Expression of small nucleolar RNA SNORD15A in acute leukemia and its clinical significance / 白血病·淋巴瘤

Objective:To investigate the expression level of small nucleolar RNA SNORD15A in bone marrow of patients with acute leukemia (AL) and its relationship with clinical characteristics and prognosis of patients.Methods:Bone marrow blood samples of 53 newly treated AL patients and 29 healthy subjects without clinical diagnosis of hematologic diseases or other malignant diseases (control group) at the Affiliated Hospital of Guangdong Medical University from March 2018 to December 2021 were collected. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to detect the relative expression of SNORD15A in bone marrow blood mononuclear cells of the two groups. The median relative expression of SNORD15A (0.148) was used as the boundary, and AL patients were divided into low expression group (<0.148) and high expression group (≥0.148). The relationship between the expression level of SNORD15A and the clinical characteristics, clinical indicators and overall survival (OS) of AL patients was analyzed. Kaplan-Meier method was used for survival analysis and log-rank test was performed; Cox proportional hazards model was used for univariate and multivariate analyses of OS of patients.Results:The relative expression of SNORD15A was 0.148 (0.012-1.376) in newly treated AL patients and 0.921 (0.513-2.288) in the control group, and the difference was statistically significant ( Z = -6.85, P < 0.01). The differences in SNORD15A relative expression between patients with different prognostic stratification, efficacy and with or without fever and bleeding were statistically significant (all P < 0.05). The differences in platelet count, plateletcrit and albumin levels between SNORD15A low expression group and high expression group were statistically significant (all P < 0.05), and the differences in molecular biology and cytogenetic characteristics were not statistically significant (all P > 0.05). The patients in SNORD15A high expression group had better OS than the low expression group ( P < 0.05). The results of univariate Cox regression analysis showed that SNORD15A was an influencing factor for patients' OS ( HR = 0.063, 95% CI 0.005-0.766, P < 0.05); the results of multivariate Cox regression analysis showed that fatigue ( HR = 4.754, 95% CI 1.014-22.290), fever ( HR = 0.147, 95% CI 0.029-0.746) and hemoglobin ( HR = 0.970, 95% CI 0.944 -0.998) were independent influencing factors for OS (all P < 0.05). Conclusions:SNORD15A is lowly expressed in AL and may be an indicator for disease monitoring and prognostic assessment in AL patients.

Research Progress of LncRNA SNHGs in Regulating the Biological Behavior of Non-small Cell Lung Cancer / 中国肺癌杂志

Lung cancer is one of the malignant tumors with the highest incidence and mortality rate in China, and its occurrence and development mechanism and treatment methods are the current research focuses. In recent years, the emergence of drugs targeting various tumor driver genes has significantly improved patients' survival and quality of life, setting off a wave of research on new therapeutic targets. Among them, long non-coding RNA (lncRNA) plays a crucial role in the malignant behavior of tumors, which has attracted widespread attention. Shown by a large number of studies, partial members of lncRNA small nucleolar RNA host gene (SNHG) family are aberrantly expressed in many maliglant tumors including non-small cell lung cancer (NSCLC) and participate in cell proliferation, invasion and migration, which may act as a new diagnostic and prognostic biomarker and can be a therapeutic target of NSCLC. In this review, we comprehensively summarize and explore the recent investigation of SNHGs in NSCLC in order to provide new ideas for the diagnosis and treatment of NSCLC.
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Effect of small nucleolar RNA host gene 5 on hypoxia/reoxygenation injury of astrocytes / 中华行为医学与脑科学杂志

