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| 1 | TRAIL-induced apoptosis of hepatocellular carcinoma cells is augmented by targeted therapies显示文摘AIM:To analyze the effect of chemotherapeutic drugs and specific kinase inhibitors,in combination with the death receptor ligand tumor necrosis factor-related apoptosis inducing ligand(TRAIL),on overcoming TRAIL resistance in hepatocellular carcinoma(HCC)and to study the efficacy of agonistic TRAIL antibodies,as well as the commitment of antiapoptotic BCL-2 proteins, in TRAIL-induced apoptosis. METHODS:Surface expression of TRAIL receptors (TRAIL-R1-4)and expression levels of the antiapoptotic BCL-2 proteins MCL-1 and BCL-xL were analyzed by flow cytometry and Western blotting,respectively. Knock-down of MCL-1 and BCL-xL was performed by transfecting specific small interfering RNAs.HCC cellswere treated with kinase inhibitors and chemotherapeutic drugs.Apoptosis induction and cell viability were analyzed via flow cytometry and 3-(4,5-Dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. RESULTS:TRAIL-R1 and-R2 were profoundly expressed on the HCC cell lines Huh7 and Hep-G2. However,treatment of Huh7 and Hep-G2 with TRAIL and agonistic antibodies only induced minor apoptosis rates.Apoptosis resistance towards TRAIL could be considerably reduced by adding the chemotherapeutic drugs 5-fluorouracil and doxorubicin as well as the kinase inhibitors LY294002[inhibition of phosphoinositol- 3-kinase(PI3K)],AG1478(epidermal growth factor receptor kinase),PD98059(MEK1),rapamycin(mam- malian target of rapamycin)and the multi-kinase inhibitor Sorafenib.Furthermore,the antiapoptotic BCL-2 proteins MCL-1 and BCL-xL play a major role in TRAIL resistance:knock-down by RNA interference increased TRAIL-induced apoptosis of HCC cells.Additionally, knock-down of MCL-1 and BCL-xL led to a significant sensitization of HCC cells towards inhibition of both c-Jun N-terminal kinase and PI3K.CONCLUSION:Our data identify the blockage of survival kinases,combination with chemotherapeutic drugs and targeting of antiapoptotic BCL-2 proteins as promising ways to overcome TRAIL resistance in HCC. | Bruno Christian Koehler Toni Urbanik Binje Vick Regina Johanna Boger Steffen Heeger Peter R Galle Marcus Schuchmann Henning Schulze-Bergkamen | 2009 | World Journal of Gastroenterology2009，15，47： | 9 |
| 2 | Bcl-x_L and Myeloid cell leukaemia-1 contribute to apoptosis resistance of colorectal cancer cells显示文摘AIM: To explore the role of Bcl-xL and Myeloid cell leukaemia (Mcl)-1 for the apoptosis resistance of colorectal carcinoma (CRC) cells towards current treat-ment modalities. METHODS: Bcl-xL and Mcl-1 mRNA and protein ex-pression were analyzed in CRC cell lines as well as human CRC tissue by Western blot,quantitative PCRand immunohistochemistry. Bcl-xL and Mcl-1 protein expression was knocked down or increased in CRC cell lines by applying specific siRNAs or expression plas-mids,respectively. After modulation of protein expres-sion,CRC cells were treated with chemotherapeutic agents,an antagonistic epidermal growth factor recep-tor (EGFR1) antibody,an EGFR1 tyrosine kinase inhibi-tor,or with the death receptor ligand TRAIL. Apoptosis induction and cell viability were analyzed. RESULTS: Here we show that in human CRC tis-sue and various CRC cell lines both Bcl-xL and Mcl-1 are expressed. Bcl-xL expression was higher in CRC tissue than in surrounding non-malignant tissue,both on protein and mRNA level. Mcl-1 mRNA expression was significantly lower in ma-lignant tissues. However,protein expression was slightly higher. Viability rates of CRC cells were significantly decreased after knock down of Bcl-xL expression,and,to a lower extent,after knock down of Mcl-1 expression. Furthermore,cells with reduced Bcl-xL or Mcl-1 expression was more sensitive towards oxaliplatin-and irinotecan-induced apoptosis,and in the case of Bcl-xL also towards 5-FU-induced apoptosis. On the other hand,upregulation of Bcl-xL by transfec-tion of an expression plasmid decreased chemothera-peutic drug-induced apoptosis. EGF treatment clearly induced Bcl-xL and Mcl-1 expression in CRC cells. Apop-tosis induction upon EGFR1 blockage by cetuximab or PD168393 was increased by inhibiting Mcl-1 and Bcl-xL expression. More strikingly,CD95-and TRAIL-induced apoptosis was increased by Bcl-xL knock down. CONCLUSION: Our data suggest that Bcl-xL and,to a lower extent,Mcl-1,are important anti-apoptotic factors in CRC. Specific downregulation of Bcl-xL is a promising approach to sensitize CRC cells towards chemotherapy and targeted therapy. | Henning Schulze-Bergkamen Roland Ehrenberg Lothar Hickmann Binje Vick Toni Urbanik Christoph C Schimanski Martin R Berger Arno Schad Achim Weber Steffen Heeger Peter R Galle Markus Moehler | 2008 | World Journal of Gastroenterology2008，14，24： | 4 |
