The MUDENG Augmentation: A Genesis in Anti-Cancer Therapy?
Adaptor Protein Complex 1
/ antagonists & inhibitors
Adaptor Protein Complex mu Subunits
/ antagonists & inhibitors
Apoptosis
/ drug effects
Apoptosis Regulatory Proteins
/ antagonists & inhibitors
Cell Proliferation
/ drug effects
Gene Expression Regulation, Neoplastic
/ drug effects
Humans
Neoplasms
/ drug therapy
Signal Transduction
/ drug effects
TNF-Related Apoptosis-Inducing Ligand
/ antagonists & inhibitors
AP5M1
BAX
MUDENG
TRAIL
cancer
therapy
Journal
International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791
Informations de publication
Date de publication:
04 Aug 2020
04 Aug 2020
Historique:
received:
03
07
2020
revised:
27
07
2020
accepted:
30
07
2020
entrez:
8
8
2020
pubmed:
8
8
2020
medline:
18
2
2021
Statut:
epublish
Résumé
Despite multitudes of reports on cancer remedies available, we are far from being able to declare that we have arrived at that defining anti-cancer therapy. In recent decades, researchers have been looking into the possibility of enhancing cell death-related signaling pathways in cancer cells using pro-apoptotic proteins. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) and Mu-2/AP1M2 domain containing, death-inducing (MUDENG, MuD) have been established for their ability to bring about cell death specifically in cancer cells. Targeted cell death is a very attractive term when it comes to cancer, since most therapies also affect normal cells. In this direction TRAIL has made noteworthy progress. This review briefly sums up what has been done using TRAIL in cancer therapeutics. The importance of MuD and what has been achieved thus far through MuD and the need to widen and concentrate on applicational aspects of MuD has been highlighted. This has been suggested as the future perspective of MuD towards prospective progress in cancer research.
Identifiants
pubmed: 32759789
pii: ijms21155583
doi: 10.3390/ijms21155583
pmc: PMC7432215
pii:
doi:
Substances chimiques
AP1M2 protein, human
0
AP5M1 protein, human
0
Adaptor Protein Complex 1
0
Adaptor Protein Complex mu Subunits
0
Apoptosis Regulatory Proteins
0
TNF-Related Apoptosis-Inducing Ligand
0
TNFSF10 protein, human
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
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