CIAPIN1 targets Na+/H+ exchanger 1 to mediate K562 chronic myeloid leukemia cells’ differentiation via ERK1/2 signaling pathway

Wang, Jian; Xu, Hua; Zhang, Hairui; Wang, Qi; Wang, Chijuan; Zhang, Hongju; Lin, Yani; Ru, Yongxin; Liang, Haoyue; Li, Qinghua; Pang, Tianxiang

doi:10.1016/j.leukres.2014.06.013

Cited by 2 publications

(1 citation statement)

References 23 publications

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“…An acidification by 0.5-0.6 pH units obtained with N-methyl-N'-nitro-N-nitrosoguanidine usually induces cell apoptosis while permitting necrotic death of cells with wide DNA lesions 13 . The decreased activity of NHE-1 mediates differentiation of K562 cells by way of extracellular signal-regulated protein kinases 1/2 (ERK1/2) mechanism, targeted by cytokine-induced antiapoptotic inhibitor 1, a downstream effector of the Ras signaling mechanism 14 . ERK1/2 are intracellular signaling molecules of type protein kinase, component of Ras-Raf-MEK-ERK signaling cascade, involved in cell proliferation and apoptosis.…”

Section: Pathophysiological Aspectsmentioning

confidence: 99%

A minireview on NHE1 inhibitors. A rediscovered hope in oncohematology

Mihăilă¹

2015

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Background. Na+ /H + exchanger-1 (NHE-1) is involved in pH regulation and is up-regulated in different malignancies. Activation of NHE-1 is one way for allowing cells to avoid intracellular acidification and protect them against apoptosis. Inhibitors of NHE-1 are able to decrease intracellular pH and induce apoptosis. Some statins can also act by partial inhibition of NHE-1. This review presents progress in understanding the mechanisms of action of these inhibitors, connections with certain genetic mutations and acquired treatment resistance, as well as new patents on them. Methods. A MEDLINE search for original and review articles using key terms, Na + /H + exchanger, leukemia, cariporide, and amiloride. Recent patents with NHE-1 inhibitors published by United States Patent and Trademark Office are also presented. Results and Conclusions. Sorafenib is used for the treatment of acute myeloid leukemia patients carrying internal tandem duplication of fms-like tyrosine kinase 3 (FLT3-ITD) mutation. 5-(N, N-hexamethylene)-amiloride can increase the suppression of FLT3 signaling by sorafenib. NHE-1 inhibitors are able to increase the sensitivity of chronic myeloid leukemia cells to tyrosine kinase inhibitors, including through the inhibition of P-glycoprotein. NHE-1 inhibitors are promising adjuvant drugs for overcoming acquired resistance to treatment in various malignant hemopathies.

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Section: Pathophysiological Aspectsmentioning

confidence: 99%