Xiaoli Du
Peking Union Medical College
17 Papers
61 Citations
Xiaoli Du is an academic researcher from Peking Union Medical College. The author has contributed to research in topics: Medicine & Biology. The author has an hindex of 11, co-authored 13 publications. Previous affiliations of Xiaoli Du include National Institutes of Health.
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Papers
Proteomic profiling of proteins dysregulted in Chinese esophageal squamous cell carcinoma
Xiaoli Du,Hai Hu,De-Chen Lin,Shu-Hua Xia,Xiao-Ming Shen,Yu Zhang,Man-Li Luo,Yan-Bin Feng,Yan Cai,Xin Xu,Ya-Ling Han,Qimin Zhan,Ming-Rong Wang +12 more
TL;DR: The proteins here identified will contribute to the understanding of the tumorigenesis and progression of Chinese ESCC and may potentially provide useful markers for diagnosis or targets for therapeutic intervention and drug development.
140
Overexpression of PLK1 is associated with poor survival by inhibiting apoptosis via enhancement of survivin level in esophageal squamous cell carcinoma
Yan-Bin Feng,De-Chen Lin,Zhi-Zhou Shi,Xiao-Chun Wang,Xiao-Ming Shen,Yu Zhang,Xiaoli Du,Man-Li Luo,Xin Xu,Ya-Ling Han,Yan Cai,Zi-Qiang Zhang,Qimin Zhan,Ming-Rong Wang +13 more
TL;DR: It is found that overexpression of PLK1 was an independent prognostic factor and significantly correlated with survivin, an antiapoptotic protein, in esophageal squamous cell carcinoma (ESCC), and data suggest thatPLK1 might be a useful prognostic marker and a potential therapeutic target for ESCC.
118
Full activity of the deleted in liver cancer 1 (DLC1) tumor suppressor depends on an LD-like motif that binds talin and focal adhesion kinase (FAK)
TL;DR: It is concluded that the LD-like motif, which binds talin and FAK, is required for the full tumor suppressor activity of DLC1 and contributes to the association of DLC 1 with focal adhesions.
109
Protein alterations in ESCC and clinical implications: a review
TL;DR: This review summarizes all the dysregulated proteins investigated in the disease from 187 published papers and analyzes their contributions to tumor development and progression, in which cyclin D1, p53, E-cadherin and VEGF appeared to have the strongest evidence as independent predictors of patient outcome.
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Exogenous expression of Esophagin/SPRR3 attenuates the tumorigenicity of esophageal squamous cell carcinoma cells via promoting apoptosis
Yu Zhang,Yan Bin Feng,Xiao Ming Shen,Bao Sheng Chen,Xiaoli Du,Man Li Luo,Yan Cai,Ya Ling Han,Xin Xu,Qi min Zhan,Ming Rong Wang +10 more
TL;DR: Exogenous expression of Esophagin/SPRR3 significantly suppressed the ability of ESCC cells to form colonies in plastic and soft agar, as well as tumor formation in vivo, and indicated that dysregulated apoptosis might contribute to reduced tumorigenicity.
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