Statins as the Controlling Agents for Non-Hodgkin's Lymphomas via Increasing the Casein Kinase 2 Interacting Protein-1: A Hypothesis.
Cell Line, Tumor
Clinical Trials as Topic
Gene Expression Regulation, Neoplastic
/ drug effects
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
/ therapeutic use
Intracellular Signaling Peptides and Proteins
/ genetics
Lymphoma, Non-Hodgkin
/ drug therapy
Phosphorylation
/ drug effects
Proto-Oncogene Proteins c-akt
/ metabolism
Signal Transduction
/ drug effects
Treatment Outcome
AKT
CKIP
Statin
apoptosis
non-hodgkin's lymphomas
signaling pathway
Journal
Current drug discovery technologies
ISSN: 1875-6220
Titre abrégé: Curr Drug Discov Technol
Pays: United Arab Emirates
ID NLM: 101157212
Informations de publication
Date de publication:
2020
2020
Historique:
received:
03
04
2019
revised:
27
05
2019
accepted:
29
05
2019
pubmed:
3
7
2019
medline:
18
9
2021
entrez:
3
7
2019
Statut:
ppublish
Résumé
Non-Hodgkin's lymphomas (NHL), derived from B- or T-cell, consist of a heterogeneous group of malignant lymphoproliferative disorders. Knockdown of Casein kinase 2 interacting protein-1 (CKIP-1) in NHL promoted cell proliferation and inhibited apoptosis via enhancing phosphorylated Protein Kinase B (PKB or AKT) expression. Statins are the class of drugs that inhibit the ratelimiting step of the mevalonate pathway, which is essential for the biosynthesis of various compounds, including cholesterol. Also, statins have anticancer properties being mediated by different mechanisms. A search on databases like Scopus and PubMed with keywords such as statin and non- Hodgkin's lymphomas was performed and Kyoto Encyclopedia of Genes and Genomes (KEGG) website was used to evaluate and reconfirm the involved cellular signaling pathway. CKIP-1 is involved in the regulation of cell proliferation and apoptosis while plays an important role in many cancers. We can hypothesize that statins may increase the expression levels of CKIP-1 which could contribute to the reductions in phospho-AKT level. Hence, they may ameliorate the NHL patients via suppressing AKT phosphorylation and increasing CKIP- expression. Present review confirms the positive effect of statins on NHL by increasing CKIP-1 and reducing cell proliferation, subsequently.
Sections du résumé
BACKGROUND
Non-Hodgkin's lymphomas (NHL), derived from B- or T-cell, consist of a heterogeneous group of malignant lymphoproliferative disorders. Knockdown of Casein kinase 2 interacting protein-1 (CKIP-1) in NHL promoted cell proliferation and inhibited apoptosis via enhancing phosphorylated Protein Kinase B (PKB or AKT) expression. Statins are the class of drugs that inhibit the ratelimiting step of the mevalonate pathway, which is essential for the biosynthesis of various compounds, including cholesterol. Also, statins have anticancer properties being mediated by different mechanisms.
METHODS
A search on databases like Scopus and PubMed with keywords such as statin and non- Hodgkin's lymphomas was performed and Kyoto Encyclopedia of Genes and Genomes (KEGG) website was used to evaluate and reconfirm the involved cellular signaling pathway.
RESULTS
CKIP-1 is involved in the regulation of cell proliferation and apoptosis while plays an important role in many cancers. We can hypothesize that statins may increase the expression levels of CKIP-1 which could contribute to the reductions in phospho-AKT level. Hence, they may ameliorate the NHL patients via suppressing AKT phosphorylation and increasing CKIP- expression.
CONCLUSION
Present review confirms the positive effect of statins on NHL by increasing CKIP-1 and reducing cell proliferation, subsequently.
Identifiants
pubmed: 31264550
pii: CDDT-EPUB-99305
doi: 10.2174/1570163816666190628165200
doi:
Substances chimiques
Hydroxymethylglutaryl-CoA Reductase Inhibitors
0
Intracellular Signaling Peptides and Proteins
0
PLEKHO1 protein, human
0
AKT1 protein, human
EC 2.7.11.1
Proto-Oncogene Proteins c-akt
EC 2.7.11.1
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
616-618Informations de copyright
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