Hong Wu

Peking University

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Roger Leng

University of Alberta

David J. Mulholland

Icahn School of Medicine at Mount Sinai

Jing Jiao

Obstetrics and Gynecology Hospital of Fudan University

Linh M. Tran

University of California, Los Angeles

Rudolf Jaenisch

Whitehead Institute for Biomedical Research

Haichuan Zhu

Wuhan University of Science and Technology

Shunyou Wang

Henan Agricultural University

Bangyan L. Stiles

University of Southern California

Ralf Lesche

Bayer (Germany)

Consolato Sergi

University of Alberta

Cooperative Institutions

University of California, Los Angeles

296

Harvard University

120

Howard Hughes Medical Institute

Peking University

UCLA Jonsson Comprehensive Cancer Center

Institute for Molecular Medicine

Zhejiang University

UCLA Health

University of California, San Francisco

Memorial Sloan Kettering Cancer Center

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Three‐Dimensional Nanostructured Substrates toward Efficient Capture of Circulating Tumor Cells

Angewandte Chemie International Edition (2009)

Shutao Wang Hao Wang Jing Jiao Kuan‐Ju Chen Gwen E. Owens

A grabby substrate: A 3D nanostructured substrate, namely, a silicon-nanopillar (SiNP) array coated with epithelial-cell adhesion-molecule antibody (anti-EpCAM), shows enhanced local topographic interactions between nanoscale cell-surface components and the substrates surface, resulting in enhanced cell-capture efficiency when employed to isolate viable cancer cells from whole-blood samples (see schematic and SEM image of a captured cancer cell).

Molecular Imaging

10.1002/anie.200901668

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Citations (496)

PTEN negatively regulates neural stem cell self-renewal by modulating G₀-G₁cell cycle entry

Proceedings of the National Academy of Sciences (2005)

Matthias Groszer Rebecca J. Erickson Deirdre D. Scripture-Adams Joseph D. Dougherty Janel Le Belle

Previous studies have demonstrated that a small subpopulation of brain tumor cells share key characteristics with neural stem/progenitor cells in terms of phenotype and behavior. These findings suggest that brain tumors might contain “cancer stem cells” that are critical for tumor growth. However, the molecular pathways governing such stem cell-like behavior remain largely elusive. Our previous study suggests that the phosphatase and tensin homologue deleted on chromosome 10 ( PTEN ) tumor suppressor gene, one of the most frequently mutated genes in glioblastomas, restricts neural stem/progenitor cell proliferation in vivo . In the present study, we sought to determine the role of PTEN in long-term maintenance of stem cell-like properties, cell cycle entry and progression, and growth factor dependence and gene expression. Our results demonstrate an enhanced self-renewal capacity and G 0 -G 1 cell cycle entry and decreased growth factor dependency of Pten null neural/stem progenitor cells. Therefore, loss of PTEN leads to cell physiological changes, which collectively are sufficient to increase the pool of self-renewing neural stem cells and promote their escape from the homeostatic mechanisms of proliferation control.

Tensin

10.1073/pnas.0509939103

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Citations (301)

Comparison of the Cardioprotective Effect of Deoxygenated Hemoglobin-based Oxygen Carrier (HBOC) Pretreatment and Ischemia Preconditioning

Artificial Cells Blood Substitutes and Biotechnology (2010)

Zhen You Tao Li Qian Yang Hong Wu Yong Zeng

This study was designed to compare the influence of deoxygenated hemoglobin-based oxygen carrier (HBOC) pretreatment and ischemia preconditioning on cardiac ischemia/reperfusion (I/R) injury. Langendorff-perfused rat hearts were pretreated with 0.1 gHb/dL deoxygenated HBOC or ischemia, then subjected to 50-min warm ischemia and 2-hr reperfusion. The results indicated that deoxygenated HBOC pretreatment and ischemia preconditioning both equally improved the recovery of cardiac function, and reduced the cardiac enzyme release and myocardial histopathological changes as compared to the control group. Therefore our study demonstrated that deoxygenated HBOC pretreatment and ischemia precondition provided equivalent protection to the isolated heart against I/R injury.

Deoxygenated Hemoglobin

Cardiac ischemia

Ischemic Preconditioning

10.3109/10731199.2010.495037

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Citations (3)

Cell Autonomous Role of PTEN in Regulating Castration-Resistant Prostate Cancer Growth

Cancer Cell (2011)

David J. Mulholland Linh M. Tran Yunfeng Li Houjian Cai Ashkan Morim

10.1016/j.ccr.2011.05.006

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Citations (487)

Suppression of Peroxiredoxin 4 in Glioblastoma Cells Increases Apoptosis and Reduces Tumor Growth

PLoS ONE (2012)

Tae Hyong Kim Jieun Song Sheila R. Alcantara Llaguno Eric Murnan Sandya Liyanarachchi

Glioblastoma multiforme (GBM), the most common and aggressive primary brain malignancy, is incurable despite the best combination of current cancer therapies. For the development of more effective therapies, discovery of novel candidate tumor drivers is urgently needed. Here, we report that peroxiredoxin 4 (PRDX4) is a putative tumor driver. PRDX4 levels were highly increased in a majority of human GBMs as well as in a mouse model of GBM. Reducing PRDX4 expression significantly decreased GBM cell growth and radiation resistance in vitro with increased levels of ROS, DNA damage, and apoptosis. In a syngenic orthotopic transplantation model, Prdx4 knockdown limited GBM infiltration and significantly prolonged mouse survival. These data suggest that PRDX4 can be a novel target for GBM therapies in the future.

