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Articles by W Shi
Total Records ( 2 ) for W Shi
  W Shi , Z Zhang , M. H Chen , J. F Angle and A. H. Matsumoto

C3H/HeJ (C3H) mice develop much smaller atherosclerotic lesions than C57BL/6 (B6) mice when deficient in apolipoprotein E (apoE–/–) or fed an atherogenic diet. The 2 strains differ in H2 haplotypes, with B6 having H2b and C3H having H2k. C3.SW-H2b/SnJ (C3.SW) is a congenic strain of C3H/HeJ in which H2k is replaced with H2b.

Methods and Results—

We performed bone marrow transplantation and found that atherosclerosis-resistant C3.SW.apoE–/– mice reconstituted with bone marrow from either C3.SW.apoE–/– or B6.apoE–/– mice after lethal irradiation had significantly larger atherosclerotic lesions than B6.apoE–/– mice receiving identical treatments and much larger lesions than C3H.apoE–/– mice reconstituted with syngeneic bone marrow. For syngeneic transplantation, C3.SW.apoE–/– mice exhibited a 21-fold increase in lesion size over C3H.apoE–/– mice (152 800±21 937 versus 7060±2290 µm2/section) and a near 4-fold increase over B6.apoE–/– mice (40 529±4675 µm2/section). C3.SW.apoE–/– mice reconstituted with syngeneic marrow exhibited enhanced lesion formation relative to those reconstituted with B6 marrow (152 800±21 937 versus 107 000±9374 µm2/section; P=0.067). Sublethal irradiation led to a 6-fold increase of lesion size in C3.SW.apoE–/– mice (9795±2804 versus 1550±607 µm2/section; P=0.008). Wild-type C3.SW mice reconstituted with apoE+/+ or apoE–/– bone marrow had significantly larger atherosclerotic lesions than C3H mice receiving identical treatments on an atherogenic diet.


These results indicate that gene(s) within the H2 region have a dramatic impact on radiation-enhanced atherosclerosis, and their effect is conveyed partially through bone marrow–derived cells.

  A. B.Y Hui , S Yue , W Shi , N. M Alajez , E Ito , S. R Green , S Frame , B O`Sullivan and F. F. Liu

Purpose: Seliciclib is a small-molecule cyclin-dependent kinase inhibitor, which has been reported to induce apoptosis and cell cycle arrest in EBV-negative nasopharyngeal carcinoma cell lines. Because most nasopharyngeal carcinoma patients harbor EBV, we proceeded to evaluate the cytotoxic effects of seliciclib in EBV-positive nasopharyngeal carcinoma models.

Experimental Design: Cytotoxicity of seliciclib was investigated in the EBV-positive cell line C666-1 and the C666-1 and C15 xenograft models. Caspase activities and cell cycle analyses were measured by flow cytometry. Efficacy of combined treatment of seliciclib with radiation therapy was also evaluated.

Results: Seliciclib caused significant cytotoxicity in the C666-1 cells in a time- and dose-dependent manner, with accumulation of cells in both sub-G1 and G2-M phases, indicative of apoptosis and cell cycle arrest, respectively. Caspase-2, -3, -8, and -9 activities were all increased, with caspase-3 being the most significantly activated at 48 h after treatment. These cells also showed a reduction of Mcl-1 mRNA and protein levels. Combined treatment of seliciclib with radiation therapy showed a synergistic interaction with enhanced cytotoxicity in C666-1 cells and delayed repair of double-strand DNA breaks. For in vivo models, significant delays in tumor growth were observed for both C666-1 and C15 tumors, which were associated with enhanced apoptosis as determined by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling and immunohistochemistry analyses.

Conclusions: Seliciclib enhanced the antitumor efficacy of radiation therapy in EBV-positive nasopharyngeal carcinoma, characterized by G2-M arrest, and apoptosis, associated with an induction in caspase activity. This process is mediated by reduction in Mcl-1 expression and by attenuation of double-strand DNA break repair.

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