Objective:To explore the effect of lncRNA SNHG5 on injury of astrocytes induced by hypoxia/reoxygenation (H/R).Methods:(1) Astrocytes were cultured in vitro. The H/R cell model was established by hypoxia culture for 6 hours and then reoxygenaion culture for 18 hours. Lipofectamine? 2000 liposome method was used to transfect lncRNA SNHG5 into astrocytes. RT-qPCR was used to detect the expression of lncRNA SNHG5 in H/R cells and after transfection. (2) Astrocytes were divided into normal control group, model group, transfection control group (pcDNA-NC was transfected first, then H/R cell model was established) and transfection group (pcDNA-lncRNA SNHG5 was transfected first, then H/R cell model was established). Then the effect of overexpression of lncRNA SNHG5 on astrocytes was observed. (3)The astrocytes transfected with lncRNA SNHG5 and H/R intervention were divided into transfection+ vehicle group (0.1% DMSO incubation) and transfection+ inhibitor group (20 μmol/L LY294002 incubation), and then observe the effect of the inhibitor of PI3K/Akt signaling pathway LY294002 on H/R astrocytes was observed. (4) CCK-8 was used to detect cell proliferation. Flow cytometry was used to detect cell apoptosis. Western blot was used to detect the expression of cell proliferation proteins (Cyclin D1 and Cyclin E), apoptotic proteins (Caspase-3 and Bax), p-PI3K and p-AKT protein. ELISA was used to detect the levels of IL-1β and TNF-α. The colorimetric method was used to detect the level of lactate dehydrogenase(LDH) in cell culture supernatants and the level of malondialdehyde(MDA) and superoxide dismutase(SOD) in cells. SPSS 22.0 software was used for independent sample t-test and one-way ANOVA, and LSD- t test was used for further pairwise comparisons. Results:(1) RT-qPCR results showed that the level of lncRNA SNHG5 in astrocytes induced by H/R was lower than that in the normal cultured cells ( t=33.28, P<0.05). (2) lncRNA SNHG5 overexpression experiment: The cell proliferation activity of the model group was lower than that in the normal control group (CCK-8 OD value: (0.64±0.02), (1.23±0.02), t=62.58, P<0.05). The levels of proliferation proteins Cyclin D1 and Cyclin E in the model group were lower than those of the normal control group ( t=33.54, 32.20, both P<0.05). The cell proliferation activity of the transfection group was higher than that of the transfection control group (CCK-8 OD value: (1.49±0.02), (0.65±0.03), t=69.89, P<0.05), the levels of cell proliferation proteins Cyclin D1 and Cyclin E in the transfection group were lower than those in the transfection control group ( t=24.96, 28.46, both P<0.05). The apoptosis rate of the model group was higher than that of the control group (flow cytometry results: (25.33±1.13)%, (9.06±0.21)%, t=42.47, P<0.05), and the levels of apoptotic proteins Caspase-3 and Bax were also higher than those of the control group ( t=57.41, 41.60, both P<0.05). The Caspase-3 rate of the transfection group was lower than that of the transfection control group((16.56±0.60)%, (25.89±1.18)%, t=21.14, P<0.05), and the levels of apoptotic proteins Caspase-3 and Bax were also higher than those of the transfection control group( t=77.79, 58.34, both P<0.05). The levels of p-PI3K and p-AKT proteins in the model group were lower than those in the control group ( t=56.35, 33.94, both P<0.05), and the levels of p-PI3K and p-AKT proteins in the transfection group were higher than those in the transfection control group ( t=130.14, 76.37, both P<0.05). The results of ELISA showed that the levels of IL-1β and TNF-α in the model group were higher than those in the control group ( t=58.04, 30.63, both P<0.05), but the levels of IL-1β and TNF-α in the transfection group were lower than those in the transfection control group ( t=33.63, 39.01, both P<0.05). The colorimetric method showed that the levels of LDH and MDA in the model group were higher than those in the control group ( t=65.51, 41.85, both P<0.05), but the level of SOD was lower than that in the control group ( t=48.82, P<0.05). The levels of LDH and MDA in the transfection group were lower than those in the transfection control group ( t=37.93, 30.72, both P<0.05), but the level of SOD was higher than that in the transfection control group ( t=30.32, P<0.05). (3) PI3K/Akt signaling pathway inhibition experiment: the cell proliferation activity of the transfection+ inhibitor group was lower than that of the transfection+ vehicle group (CCK-8 OD value: (0.97±0.02), (1.46±0.03), t=15.24, P<0.05), and the related proliferation proteins Cyclin D1 and Cyclin E were also lower ( t=11.41, 13.15, both P<0.05). The apoptosis rate of the transfection+ inhibitor group was higher than that of the transfection+ vehicle group (Flow cytometry: (26.11±0.86)%, (16.06±0.44)%, t=10.45, P<0.05). The apoptosis rate of the transfection+ inhibitor group was higher than that of the transfection+ vehicle group (Flow cytometry: (26.11±0.86)%, (16.06±0.44)%, t=10.45, P<0.05), and the related apoptosis protein Caspase-3 and Bax were also higher ( t=19.06, 13.54, both P<0.05). The expression levels of p-PI3K and p-AKT protein in the transfection+ inhibitor group were lower than those in the transfection+ vehicle group ( t=36.67, 27.34, both P<0.05). ELISA results showed that the levels of IL-1β and TNF-α in the transfection+ inhibitor group were higher than those in the transfection+ vehicle group ( t=15.17, 9.44, both P<0.05). The colorimetric method results showed that the levels of LDH and MDA in the transfection+ inhibitor group were the same as those in the transfection+ vehicle group ( t=15.33, 9.05, both P<0.05), but the level of SOD was lower than the transfection+ vehicle group ( t=11.04, P<0.05). Conclusion:Overexpression of lncRNA SNHG5 may promote the proliferation of astrocytes induced by hypoxia/reoxygenation, and inhibit cell apoptosis, inflammation and oxidative stress.

