Qianfoshan Hospital of Shandong

Jinan, China

Qianfoshan Hospital of Shandong

Jinan, China

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Yuan X.,Shandong Academy of Sciences | Yuan X.,University of Jinan | Wang X.,Peoples Hospital of Zhangqiu City | Bi K.,Qianfoshan Hospital of Shandong | Jiang G.,Shandong Academy of Sciences
International Journal of Oncology | Year: 2015

Ecotropic virus integration site-1 (EVI-1) gene, locus on chromosome 3 (3q26.2) in the human genome, was first found in the AKXD strain of mice, in a model of retrovirus-induced acute myeloid leukemia (AML) established twenty years ago. Since then, EVI-1 was regarded as one of the most invasive proto-oncogenes in human leukemia. EVI-1 can encode a unique zinc-finger protein of 145 kDa that can bind with DNA, and its overexpression was closely related to human hemopoietic diseases. Furthermore, accumulating research indicates that EVI-1 is involved in the differentiation, apoptosis and proliferation of leukemia cells. The present review focuses on the biochemical properties of EVI-1 which plays a role in myeloid malignancies.


PubMed | Qianfoshan Hospital of Shandong, Shandong Academy of Sciences and Peoples Hospital of Zhangqiu City
Type: Journal Article | Journal: International journal of oncology | Year: 2015

Ecotropic virus integration site-1 (EVI-1) gene, locus on chromosome 3 (3q26.2) in the human genome, was first found in the AKXD strain of mice, in a model of retrovirus-induced acute myeloid leukemia (AML) established twenty years ago. Since then, EVI-1 was regarded as one of the most invasive proto-oncogenes in human leukemia. EVI-1 can encode a unique zinc-finger protein of 145 kDa that can bind with DNA, and its overexpression was closely related to human hemopoietic diseases. Furthermore, accumulating research indicates that EVI-1 is involved in the differentiation, apoptosis and proliferation of leukemia cells. The present review focuses on the biochemical properties of EVI-1 which plays a role in myeloid malignancies.


Song G.,Shandong Academy of Sciences | Li Y.,Shandong Academy of Sciences | Zhang Z.,Shandong Academy of Sciences | Ren X.,Shandong Academy of Sciences | And 7 more authors.
Oncology Reports | Year: 2013

Vascular endothelial growth factor (VEGF) plays an important role in solid tumor growth, progression and metastasis as well as in the proliferation and differentiation of hematological malignancies. However, the molecular mechanism that modulates VEGF expression and secretion in leukemia cells has not yet to be elucidated. The purpose of the present study was to investigate the role of the signal pathway in modulating the expression of VEGF in HL-60 cells. Specific siRNAs targeting VEGF were transfected into HL-60 cells and the VEGF expression was measured with reverse transcription-polymerase chain reaction (RT-PCR) and western blot assay. The cell proliferation of HL-60 cells was detected by the cell counting kit-8 (CCK-8) assay and the differentiation of HL-60 cells induced by all-trans-retinoic acid (ATRA) was detected by the RT-PCR assay and flow cytometry assay for CD11b. The upstream transcription factors that were related to VEGF expression such as P53, SP-1, c-jun, VHL, cox-2, c-myc and stat3 were detected by RT-PCR assay. In addition, the chromatin immunoprecipitation (ChIP) assay was used to reveal the role of c-myc by binding the target gene VEGF. The results demonstrated the hypoxia-inducible factor 1α-related signaling pathway, not the same as in solid tumors, might not play a key role in modulating VEGF expression. c-myc contributes to the modulation of VEGF expression by targeting the promoter of VEGF, which was indicated by the ChIP assay. In conclusion, our data demonstrate that VEGF plays an important role in the differentiation and proliferation of HL-60 cells; c-myc-dependent downregulation of VEGF induced by ATRA contributes to the differentiation of HL-60 cells.


Song G.,Shandong Academy of Sciences | Shi L.,Shandong Academy of Sciences | Guo Y.,Shandong Academy of Sciences | Yu L.,Shandong Academy of Sciences | And 8 more authors.
Oncotarget | Year: 2016

All-trans retinoic acid (ATRA) treatment yields cure rates > 80% through proteasomal degradation of the PML-RARa fusion protein that typically promotes acute promyelocytic leukemia (APL). However, recent evidence indicates that ATRA can also promote differentiation of leukemia cells that are PML-RARa negative, such as HL-60 cells. Here, gene expression profiling of HL-60 cells was used to investigate the alternative mechanism of impaired differentiation in APL. The expression of peptidylarginine deiminase 4 (PADI4), encoding PAD4, a protein that post-translationally converts arginine into citrulline, was restored during ATRAinduced differentiation. We further identified that hypermethylation in the PADI4 promoter was associated with its transcriptional repression in HL-60 and NB4 (PMLRARa positive) cells. Functionally, PAD4 translocated into the nucleus upon ATRA exposure and promoted ATRA-mediated differentiation. Mechanistic studies using RNAi knockdown or electroporation-mediated delivery of PADI4, along with chromatin immunoprecipitation, helped identify PU.1 as an indirect target and SOX4 as a direct target of PAD4 regulation. Indeed, PAD4 regulates SOX4-mediated PU.1 expression, and thereby the differentiation process, in a SOX4-dependent manner. Taken together, our results highlight an association between PAD4 and DNA hypermethylation in APL and demonstrate that targeting PAD4 or regulating its downstream effectors may be a promising strategy to control differentiation in the clinic.


Zhang Y.,Shandong University | Lin H.,Qianfoshan Hospital of Shandong | Yi W.-B.,Shandong University
Experimental and Therapeutic Medicine | Year: 2016

Spinal anesthesia or regional anesthesia is a potent anesthetic procedure. Additional modalities have been sought to increase the duration of block in spinal anesthesia. Ketamine is an N-methyl-D-aspartate (NMDA) receptor blocker that has an anesthetic effect when injected intrathecally and has a synergic effect with bupivacaine. Ketamine also has potent analgesic properties. The present study investigated the effect of intrathecally administered ketamine on spinal anesthesia with levobupivacaine or ropivacaine. Sprague-Dawley rats at post-natal day 21 were exposed to spinal anesthesia with 0.5% levobupivacaine or 0.5% ropivacaine. Separate groups of rats were treated with intrathecal ketamine at a 5 or 10 mg/kg bodyweight dose along with ropivacaine or levobupivacaine. The thermal and mechanical withdrawal latencies of the animals were determined using hot plate and von Frey filaments, respectively. A rotarod apparatus was employed to assess the capacity of the rats to rotate the spindle at 24 h following anesthesia. The gait of the rat pups was also assessed. Intrathecal administration of ketamine resulted in dense blocks and extended the duration of spinal blocks as evidenced by thermal latencies and responses to von Frey filaments. The latency to fall was shorter in rats exposed to ketamine along with ropivacaine or levobupivacaine spinal anesthesia. The gait parameters were also more disturbed upon ketamine administration. In conclusion, ketamine administration with ropivacaine or levobupivacaine increased the intensity and duration of spinal blockade, thereby increasing the anesthetic effects. © 2016, Spandidos Publications. All rights reserved.

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