Curcumol induces cell cycle arrest and apoptosis by inhibiting IGF-1R/PI3K/Akt signaling pathway in human nasopharyngeal carcinoma CNE-2 cells

2018 ◽  
Vol 32 (11) ◽  
pp. 2214-2225 ◽  
Author(s):  
Xumei Li ◽  
Haowei Liu ◽  
Juan Wang ◽  
Jianli Qin ◽  
Zhun Bai ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Nasopharyngeal Carcinoma ◽  
Cell Cycle Arrest ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Cycle Arrest ◽  
Human Nasopharyngeal Carcinoma

DNA damage–induced cell-cycle arrest of hematopoietic cells is overridden by activation of the PI-3 kinase/Akt signaling pathway

Blood ◽  
2001 ◽  
Vol 98 (3) ◽  
pp. 834-841 ◽  
Author(s):  
Matthew K. Henry ◽  
Jeffrey T. Lynch ◽  
Alex K. Eapen ◽  
Frederick W. Quelle
Keyword(s):  
Cell Cycle ◽  
Dna Damage ◽  
Cell Cycle Arrest ◽  
Signaling Pathway ◽  
Growth Arrest ◽  
Hematopoietic Cells ◽  
Akt Signaling ◽  
Dominant Negative ◽  
Akt Signaling Pathway ◽  
Cycle Arrest

Abstract Exposure of hematopoietic cells to DNA-damaging agents induces cell-cycle arrest at G1 and G2/M checkpoints. Previously, it was shown that DNA damage–induced growth arrest of hematopoietic cells can be overridden by treatment with cytokine growth factors, such as erythropoietin (EPO) or interleukin-3 (IL-3). Here, the cytokine-activated signaling pathways required to override G1 and G2/M checkpoints induced by γ-irradiation (γ-IR) are characterized. Using factor-dependent myeloid cells stably expressing EPO receptor (EPO-R) mutants, it is shown that removal of a minimal domain required for PI-3K signaling abrogated the ability of EPO to override γ-IR–induced cell-cycle arrest. Similarly, the ability of cytokines to override γ-IR–induced arrest was abolished by an inhibitor of PI-3K (LY294002) or by overexpression of dominant-negative Akt. Moreover, the ability of EPO to override these checkpoints in cells expressing defective EPO-R mutants could be restored by overexpression of a constitutively active Akt. Thus, activation of a PI-3K/Akt signaling pathway is required for cytokine-dependent suppression of DNA-damage induced checkpoints. Together, these findings suggest a novel role for PI-3K/Akt pathways in the modulation of growth arrest responses to DNA damage in hematopoietic cells.

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