Association of the Epithelial-Mesenchymal Transition (EMT) with Cisplatin Resistance.
Antineoplastic Agents
/ pharmacology
Cell Differentiation
Cisplatin
/ pharmacology
Drug Resistance, Neoplasm
Epithelial-Mesenchymal Transition
/ drug effects
Forkhead Box Protein O1
/ metabolism
Humans
MicroRNAs
/ metabolism
NF-kappa B
/ metabolism
Neoplasms
/ drug therapy
Phosphatidylinositol 3-Kinases
/ metabolism
Signal Transduction
/ drug effects
TOR Serine-Threonine Kinases
/ metabolism
cancer therapy
chemoresistance
cisplatin
epithelial–mesenchymal transition (EMT)
signal transduction
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:
03 Jun 2020
03 Jun 2020
Historique:
received:
13
04
2020
revised:
14
05
2020
accepted:
26
05
2020
entrez:
7
6
2020
pubmed:
7
6
2020
medline:
1
4
2021
Statut:
epublish
Résumé
Therapy resistance is a characteristic of cancer cells that significantly reduces the effectiveness of drugs. Despite the popularity of cisplatin (CP) as a chemotherapeutic agent, which is widely used in the treatment of various types of cancer, resistance of cancer cells to CP chemotherapy has been extensively observed. Among various reported mechanism(s), the epithelial-mesenchymal transition (EMT) process can significantly contribute to chemoresistance by converting the motionless epithelial cells into mobile mesenchymal cells and altering cell-cell adhesion as well as the cellular extracellular matrix, leading to invasion of tumor cells. By analyzing the impact of the different molecular pathways such as microRNAs, long non-coding RNAs, nuclear factor-κB (NF-ĸB), phosphoinositide 3-kinase-related protein kinase (PI3K)/Akt, mammalian target rapamycin (mTOR), and Wnt, which play an important role in resistance exhibited to CP therapy, we first give an introduction about the EMT mechanism and its role in drug resistance. We then focus specifically on the molecular pathways involved in drug resistance and the pharmacological strategies that can be used to mitigate this resistance. Overall, we highlight the various targeted signaling pathways that could be considered in future studies to pave the way for the inhibition of EMT-mediated resistance displayed by tumor cells in response to CP exposure.
Identifiants
pubmed: 32503307
pii: ijms21114002
doi: 10.3390/ijms21114002
pmc: PMC7312011
pii:
doi:
Substances chimiques
Antineoplastic Agents
0
FOXO1 protein, human
0
Forkhead Box Protein O1
0
MicroRNAs
0
NF-kappa B
0
MTOR protein, human
EC 2.7.1.1
TOR Serine-Threonine Kinases
EC 2.7.11.1
Cisplatin
Q20Q21Q62J
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Déclaration de conflit d'intérêts
The authors declare no conflicts of interest.
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