[Relationship between Polymorphism of miR-155 and Its Target Gene MyD88 and Clinicopathological Features of Diffuse Large B-cell Lymphoma].

OBJECTIVE: To investigate the relationship between the polymorphism of miR-155 and its target gene MyD88 and clinicopathological features of diffuse large B-cell lymphoma (DLBCL). METHODS: 135 cases of DLBCL patients in our hospital from March 2015 to August 2017 were selected, and 90 cases of reactive hyperplasia of lymph nodes were selected as the control group. The relative expression of miR-155 and MyD88 gene polymorphism were detected in the two groups, and the relationship between miR-155 and MyD88 gene polymorphism and clinicopathological characteristics of DLBCL was analyzed. RESULTS: The relative expression of miR-155 in DLBCL patients was significantly higher than that in the control group (P<0.05). The mutation rate of MyD88 L265P in DLBCL group was significantly higher than that in control group (P<0.05). The relative expression of miR-155 in patients with MyD88 L265P mutation was significantly higher than that in patients with wild-type DLBCL (P<0.05). The relative expression of miR-155 and the polymorphism of MyD88 L265P were associated with lesion location, stage, BCL-2 protein expression and MyD88 protein expression in DLBCL patients (t=7.461、8.804、6.487、10.812； χ2=10.681、8.599、7.251、23.008；P<0.05). The survival of DLBCL patients with low miR-155 expression was significantly better than that with high miR-155 expression (P<0.05). The survival of wild-type DLBCL patients with MyD88 L265P locus was significantly better than that of mutant DLBCL patients (P<0.05). There was a significant positive correlation between the relative expression of miR-155 and the expression of MyD88 protein (r=0.428, P=0.000). CONCLUSION: The abnormal expression of miR-155 and the mutation rate of MyD88 gene in DLBCL patients are increased, and the expression of miR-155 and the mutation of MyD88 gene affect the disease progression and prognosis of patients, which may be potential biological indicators for the diagnosis, treatment and prognosis of DLBCL.

[Effects of Long Non-coding RNA-TUC338 on the Migration and Proliferation of Lymphoma Cells via PI3K/AKT Signaling Pathway].

OBJECTIVE: To investigate the effect of long non-coding RNA-TUC338 on the proliferation and migration of lymphoma cells. METHODS: The expression of TUC338 in different lymphoma cells was detected by fluorescence quantitative PCR, cell proliferation by sulforhodamine B (SRB) assay, migration of lymphoma cells by transwell assay, and protein expression in PI3K/AKT signaling pathway by Western blot. RESULTS: The expression levels of TUC338 in lymphoma cells Daudi, U937, BC-3, and Raji significantly increased in comparison with human normal T lymphocytes H9 (t=13.277, 10.103, 16.200, and 26.687, P=0.002, 0.005, 0.001, and 0.000). Compared with NC-siRNA group, the number of cells crossing the chamber of TUC338-siRNA group was significantly reduced (t=30.508, P=0.000), the protein expression levels of p-PI3K and p-AKT significantly decreased (t=16.872 and 18.371, P=0.000 and 0.000), and OD530 absorbance values at 24 h, 48 h, and 72 h were significantly lower (P<0.05). CONCLUSION: The expression of TUC338 significantly increases in lymphoma cells, and silence of TUC338 effectively inhibits the activation of PI3K/AKT signaling pathway, thereby inhibiting the proliferation and migration of lymphoma cells, which has a potential application value in diagnosis and treatment of lymphoma.

[Relationship of Expression of Circ_cgga162 with the Prognosis of Patients with Mantle Cell Lymphoma].

OBJECTIVE: To investigate the expression of Circ_cgga162 in serum of mantle cell lymphoma (MCL) patients and analyze its potential as a prognostic biomarker. METHODS: The expression of Circ_cgga162 in 86 cases of mantle cell lymphoma and 50 cases of lymph node reactive hyperplasia (RH) were detected by real-time quantitative polymerase chain reaction (qRT-PCR). The relationship between the expression of Circ_cgga162 and clinicopathological features was analyzed by univariate analysis. The relationship of Circ_cgga162 expression with progression-free survival time and overall survival time was analyzed by Kaplan-Meier. The relationship between expression of Circ_cgga162 and prognosis of patients was analyzed by univariate and multivariate analysis. RESULTS: The expression level of Circ_cgga162 in MCL patients was significantly higher than that in control (RH) group (P＜0.01). The expression of Circ_cgga162 not correlated with age, gender, B symptoms and LDH (all P＞0.05), but correlated with the expression of MCL International Prognostic Index (IPI), Ann Arbor stage, bone marrow infiltration and Ki67 (all P＜0.05). In addition, Kaplan-Meier analysis showed that the progression-free survival time and overall survival time of the MCL patients with high expression of Circ_cgga162 were significantly shorter than those of the MCL patients with low expression (P＜0.01). Univariate analysis showed that Ann Arbor stage, Circ_cgga162 expression, MIPI, bone marrow infiltration and Ki67 were the prognostic factors for MCL patients (all P＜0.05). Multivariate Cox regression analysis showed that Ann Arbor stage, Circ_cgga162 expression and MIPI were independent factors affecting the prognosis of MCL patients (all P＜0.05). CONCLUSION: Circ_cgga162 is highly expressed in serum of patients MCL, which relates with the prognosis of MCL patients. Circ_cgga162 can be used as a potential prognostic marker and therapeutic target for MCL patients.

