Qimin Zhan
Peking Union Medical College
215 Papers
1.3K Citations
Qimin Zhan is an academic researcher from Peking Union Medical College. The author has contributed to research in topics: Biology & Cancer. The author has an hindex of 54, co-authored 186 publications. Previous affiliations of Qimin Zhan include National Institutes of Health.
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Papers
Aurora-A enhances malignant development of esophageal squamous cell carcinoma (ESCC) by phosphorylating β-catenin.
Shunqian Jin,Shunqian Jin,Xiaoxia Wang,Xiaoxia Wang,Tong Tong,Dongdong Zhang,Ji Shi,Jie Chen,Qimin Zhan +8 more
TL;DR: It is proposed that Aurora‐A‐mediated phosphorylation of β‐catenin is a novel mechanism of malignancy development of tumor.
Silencing DACH1 promotes esophageal cancer growth by inhibiting TGF-β signaling.
Liang Wu,James G. Herman,Malcolm V. Brock,Kongming Wu,Gaoping Mao,Wenji Yan,Yan Nie,Hao Liang,Qimin Zhan,Wen Li,Mingzhou Guo +10 more
TL;DR: Dachshund homologue 1 is frequently methylated in human esophageal cancer and methylation of DACH1 is involved in the early stage of esphageal carcinogenesis.
Overexpression of stefin A in human esophageal squamous cell carcinoma cells inhibits tumor cell growth, angiogenesis, invasion, and metastasis.
Wendong Li,Fang Ding,Liyong Zhang,Zhongmin Liu,Yu Wu,Aiping Luo,Min Wu,Ming-Rong Wang,Qimin Zhan,Zhihua Liu +9 more
TL;DR: The data strongly indicate that stefin A plays an important role in the growth, angiogenesis, invasion, and metastasis of human esophageal squamous cell carcinoma cells and suggest that stecin A may be useful in cancer therapy.
CDX2 serves as a Wnt signaling inhibitor and is frequently methylated in lung cancer
TL;DR: CDX2 may serve as a tumor suppressor in lung cancer and inhibits lung cancer cell proliferation by suppressing Wnt signaling and expression of CDX2 is regulated by promoter region hypermethylation.
Association with Cdc2 and inhibition of Cdc2/Cyclin B1 kinase activity by the p53-regulated protein Gadd45.
Qimin Zhan,Michael J. Antinore,Xin Wei Wang,F. Carrier,F. Carrier,Martin L. Smith,Martin L. Smith,Chris Harris,Albert J. Fornace +8 more
TL;DR: With the use of an antisense approach, reduced Gadd45 expression attenuated the suppression of Cdc2/Cyclin B1 activity in UV-irradiated human cells and implicate Gadd 45 in the control of G2/M cell cycle progression after certain stresses.