2016
DOI: 10.3324/haematol.2015.141143
|View full text |Cite
|
Sign up to set email alerts
|

Optimal interleukin-7 receptor-mediated signaling, cell cycle progression and viability of T-cell acute lymphoblastic leukemia cells rely on casein kinase 2 activity

Abstract: I nterleukin-7 and interleukin-7 receptor are essential for normal T-cell development and homeostasis, whereas excessive interleukin-7/interleukin-7 receptor-mediated signaling promotes leukemogenesis. The protein kinase, casein kinase 2, is overexpressed and hyperactivated in cancer, including T-cell acute lymphoblastic leukemia. Herein, we show that while interleukin-7 had a minor but significant positive effect on casein kinase 2 activity in leukemia T-cells, casein kinase 2 activity was mandatory for optim… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1

Citation Types

0
15
0

Year Published

2017
2017
2021
2021

Publication Types

Select...
8
1

Relationship

3
6

Authors

Journals

citations
Cited by 16 publications
(15 citation statements)
references
References 52 publications
0
15
0
Order By: Relevance
“…IL7 and IL7R are essential for normal T-cell development and homeostasis, whereas disregulated IL7/IL7R activity promotes T-ALL [ 8 ]. In T-ALL, gain of function mutations of IL7Rα, which could be detected in about 10% of pediatric patients, resulted in the activation of PI3K/Akt/mTOR signaling [ 86 , 87 ]. Interestingly, both IGF1/IGF1R and IL7/IL7R activate not only PI3K/Akt but also the MEK/ERK module [ 81 , 88 ] ( Figure 1 ).…”
Section: Activation Of Mtorc1 and Mtorc2 In T-all Cellsmentioning
confidence: 99%
“…IL7 and IL7R are essential for normal T-cell development and homeostasis, whereas disregulated IL7/IL7R activity promotes T-ALL [ 8 ]. In T-ALL, gain of function mutations of IL7Rα, which could be detected in about 10% of pediatric patients, resulted in the activation of PI3K/Akt/mTOR signaling [ 86 , 87 ]. Interestingly, both IGF1/IGF1R and IL7/IL7R activate not only PI3K/Akt but also the MEK/ERK module [ 81 , 88 ] ( Figure 1 ).…”
Section: Activation Of Mtorc1 and Mtorc2 In T-all Cellsmentioning
confidence: 99%
“…In addition to the impact of CK2 on PTEN and PI3K/Akt-mediated signaling, CK2 can promote B-and T-ALL also via regulation of Ikaros [22]. Moreover, there is evidence for a crosstalk between CK2 and JAK/STAT signaling pathway that can contribute to leukemia cell survival and proliferation [23][24][25], including in response to critical microenvironmental stimuli, such as interleukin-7 (IL-7) [25,26].…”
Section: Introductionmentioning
confidence: 99%
“…Importantly, CK2 activity was required for the viability of T-ALL cells expressing a mutant IL-7R. 56 Overall, this study identified CK2 as a major effector of IL-7/IL-7R signaling in T-ALL.…”
Section: Ck2 In Acute and Chronic Leukemiasmentioning
confidence: 59%
“… 55 While IL-7 had a minor but significant positive effect on CK2 activity in leukemic T-cells, CK2 activity was mandatory for optimal IL-7/IL-7R-dependent signaling. 56 Indeed, CK2 pharmacological inhibition impaired both JAK1/STAT5 and PI3K/Akt pathway activation triggered by either IL-7 or by mutational activation of IL-7R. As a consequence, viability, growth and cell cycle progression of T-ALL cell lines and lymphoblasts were negatively affected.…”
Section: Ck2 In Acute and Chronic Leukemiasmentioning
confidence: 98%