scholarly journals Deltonin Isolated from Dioscorea zingiberensis Inhibits Cancer Cell Growth through Inducing Mitochondrial Apoptosis and Suppressing Akt and Mitogen Activated Protein Kinase Signals

2011 ◽  
Vol 34 (8) ◽  
pp. 1231-1239 ◽  
Author(s):  
Dan Shu ◽  
Yong Qing ◽  
Qingyi Tong ◽  
Yang He ◽  
Zhihua Xing ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cell Growth ◽  
Cancer Cell ◽  
Mitogen Activated Protein Kinase ◽  
Mitochondrial Apoptosis ◽  
Cancer Cell Growth ◽  
Dioscorea Zingiberensis ◽  
Mitogen Activated Protein

scholarly journals Heparin regulates colon cancer cell growth through p38 mitogen-activated protein kinase signalling

2010 ◽  
Vol 43 (1) ◽  
pp. 9-18 ◽  
Author(s):  
G. Chatzinikolaou ◽  
D. Nikitovic ◽  
A. Berdiaki ◽  
A. Zafiropoulos ◽  
P. Katonis ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Protein Kinase ◽  
Cell Growth ◽  
Cancer Cell ◽  
Colon Cancer Cell ◽  
Mitogen Activated Protein Kinase ◽  
Cancer Cell Growth ◽  
Mitogen Activated Protein ◽  
Protein Kinase Signalling

scholarly journals Oncogenic Activation of AKT by MAPK6

2020 ◽  
Author(s):  
Qinbo Cai ◽  
Wei Wang ◽  
Bingning Dong ◽  
Wolong Zhou ◽  
Tao Shen ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Cell Growth ◽  
Cancer Cell ◽  
Kinase Domain ◽  
Mitogen Activated Protein Kinase ◽  
Breast Cancer Patients ◽  
Cancer Cell Growth ◽  
Growth And Survival ◽  
Mitogen Activated Protein ◽  
Normal Human

AbstractMitogen-activated protein kinase 6 (MAPK6) is an atypical MAPK closely related to MAPK4. We recently reported that MAPK4 can promote cancer by activating the Protein Kinase B (PKB/AKT) pathway of cell growth and survival. Here we report that MAPK6 overexpression also activates AKT to induce oncogenic outcomes, including transforming “normal” human epithelial cells into anchorage-independent growth and enhancing cancer cell growth. Knockdown of MAPK6 inhibited cancer cell growth and xenograft growth, supporting the tumor-promoting activities of endogenous MAPK6. Unlike MAPK4, which binds AKT through its kinase domain and phosphorylates AKT at T308, MAPK6 interacts with AKT through its C34 region and the unique C-terminal tail and phosphorylates AKT at S473 independent of mTORC2, the major AKT S473 kinase. MAPK6 overexpression is associated with decreased overall survival and the survival of lung adenocarcinoma, mesothelioma, uveal melanoma, and breast cancer patients. We conclude that MAPK6 can promote cancer by activating AKT and that targeting MAPK6 may be effective in human cancers.

scholarly journals Role of Reactive Oxygen Species in Cancer Progression: Molecular Mechanisms and Recent Advancements

Biomolecules ◽  
2019 ◽  
Vol 9 (11) ◽  
pp. 735 ◽  
Author(s):  
Vaishali Aggarwal ◽  
Hardeep Tuli ◽  
Ayşegül Varol ◽  
Falak Thakral ◽  
Mukerrem Yerer ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Kinase ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Reactive Oxygen ◽  
Mitogen Activated Protein Kinase ◽  
Oxygen Species ◽  
Mitogen Activated Protein ◽  
High Concentrations

Reactive oxygen species (ROS) play a pivotal role in biological processes and continuous ROS production in normal cells is controlled by the appropriate regulation between the silver lining of low and high ROS concentration mediated effects. Interestingly, ROS also dynamically influences the tumor microenvironment and is known to initiate cancer angiogenesis, metastasis, and survival at different concentrations. At moderate concentration, ROS activates the cancer cell survival signaling cascade involving mitogen-activated protein kinase/extracellular signal-regulated protein kinases 1/2 (MAPK/ERK1/2), p38, c-Jun N-terminal kinase (JNK), and phosphoinositide-3-kinase/ protein kinase B (PI3K/Akt), which in turn activate the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), matrix metalloproteinases (MMPs), and vascular endothelial growth factor (VEGF). At high concentrations, ROS can cause cancer cell apoptosis. Hence, it critically depends upon the ROS levels, to either augment tumorigenesis or lead to apoptosis. The major issue is targeting the dual actions of ROS effectively with respect to the concentration bias, which needs to be monitored carefully to impede tumor angiogenesis and metastasis for ROS to serve as potential therapeutic targets exogenously/endogenously. Overall, additional research is required to comprehend the potential of ROS as an effective anti-tumor modality and therapeutic target for treating malignancies.

scholarly journals Protein kinase C alpha-dependent signaling mediates endometrial cancer cell growth and tumorigenesis

2009 ◽  
Vol 125 (11) ◽  
pp. 2556-2564 ◽  
Author(s):  
James M. Haughian ◽  
Elaine M. Reno ◽  
Alicia M. Thorne ◽  
Andrew P. Bradford
Keyword(s):  
Endometrial Cancer ◽  
Protein Kinase C ◽  
Protein Kinase ◽  
Cell Growth ◽  
Cancer Cell ◽  
Cancer Cell Growth ◽  
Endometrial Cancer Cell ◽  
Kinase C ◽  
Protein Kinase C Alpha
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