Syngenic

Peroxiredoxin

10.1371/journal.pone.0042818

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Citations (54)

Genetic deletion of the Pten tumor suppressor gene promotes cell motility by activation of Rac1 and Cdc42 GTPases

Current Biology (2000)

Joanna Liliental Sun Young Moon Ralf Lesche Ramanaiah Mamillapalli Daming Li

Tensin

10.1016/s0960-9822(00)00417-6

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Citations (292)

Evaluation of well‐differentiated/de‐differentiated liposarcomas by high‐resolution oligonucleotide array‐based comparative genomic hybridization

Genes Chromosomes and Cancer (2010)

William D. Tap Fritz C. Eilber Charles Ginther Sarah Dry Nicholas Reese

Abstract Well‐differentiated/de‐differentiated liposarcomas (WDLS/DDLS) encompass an intriguing disease model in which a temporal intersection occurs between the malignant transformation of mesenchymal cells and the process of adipogenesis. Deciphering the molecular events that trigger and are characteristic of the intersection of these oncogenic and normal processes is critical to affect the often morbid and lethal consequences of malignant tumors of fat. High‐resolution genome‐wide oligonucleotide array‐based comparative genomic hybridization (aCGH) with matched gene expression analyses was performed on seven lipomas, one hibernoma, and 38 WD and DDLS to define and compare the genomic events associated with these tumors. WD and DDLS had complex karyotypes. On average, WDLS had 11.1 and DDLS had 22.7 chromosomal copy number aberrations. All of the liposarcomas had 12q13‐q15 amplifications with varying peaks at CDK4 (12q14.1), HMGA2 (12q14.3), and MDM2 (12q15); 24% of the DDLS and no WDLS had 1p32.2 ( JUN ) amplifications; 33% WDLS and 35% DDLS had 1q24.3 amplifications involving DNM3 and miR‐214/miR‐199a2; 24% of the liposarcomas had 6q23‐q24 amplifications (including MAP3K5 ). Amplifications in GLI1 (12q13.3), JUN , and MAP3K5 (6q23.3) were mutually exclusive and occurred predominately in the DDLS. 6q amplifications occurred primarily in retroperitoneal tumors and females represented the majority of those patients who developed fatty tumors prior to the age of 50 years old. This detailed genetic mapping provides insight into the heterogeneity of WD and DDLS and the chromosomal and genetic abnormalities that are present in and distinguish these mesenchymal malignancies. © 2010 Wiley‐Liss,Inc.

Comparative genomic hybridization

10.1002/gcc.20835

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Citations (88)

Maternal embryonic leucine zipper kinase (MELK) regulates multipotent neural progenitor proliferation

The Journal of Cell Biology (2005)

Ichiro Nakano Andres A. Paucar Ruchi Bajpai Joseph D. Dougherty Amani Zewail

Maternal embryonic leucine zipper kinase (MELK) was previously identified in a screen for genes enriched in neural progenitors. Here, we demonstrate expression of MELK by progenitors in developing and adult brain and that MELK serves as a marker for self-renewing multipotent neural progenitors (MNPs) in cultures derived from the developing forebrain and in transgenic mice. Overexpression of MELK enhances (whereas knockdown diminishes) the ability to generate neurospheres from MNPs, indicating a function in self-renewal. MELK down-regulation disrupts the production of neurogenic MNP from glial fibrillary acidic protein (GFAP)–positive progenitors in vitro. MELK expression in MNP is cell cycle regulated and inhibition of MELK expression down-regulates the expression of B-myb, which is shown to also mediate MNP proliferation. These findings indicate that MELK is necessary for proliferation of embryonic and postnatal MNP and suggest that it regulates the transition from GFAP-expressing progenitors to rapid amplifying progenitors in the postnatal brain.

Progenitor

Forebrain

Neurosphere

10.1083/jcb.200412115

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Citations (148)

Negative Regulation of Neural Stem/Progenitor Cell Proliferation by the Pten Tumor Suppressor Gene in Vivo

Science (2001)

Matthias Groszer Rebecca J. Erickson Deirdre D. Scripture-Adams Ralf Lesche Andreas Trumpp

The mechanisms controlling neural stem cell proliferation are poorly understood. Here we demonstrate that the PTEN tumor suppressor plays an important role in regulating neural stem/progenitor cells in vivo and in vitro. Mice lacking PTEN exhibited enlarged, histoarchitecturally abnormal brains, which resulted from increased cell proliferation, decreased cell death, and enlarged cell size. Neurosphere cultures revealed a greater proliferation capacity for tripotent Pten-/- central nervous system stem/progenitor cells, which can be attributed, at least in part, to a shortened cell cycle. However, cell fate commitments of the progenitors were largely undisturbed. Our results suggest that PTEN negatively regulates neural stem cell proliferation.

Neurosphere

Progenitor

10.1126/science.1065518

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Citations (782)

Additional file 7 of Systematic prediction of degrons and E3 ubiquitin ligase binding via deep learning

Figshare (2022)

Chao Hou Yuxuan Li Mengyao Wang Hong Wu Tingting Li

Additional file 7: Table S6. Enriched function groups of short-lived proteins.

10.6084/m9.figshare.20317678

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Citations (0)