[The role of EGF-like factor signaling pathway in granulosa cells in regulation of oocyte maturation and development].

The surge of luteinizing hormone (LH) in preovulatory ovarian follicles triggers the resumption of meiosis in oocytes and induces the proliferation of surrounding cumulus granulosa cells. It is believed that LH receptors are expressed in the mural granulosa cells, but not the oocytes and the surrounding cumulus cells, suggesting that the LH signaling is mediated by factors produced by the granulosa cells. However, the mechanism underlying oocyte maturation induced by LH before ovulation has been controversial. Current studies suggest that LH binds on to its receptor on granulosa cells of the follicular wall to promote the production of EGF-like factors, which activate various signaling cascades and induce oocyte maturation and development. Since the in vitro maturation system is difficult to simulate the in vivo physiological environment, in vitro cultured follicles are likely to be de?cient in the EGF-like factors, which could result in the poor developmental competency of in vitro cultured oocytes and restrict their efficient utilization. In this review, we summarize the EGF-like factor signaling system in granulosa cells and its regulation of oocyte maturation and development. It aims to optimize the in vitro maturation culture system of oocytes and increase the EGF-like factor signaling system in cumulus granulosa cells, thereby providing a framework for improving the efficiency on in vitro maturation of oocytes.

[Expression and Clinical Significance of LncRNA KCNQ1OT1 in Patients with Acute Myeloid Leukemia].

OBJECTIVE: To investigate the expression of LncRNA KCNQ1OT1 in patients with acute myeloid leukemia (AML) and to analyze the relation of LncRNA KCNQ1OT1 expression levels with clinicopathological features. METHODS: A total of 68 patients with AML were enrolled in the study, 48 out of them were suffered from acute myeloid leukemia (AML) and 20 reached to complete remission (CR), 30 age-matched patients with iron-deficient anemia were included in control group, the peripheral blood samples of all the patients were collected, and the real-time fluorescent quantitative PCR (qRT-PCR) was used to detect the expression of LncRNA KCNQ1OT1, meanwhile, the correlation of its expression with clinicopathological characteristics and prognosis was analyzed. RESULTS: The expression of LncRNA KCNQ1OT1 in AML patients was significantly higher than that in the patient with complete remission and iron-deficient anemia (F=14.67, P<0.01). The expression of LncRNA KCNQ1OT1 was not significantly different between 20 cases of AML-CR and 30 cases of iron-deficient anemia (P>0.05). The expression of LncRNA KCNQ1OT1 was associated with NCCN risk grade and survival status in patients with AML. The median overall survival time was significantly shorter in patients with high expression of LncRNA KCNQ1OT1 than that in patients with low expression(P<0.05). CONCLUSION: LncRNA KCNQ1OT1 may be involved in the regulation of AML. Expression of LncRNA KCNQ1OT1 and NCCN risk score can be used as biomarkers of prognosis in the patients with AML and may be a potential prognostic marker and therapeutic target for AML patients.

Mitochondria and pluripotent stem cells function.

Mitochondria are important intracellular organelles which provide energy for cellular activities through oxidative phosphorylation. Recently, mitochondria have been shown to exhibit peculiar features in pluripotent stem cells (PSCs), namely, PSCs rely mainly on glycolysis for energy supply in pluripotent states while mitochondrial oxidative phosphorylation function is gradually enhanced during PSCs differentiation. In contrast, during somatic reprogramming, the metabolic transition from mitochondrial oxidative phosphorylation to glycolysis is necessary for successful reprogramming. Moreover, mitochondrial biogenesis and dynamics are also actively involved in the maintenance of pluripotency, induction of differentiation and induced pluripotent stem cells (iPSCs) reprogramming. Here we reviewed mitochondrial structure and function in regulating PSCs pluripotency, anabolism, redox homeostasis, differentiation, and reprogramming, which may provide reference for further understanding the role of mitochondria in PSCs.

Mechanisms of TET protein-mediated DNA demethylation and its role in the regulation of mouse development.

TET (ten-eleven translocation) protein family includes three members TET1, TET2 and TET3, which belong to alpha-ketoglutaric acid ( α-KG )- and Fe(2+)-dependent dioxygenase superfamily, and have the capacity to convert 5-methylcytosine (5 mC) to 5-hydroxymethylcytosine (5 hmC), 5-formylcytosine (5 fC) and 5-carboxylcytosine (5 caC). At present, growing lines of evidence indicate that TET proteins are involved in the control of active or passive DNA demethylation via different mechanisms; moreover, their activities may be regulated by some cellular factors. TET proteins play vital roles in modulating mammal development, including primordial germ cell formation, embryonic development, stem cells pluripotency, nerve and brain development, etc. The identification of biological roles of TET proteins will open a new field in epigenetic research, and these studies on TET proteins are of great significance to life science research. Here, we review TET proteins from their structure, molecular mechanisms of DNA demethylation and function in the regulation of mouse development, which may provide the basis for understanding the functions of TET proteins.