期刊
TRENDS IN CANCER
卷 8, 期 3, 页码 190-209出版社
CELL PRESS
DOI: 10.1016/j.trecan.2021.12.002
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资金
- EU-program ERDF (European Regional Development Fund)
- Wilhelm Sander-Foundation [2017.008.02]
- ACTREC
- Indo-Russia Bilateral Funding [INT/RUS/RFBR/395]
- RBFR [19-54-45015a]
- German Research Foundation [DFG LA 2386]
- OvGU
- TMC Institutional Funding
- [0259-2021-0009]
This article discusses the role and regulatory mechanisms of cellular FLICE inhibitory protein (c-FLIP) in the extrinsic pathway of cancer networks. In addition to its key role in apoptosis, c-FLIP may regulate other cellular functions and serve as a therapeutic target for cancer treatment.
The extrinsic pathway is mediated by death receptors (DRs), including CD95 (APO-1/Fas) or TRAILR-1/2. Defects in apoptosis regulation lead to cancer and other malignancies. The master regulator of the DR networks is the cellular FLICE inhibitory protein (c-FLIP). In addition to its key role in apoptosis, c-FLIP may exert other cellular functions, including control of necroptosis, pyroptosis, nuclear factor kappa B (NF-kappa B) activation, and tumorigenesis. To gain further insight into the molecular mechanisms of c-FLIP action in cancer networks, we focus on the structure, isoforms, interactions, and post-translational modifications of c-FLIP. We also discuss various avenues to target c-FLIP in cancer cells for therapeutic benefit.
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