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Wei Dai

Wei Dai, PhD

Professor, Department of Medicine

Professor, Department of Biochemistry and Molecular Pharmacology

Keywords
cell cycle, checkpoint control, mitosis, genomic instability, carcinogenesis, cancer, genome integrity, pharmacology
Summary

Progression of the cell cycle is tightly regulated in order to ensure that genetic integrity is maintained and genetic information is passed correctly to daughter cells. Extensive research over the past two decades has revealed the existence of important surveillance mechanisms (referred to as checkpoints) that regulate cell cycle progression. These checkpoints monitor specific cell cycle?related processes and block cell cycle progression until these processes are completed with high fidelity. Cancer results from damage to multiple genes controlling cell division or cell death. An underlying genetic instability is required for the generation of multiple lesions that are characteristic of cancer. Genetic instability could be manifested as alterations in chromosome number as well as translocations, deletions, and insertions. Aneuploidy is frequently present in many types of tumor cell. A loss of the spindle checkpoint function and the control of anaphase entry appear to be causes leading to gross aneuploidy, a condition from which cells with an advantage for tumor growth will be selected. Thus, studying the mechanism underlying cohesion of sister chromatids and centrioles has the potential for identifying new targets for rational designing of anti-cancer drugs. In addition, a better understanding of biochemical pathways controlling checkpoint-induced programmed cell death may help us to better therapeutically induce resistant tumor cells to undergo apoptosis. We have been studying the function of molecular components in cell cycle regulation and in suppression tumorigenesis. Our recent studies on the function of Plk1, BubR1, and Sgo1 reveal that these cell cycle checkpoint regulators play an important role in the maintenance of genomic stability and suppression of tumor formation. We have obtained a series of mice with ablation of checkpoint genes. We believe these mice will be excellent animal models with which the effect of environmental agents on cacinogenesis can be studied.

Phone

212-263-5521

Academic office

341 East 25 Street

New York, NY 10010

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These focus areas and their associated publications are derived from medical subject headings from PubMed.
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Tran, Franklin; Lee, Eunji; Cuddapah, Suresh; Choi, Byeong Hyeok; Dai, Wei

Cancers. 2022 Nov 25; 14(23):

Kou, Ziyue; Yang, Rui; Lee, Eunji; Cuddapah, Suresh; Choi, Byeong Hyeok; Dai, Wei

Toxicology & applied pharmacology. 2022 Nov 09; 457:116314

Wang, Hanlu; Yang, Tiantian; Jiang, Wenhong; Qin, Meng; Sun, Ziyong; Dai, Wei; Jiang, Yongping

Scientific reports. 2022 Sep 19; 12(1):15668

Dai, Wei; Xie, Suqing; Chen, Changyan; Choi, Byeong Hyeok

Seminars in cancer biology. 2021 Nov; 76:301-309

Choi, Byeong Hyeok; Kou, Ziyue; Colon, Tania Marlyn; Chen, Chih-Hong; Chen, Yuan; Dai, Wei

Journal of biological chemistry. 2021 Jan 19; 100314

Guan, Xin; Wang, Lan; Wang, Hanlu; Wang, Huihui; Dai, Wei; Jiang, Yongping

Clinical & translational science. 2020 Nov; 13(6):1115-1126

Zhang, Yu; Shen, Bin; Guan, Xin; Qin, Meng; Ren, Zhihua; Ma, Yupo; Dai, Wei; Ding, Xinxin; Jiang, Yongping

Stem cell research & therapy. 2019 Jun 13; 10(1):173

Zhu, Junlan; Huang, Grace; Hua, Xiaohui; Li, Yang; Yan, Huiying; Che, Xun; Tian, Zhongxian; Liufu, Huating; Huang, Chao; Li, Jingxia; Xu, Jiheng; Dai, Wei; Huang, Haishan; Huang, Chuanshu

Oncogene. 2019 Apr; 38(17):3301-3315