| 3 | Whole-blood sorting,enrichment and in situ immunolabeling of cellular subsets using acoustic microstreaming显示文摘Analyzing undiluted whole human blood is a challenge due to its complex composition of hematopoietic cellular populations,nucleic acids,metabolites,and proteins.We present a novel multi-functional microfluidic acoustic streaming platform that enables sorting,enrichment and in situ identification of cellular subsets from whole blood.This single device platform,based on lateral cavity acoustic transducers(LCAT),enables(1)the sorting of undiluted donor whole blood into its cellular subsets(platelets,RBCs,and WBCs),(2)the enrichment and retrieval of breast cancer cells(MCF-7)spiked in donor whole blood at rare cell relevant concentrations(10 mL^(−1)),and(3)on-chip immunofluorescent labeling for the detection of specific target cellular populations by their known marker expression patterns.Our approach thus demonstrates a compact system that integrates upstream sample processing with downstream separation/enrichment,to carry out multi-parametric cell analysis for blood-based diagnosis and liquid biopsy blood sampling. | Neha Garg Trisha M.Westerhof Vick Liu Robin Liu Edward L.Nelson Abraham P.Lee | 2018 | Microsystems & Nanoengineering2018，4，1： | 3 |
| 4 | Umbilical Herniorrhapy in Cirrhosis: Improved Outcomes with Elective Repair显示文摘 | Stephen H. Gray Catherine C. Vick Laura A. Graham Kelly R. Finan Leigh A. Neumayer Mary T. Hawn | 2008 | Journal of Gastrointestinal Surgery2008，，4： | 2 |
| 5 | Transscleral diode laser constact cyclophotocoagulation in the treatment of different glaucoma also as primary surgery 显示文摘 | Kramp K Vick HP Guthoff R | 2002 | Graeefe Arch Clin Exp Ophthalmol2002，240，9： | 1 |
| 6 | Transgenic birds from tnmsformed primordial germ cells显示文摘 | Vick L Li Y Simkisa K | 1993 | Proc R Soc Lond1993，251，： | 1 |
| 7 | 显示文摘 | Vick Roy T B Blanch H W Wilke C R | 1983 | Trends of Biotecnology1983，1，： | 1 |
| 8 | Interstitial chemotherapy with drug polymer implants for the treatment of recurrent gliomas显示文摘 | BREM H MAHALEY MS VICK NA | 1991 | J Neurosurg1991，74，2： | 1 |
| 9 | Genetic Control of High Oleic Acid Content in Sunflower Oil 显示文摘 | Miller J F Zimmerman D C Vick B A | 1987 | Crop Science1987，27，5： | 1 |
| 10 | Sound detection of stored-product insects that feed inside kernels of grain 显示文摘 | VICK K M WEBB J C WEABER B A | 1988 | Journal of Economic Entomology1988，81，5： | 1 |
| 11 | Target region amplification polymorphism:A novel marker technique for plant genotyping plant显示文摘 | Hu J Vick BA | | 0，，： | 1 |
| 12 | Bildgebung bei neuroendokrinentumoren des Pankreas显示文摘 | Vick C Zech CJ H?pfner S | | 0，，04： | 1 |
| 13 | Target region amplification polymorphism: a novel marker technique for plant genotyping显示文摘 | Hu J Vick B A | 2003 | Plant Molecular Biology Reporter2003，21，： | 1 |
| 14 | Porous Thin Films for Thermal Barrier Coatings 显示文摘 | Harris K D Vick D Robbie K | 2001 | Surface and Coatings Technology2001，138，： | 1 |
| 15 | Geological model for tunnel cost model显示文摘 | EINSTEIN H H VICK S G | 1974 | Proc Rapid Excavation and Tunneling Conf1974，，2： | 1 |
| 16 | Loss of lymphotoxin α but not tumor necrosis factor-α reduces atherosclerosis in mice 显示文摘 | Schreyer SA Vick CM LeBoeuf RC | 2002 | J Biol Chem2002，277，12： | 1 |
| 17 | A Basic Theoretical Study of the Temperature Rising Contact with Multiple Contacts显示文摘 | Vick B Furey M J | 2001 | Tribology International2001，34，： | 1 |
| 18 | Thin film microstructure control using glancing angle deposition by sputtering 显示文摘 | J C Sit D Vick K Robbie | 1999 | Journal of Materials Research1999，14，4： | 1 |
| 19 | Cure of phenol-formaldehyde adhe- sive in the presence of CCA-treated wood by differential scanning calorimetry显示文摘 | Vick C B Christiansen A W | 1993 | Wood and Fiber Science1993，25，1： | 1 |
| 20 | Coupling of stochastic elec- tromagnetic fields to a transmission line in a reverberation chamber显示文摘 | Magdowski M Tkachenko S V Vick R | 2011 | IEEE Transactions on Electromagnetic Compatibility2011，53，2： | 1 |
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