angiostatin can inhibit new vascular formation, and it has potential clinical practical value. Human plasminogen was purified from human plasma by affinity chromatograph, and then in situ digestion of plasminogen by elastase was carried out to produce angiostatin fragments. After washing, angiostain was eluted specifically by 0.2 mol/L 6-aminocaproic acid solution. This improvement made this method be simpler, rapider and more efficient. In vitro and in vivo experiments indicated that this purified protein has potent antiangiogenic activity.

    • 作者:

      Fu Yang Li;Peng He;Xin Ping Liu;Ying Qi Zhang;Jing Hua Yang;代明 樊;Li Bo Yao

    • 刊名:

      Progress in Biochemistry and Biophysics

    • 在线出版时间:

      2000

  • I148M variant of PNPLA3 confer increased risk for nonalcoholic fatty liver disease not only in European population, but also in Chinese population

    • 摘要:

    • 作者:

      Xiaohua Li;Qingchuan Zhao;Kaichun Wu;代明 樊

    • 刊名:

      Hepatology

    • 在线出版时间:

      2011-12

  • Antisense to cyclin D1 reverses the transformed phenotype of human gastric cancer cells

    • 摘要:

      AIM: To further investigate the effect of cyclin D1 on the biologic behavior of cancer cells and its potential role in gene therapy of tumor. METHODS: A cyclin D1 subcloning plasmid termed BKSD1 was constructed by subcloning the human cyclin D1 cDNA into Bluescript-KS, a plasmid vector with a pair of T7 and T3 promoters, with recombinant DNA technology of molecular biology. So, it is easy to generate digoxigenin (DIG)-labeled RNA probes of antisense and sense to cyclin D1 using RKSD1 as a template vector. PDORD1AS, an eukaryotic expression vector containing the full-length human cyclin D1 cDNA in its antisense orientation cloned into the retroviral vector pDOR-neo, was successfully constructed with BKSD1 to change restriction sites. A gastric cancer cell line, SGC7901/ VCR, was transfected with pDORD1AS by Lipofect Amine mediated introduction and a subline termed SGC7901/ VCRD1AS, which had stable overexpression of antisense RNA to cyclin D1, was obtained by selection in G418. The subline, control subline transfected pDOR-neo and SGC7901/ VCR were evaluated by methods of immunohistochemistry, flow cytometry, molecular hybridization, morphology and cell biology. RESULTS: Compared with control cell lines, SGC7901/ VCRD1AS had a reduced expression of cyclin D1 (inhibition rate was about 36%), increased cell size and cytoplasm to nucleus ratio, increased doubling time (42.2 h to 26.8 h and 26.4 h), decreased saturation density (18.9 × 104 to 4.8 × 105 and 4.8 × 105), increased percentage of cells in the G1/ G0 phase (80.9% - 64.6% and 63.8%), reacquired serum dependence, and a loss of tumorigenicity in nude mice (0/ 4 to 4/ 4 and 4/ 4). CONCLUSION: Stable overexpression of antisense RNA to cyclin D1 can reverse the transformed phenotype of human gastric cancer cells and may provide an approach of gene therapy for gastric cancer.

    • 作者:

      Bing Chen;Xue Yong Zhang;Yu Jing Zhang;Ping Zhou;Yan Gu;代明 樊

    • 刊名:

      World Journal of Gastroenterology

    • 在线出版时间:

      1999-2

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