c-Myc, RMRP, and miR-34a-5p form a positive-feedback loop to regulate cell proliferation and apoptosis in multiple myeloma.

Long non-coding RNA (lncRNA) component of mitochondrial RNA processing endoribonuclease (RMRP) has been demonstrated to be implicated in human cancer processes. However, the role of lncRNA RMRP in multiple myeloma (MM) remains unknown. In this paper, we proved that RMRP and c-Myc were upregulated, while miR-34a-5p was downregulated in MM cell lines and bone marrows of MM patients.

PML/RARa blocks the differentiation and promotes the proliferation of acute promyelocytic leukemia through activating MYB expression by transcriptional and epigenetic regulation mechanisms.

The promyelocytic leukemia (PML)/retinoic acid receptor-alpha (RARα) onco-fusion protein that is generated from t(15;17) chromosome translocation is crucial for the leukemogenesis of acute promyelocytic leukemia (APL) and is well documented as a transcriptional repressor. To understand the relationship between PML/RARα and the oncogene in the development of APL, we investigate the regulation mechanism of PML/RARα to MYB proto-oncogene and the role of this regulation on the proliferation and differentiation of APL cells. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) assays show that MYB expression was significantly higher in PML/RARα positive cell lines.

[Effect of SHIP-1 on Invasion, Migration and PI3K-AKT Signaling Pathway of Leukemic Cells].

Objective: To investigate the effect of SH2-containing inositol phosphatase-1 (SHIP-1) on the proliferation, invasion and migration of human leukemia cells as well as phosphatidylinositol-3 kinase (PI3K) / protein kinase B (AKT) signaling pathway.

Methods: The overexpression vector pCDNA3.1-SHIP1 was transfected into THP-1 cells by Lipofectamine 2000.

LncRNA MALAT1 acts as an oncogene in multiple myeloma through sponging miR-509-5p to modulate FOXP1 expression.

Previous studies showed that Metastasis associated lung adenocarcinoma transcript 1(MALAT1) acted as an oncogene in Multiple Myeloma (MM). However, the underlying mechanism of MALAT1 in MM remains unclear. Quantitative real time-PCR(qRT-PCR) was used to determine MALAT1 expression in MM samples and cell lines.

AML1/ETO trans-activates c-KIT expression through the long range interaction between promoter and intronic enhancer.

The AML1/ETO onco-fusion protein is crucial for the genesis of t(8;21) acute myeloid leukemia (AML) and is well documented as a transcriptional repressor through dominant-negative effect. However, little is known about the transactivation mechanism of AML1/ETO. Through large cohort of patient's expression level data analysis and a series of experimental validation, we report here that AML1/ETO transactivates c-KIT expression through directly binding to and mediating the long-range interaction between the promoter and intronic enhancer regions of c-KIT.

[Change of Plasma Interleukin-16 Level in Patients with Multiple Myeloma and Its Clinical Significance].

Objective: To investigate the change of plasma IL-16 level in patients with multiple myeloma(MM) and its clinical significance.

Methods: Sixty-two patients with multiple myeloma were admitted in our hospital from June 2008 to June 2015. Forty healthy volunteers were selected as control group.

[Effects of Different Dosages of rhG-CSF on Duration of Aleucocytosis and Leukocytes Level after Chemotherapy of Patients with Hematologic Malignancies].

Objective: To compare the effects of different dosages of rhG-CSF on duration of aleucocytosis and white blood cell counts after chemotherapy of patients with hematologic malignancies.

Methods: Ninety patients in our hospital from December 2011 to June 2016 were chosen as study objects, and all of them were divided into 3 groups: group A (rhG-CSF 200 µg/m), group B(rhG-CSF 300 µg/m) and group C(rhG-CSF 400 µg/m); 30 patients from January 2004 to January 2007 were chosen as control(control group). The WBC and its duration, WBC and its timepoint were compared among different groups.

miR-92a Inhibits Proliferation and Induces Apoptosis by Regulating Methylenetetrahydrofolate Dehydrogenase 2 (MTHFD2) Expression in Acute Myeloid Leukemia.

Aberrant expression of microRNA-92a (miR-92a) has been investigated in various cancers. However, the function and mechanism of miR-92a in acute myeloid leukemia (AML) remain to be elucidated. Our data showed that miR-92a was evidently downregulated and methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) was remarkably upregulated in AML cell lines HL-60 and THP-1.