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Cross-Talk between extracellular S1P/S1P2 and P42/44 MAPK in bcr/abl Positive Chronic Myeloid Leukemia Cells

Chinese Journal of Cancer Research 2009年第1期21卷 20-27页

作者： Yin Xu Fei-qun Zheng Qun-wei Zhang Yang Liu Hai-feng Duan Chun-ping Cui Bin Wu Yi-de Qin Deparment of Biochemistry and Molecular Biology Anhui Medical University Hefei 230032 China Department of Experimental Hematology Beijing Institute of Radiation Medicine Beijing 100850 China Key Laboratory of Carcinogenesis and Translational Research （Ministry of Education） Department of lnterventional Therapy Peking University School of Oncology Beijing Cancer Hospital ＆ Institute Beijing 100142 China

Objective： BCR/ABL oncoprotein-expression is associated with uncontrolled cell growth. Sphingosine kinase 1 （SPK1） regulates the production of sphingosine 1-phosphate （S1P）, a key lipid signal molecular in cell proliferation and survival. The objective of this study was to elucidate the roles of S1P and its receptors in bcr/abl positive chronic myeloid leukemia （CML） cells. Methods： The expressions of SIP receptors： S1P1, S1P2 and S1P3 in CML cells were detected by RT-PCR. SPK1 expression, activity and extracellular S1P were determined in ECV304 and HL-60 cells which were transfected with bcr/abl gene. To elucidate the relationship between the BCR/ABL, ERK/MAPK （extracellular signal-regulated kinase/mitogen-activated protein kinase）, SPK/S 1P and S 1P/S 1 P2 signal pathways, bcr/abl positive CML cell line K562 was treated with STI571, PD98059, N,N-dimethyl sphingosine （DMS） and JTE-013. Results： Retrovirus-mediated overexpression of bcr/abl gene in ECV304 and HL-60 cells resulted in upregulation of the expression, activity of SPK1 and increase of the secretion of SIP, whereas treatment of STI571 and PD98059 decreased the BCR/ABL-induced S1P secretion. Treatment of DMS reduced S1P secretion and P42/44MAPK phosphorylation. S1P2-selective antagonist JTE-013 could also decrease P42/44MAPK phosphorylation. Conclusion： These results suggest that BCR/ABL up-regulates extracellular sphingosine 1-phosphate through sphingosine kinase 1 and there is cross-talk between SPK1/S1P/S1P2 and P42/44MAPK in bcr/abl positive CML cells.

关键词： Sphingosine kinase Sphingosine 1-phosphate CML extracellular signal-regulated kinase/mitogen-activated protein kinase Cross-talk

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Speedy/RINGO: a molecular savior in spinal cord injury-based neurodegeneration?

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Neuroimmunology and Neuroinflammation 2019年第3期6卷 6-20页

作者： Yesim Kaya Aysegul Yildiz Department of Molecular Biology and Genetics Faculty of ScienceMugla Sitki Kocman UniversityKotekliMenteseMugla 48000Turkey

Endogenous or exogenous insults can cause spinal cord injury(SCI),often resulting in the loss of motor,autonomic,sensory and reflex functions.The pathogenesis of SCI comprises two stages.The primary injury stage occurs at the moment of trauma and is characterized by hemorrhage and rapid cell death.The secondary injury stage occurs due to progression of primary damage and is characterized by tissue loss and functional disorder.One of the most important cellular mechanisms underlying secondary injury is glutamate excitotoxicity,which overactivates the calpain protease via excessive Ca2+influx and induces neuronal apoptosis via p53 induction.Furthermore,Ca2+influx elicits apoptosis by inducing p53,thus negatively affecting two pathways:the mitogenic extracellular signal-regulated kinase/mitogenactivated protein kinase(ERK/MAPK)pathway and the survival phosphoinositide 3-kinase/protein kinase B(PI3K/AKT)pathway.Speedy/rapid inducer of G2/M progression in oocytes(Speedy/RINGO)is a cell cycle regulatory protein that increases survival of p53-positive mitotic cells by inhibiting the apoptotic machinery.Moreover,this protein elicits p53-dependent anti-apoptotic effects on calpain-induced degeneration of primary hippocampal neurons,amyotrophic lateral sclerosis motor neurons,and astrocytes and microglia in spinal cord lesions.The pathophysiology of SCI has not been fully elucidated and this hinders the development of powerful therapeutic strategies.This review focuses on the cellular mechanisms underlying the anti-apoptotic effects of Speedy/RINGO and discusses how this protective function can possibly be exploited to facilitate recovery from SCI.Particular attention is paid to reversal of the negative effects on the ERK/MAPK and PI3K/AKT pathways via induction of p53.

关键词： Speedy/RINGO calpain p53 extracellular signal-regulated kinase/mitogen-activated protein kinase phosphoinositide 3-kinase/protein kinase B spinal cord injury glutamate excitotoxicity calcium influx

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