Wanjing Ding
Zhejiang University
6 Papers
56 Citations
Wanjing Ding is an academic researcher from Zhejiang University. The author has contributed to research in topics: Celastrol & Cell cycle checkpoint. The author has an hindex of 6, co-authored 6 publications. Previous affiliations of Wanjing Ding include East China Normal University.
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Papers
Synergistic Anti-Cancer Activity by the Combination of TRAIL/APO-2L and Celastrol
Hong Zhu,Wanjing Ding,Rui Wu,Qinjie Weng,Jianshu Lou,Rong-Jia Jin,Wei Lu,Bo Yang,Qiao-Jun He +8 more
TL;DR: The combination of TRAIL/APO-2L and celastrol exerts strong synergistic antiproliferative effect against human cancer cells including ovary cancer OVCAR-8, colon cancer SW620, and lung cancer 95-D, with the combination indices below 0.8.
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GDC-0941 sensitizes breast cancer to ABT-737 in vitro and in vivo through promoting the degradation of Mcl-1
Lin Zheng,Wei Yang,Chong Zhang,Wanjing Ding,Hong Zhu,Nengming Lin,Honghai Wu,Qiaojun He,Bo Yang +8 more
TL;DR: The present study showed that GDC-0941 potently sensitized breast cancer to ABT-737 in vitro and in vivo and exerted increased anti-tumor efficacy on MDA-MB-231 xenograft models.
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Synergistic antitumor effect of TRAIL in combination with sunitinib in vitro and in vivo
Wanjing Ding,Tianyu Cai,Hong Zhu,Rui Wu,Chongxing Tu,Liu-qing Yang,Wei Lu,Qiaojun He,Bo Yang +8 more
TL;DR: The present data showed that sunitinib potentiated the in vitro and in vivo anticancer capabilities of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), also known as Apo2 ligand, which seems highly encouraging and warrants further investigation in a clinical setting.
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XN05, a novel synthesized microtubule inhibitor, exhibits potent activity against human carcinoma cells in vitro.
TL;DR: The data demonstrated that XN05 exhibited its antitumor activity through disrupting the microtubule assembly, causing cell cycle arrest and consequently inducing apoptosis in BEL-7402 cells, which has great potential for therapeutic treatment of various malignancies.
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E2F1 impairs all-trans retinoic acid-induced osteogenic differentiation of osteosarcoma via promoting ubiquitination-mediated degradation of RARα.
TL;DR: E2F1 is identified as a novel regulator involved in ATRA-induced osteogenic differentiation of osteosarcoma cells and found to downregulate retinoic acid receptor α (RARα), a key factor determines the effectiveness of ATRA.
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