PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers

Multidrug resistance (MDR) is the dominant challenge in the failure of chemotherapy in cancers. Phosphatidylinositol 3-kinase (PI3K) is a lipid kinase that spreads intracellular signal cascades and regulates a variety of cellular processes. PI3Ks are considered significant causes of chemoresistance...

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Vydané v:Cell death & disease Ročník 11; číslo 9; s. 797
Hlavní autori: Liu, Rui, Chen, Youwen, Liu, Guangzhi, Li, Chenxi, Song, Yurong, Cao, Zhiwen, Li, Wen, Hu, Jinghong, Lu, Cheng, Liu, Yuanyan
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: London Nature Publishing Group UK 24.09.2020
Predmet:
631/67/1059/602
631/67/2327
Antibodies
Biochemistry
Biomedical and Life Sciences
Cell Biology
Cell Culture
Cell Proliferation
Drug Resistance, Multiple - genetics
Humans
Immunology
Life Sciences
Neoplasms - drug therapy
Neoplasms - genetics
Proto-Oncogene Proteins c-akt - metabolism
Review
Review Article
Signal Transduction
ISSN:2041-4889, 2041-4889
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Shrnutí:Multidrug resistance (MDR) is the dominant challenge in the failure of chemotherapy in cancers. Phosphatidylinositol 3-kinase (PI3K) is a lipid kinase that spreads intracellular signal cascades and regulates a variety of cellular processes. PI3Ks are considered significant causes of chemoresistance in cancer therapy. Protein kinase B (AKT) is also a significant downstream effecter of PI3K signaling, and it modulates several pathways, including inhibition of apoptosis, stimulation of cell growth, and modulation of cellular metabolism. This review highlights the aberrant activation of PI3K/AKT as a key link that modulates MDR. We summarize the regulation of numerous major targets correlated with the PI3K/AKT pathway, which is further related to MDR, including the expression of apoptosis-related protein, ABC transport and glycogen synthase kinase-3 beta (GSK-3β), synergism with nuclear factor kappa beta (NF-κB) and mammalian target of rapamycin (mTOR), and the regulation of glycolysis.
Bibliografia:ObjectType-Article-1
SourceType-Scholarly Journals-1
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ObjectType-Review-3
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ISSN:2041-4889
2041-4889
DOI:10.1038/s41419-020-02998-6