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Reactive oxygen species in cancer stem cells.
- Xiaoke Shi, Yan Zhang, Junheng Zheng, Jingxuan Pan
- Biology, MedicineAntioxidants & redox signaling
- 1 June 2012
This work has shown that normal stem cells such as hematopoietic stem cells reside in niches characterized by hypoxia and low ROS, both of which are critical for maintaining the potential for self-renewal and stemness, and the roles of ROS in CSCs remain poorly understood.
Antineoplastic mechanisms of niclosamide in acute myelogenous leukemia stem cells: inactivation of the NF-kappaB pathway and generation of reactive oxygen species.
Niclosamide inhibited the NF-kappaB pathway and increased ROS levels to induce apoptosis in AML cells and these results support further investigation of niclosamide in clinical trials of AML patients.
Identification of Niclosamide as a New Small-Molecule Inhibitor of the STAT3 Signaling Pathway.
Niclosamide, an FDA-approved anthelmintic drug, is identified as a new small-molecule inhibitor of the STAT3 signaling pathway and consequently induced cell growth inhibition, apoptosis, and cell cycle arrest of cancer cells with constitutively active STAT3.
Farnesyltransferase inhibitors induce DNA damage via reactive oxygen species in human cancer cells.
- Jingxuan Pan, M. She, Zhi-xiang Xu, Lily Sun, S. J. Yeung
- Biology, ChemistryCancer research
- 1 May 2005
It is concluded that FTIs induced oxidative DNA damage by inducing ROS and initiated DNA damage responses, including RhoB induction, and there was a complex relationship among FTIs, farnesyltransferase, ROS, and RHoB.
Pristimerin induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation by blocking NF-κB signaling and depleting Bcr-Abl
- Zhongzheng Lu, Yanli Jin, Chun Chen, Juan Li, Q. Cao, Jingxuan Pan
- Biology, ChemistryMolecular Cancer
- 19 May 2010
This is the first report to show that pristimerin is effective in vitro and in vivo against CML cells, including those with the T315I mutation, indicating that NF-κB inactivation and Bcr-Abl inhibition may be parallel independent pathways.
Blocking EZH2 methylation transferase activity by GSK126 decreases stem cell-like myeloma cells
The findings suggest that EZH2 inactivation by GSK126 is effective in killing MM cells and CSCs as a single agent or in combination with bortezomib.
Sustained c-Jun-NH2-Kinase Activity Promotes Epithelial-Mesenchymal Transition, Invasion, and Survival of Breast Cancer Cells by Regulating Extracellular Signal-Regulated Kinase Activation
- Jinhua Wang, I. Kuiatse, Adrian V. Lee, Jingxuan Pan, A. Giuliano, X. Cui
- BiologyMolecular Cancer Research
- 1 February 2010
The data suggest that the role of JNK changes when its activity is elevated persistently above the basal levels associated with cell apoptosis, and that JNK activation may serve as a marker of breast cancer progression and resistance to cytotoxic drugs.
Class III-specific HDAC inhibitor Tenovin-6 induces apoptosis, suppresses migration and eliminates cancer stem cells in uveal melanoma
In conclusion, the findings suggest that Tenovin-6 may be a promising agent to kill UM bulk tumor cells and CSCs.
Celastrol, a novel HSP90 inhibitor, depletes Bcr-Abl and induces apoptosis in imatinib-resistant chronic myelogenous leukemia cells harboring T315I mutation.
Gas6/AXL Signaling Regulates Self-Renewal of Chronic Myelogenous Leukemia Stem Cells by Stabilizing β-Catenin
The findings improve the understanding of LSC regulation and validate Gas6/AXL as a pair of therapeutic targets to eliminate CML LSCs.