Abstract:
:Cancer-associated fibroblasts (CAFs) are the predominant cell type in tumor microenvironment (TM) and featured with the distinct energy metabolism reprogramming (EMR) phenotype caused by many factors such as hypoxia and growth factors. The EMR of CAFs plays a key role in biological behaviors of cancer cells including proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT). Recently, accumulative evidence indicates that oxidative stress (OS) mediates the EMR of CAFs under conditions of various stimuli. However, the precise mechanism by which OS causes the EMR of CAFs is not clear. Interestingly, our previous work suggested that ataxia-telangiectasia mutated (ATM) signaling is activated independent of DNA double strand breaks (DSBs) in CAFs derived from human breast cancers compared with paired normal fibroblasts (NFs). Recent studies have shown that ATM protein kinase, as a redox sensor, is closely associated with cellular energy metabolism. Thus, it is very possible that ATM protein kinase regulates the EMR of CAFs. So, it is necessary to perform an integral study on how oxidized ATM regulates the EMR of CAFs in response to various stimuli evoking OS. This will facilitate to develop a new powerful strategy of preventing and treating cancers.
journal_name
Cancer Lettjournal_title
Cancer lettersauthors
Tang S,Yang L,Tang X,Liu Mdoi
10.1016/j.canlet.2014.07.028subject
Has Abstractpub_date
2014-10-28 00:00:00pages
133-44issue
2eissn
0304-3835issn
1872-7980pii
S0304-3835(14)00375-9journal_volume
353pub_type
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