SNHG6 promotes invasion and metastasis of esophageal squamous cell carcinoma TE1 cells via upregulating ZEB1 / 中国肿瘤生物治疗杂志

@# Objective: To explore the roles and mechanisms of long non-coding RNA (lncRNA) small nucleolar RNA host gene 6 (SNHG6) in promoting invasion and metastasis of esophageal squamous carcinoma (ESCC). Methods: Real time quantitative polymerase chain reaction (qPCR) was used to detect the expression of SNHG6 in ESCC and matched para-carcinoma tissues. Reverse transcription-polymerase chain reaction (RT-PCR) was performed to detect the expression of SNHG6 in ESCC cell lines (TE1, Yes-2, Eca9706 and Kyse150). Then, TE1 cell line which harbored highest expression of SNHG6 was used in following experiments. siRNAs were used to knock down the expression of SNHG6. Clone formation, wound-healing and transwell assay were used to detect the abilities of proliferation, migration andinvasionofTE1cells,respectively.Westernblottingwasusedtodetecttheexpressions of MMP-2, MMP-9andZEB1 protein before and after knockdownofSNHG6inTE1cells.Results:SNHG6washighlyexpressedinESCC tissues, compared to para-carcinoma tissues (P<0.01). The expression of SNHG6 was significantly decreased after transfection of SNHG6siRNA (all P<0.01). The abilities of proliferation, migration and invasion of TE1 cells in si-SNHG6-1 and si-SNHG6-2 group were significantly lower than those in the control group (all P<0.01). The expressions of ZEB1, MMP-2and MMP-9 in si-SNHG6-1 and si-SNHG6-2 group were significantly lower than those in the control group (all P<0.05). Conclusion: SNHG6 is highly expressed in ESCC tissues and promotes the malignant biological behavior of ESCC cells. Its mechanism of promoting the occurrence and development of ESCC may be related to the upregulation of ZEB1 expression.

Expression and mechanisms of long non-coding RNAs SNHG15 in cancers / 国际肿瘤学杂志

As a kind of long non-coding RNAs (lncRNAs),small nucleolar RNA host gene 15 (SNHG15) is located on chromosome 7.In recent years,studies have shown that lncRNA SNHG15 is over expressed in various types of cancers such as glioma,thyroid cancer,breast cancer,lung cancer,gastric cancer,colorectal cancer,liver cancer,renal carcinoma,pancreatic cancer,osteosarcoma,and it can promote the proliferation,invasion,metastasis of malignant tumors and lead to poor prognosis of tumor patients through different signal pathways.

Expression of long non-coding RNA SNHG3 in breast cancer and its clinical significance / 医学研究生学报

ObjectiveThere are a few reports about the expression of SNHG3 in breast cancer and its effects. This study aimed to detect the expression of SNHG3 in breast cancer and paracancerous tissues, along with its relevance to clinicopathological parameters.MethodsSeventy-four patients with breast cancer were confirmed pathologically in our hospital from Jan. 2014 to Dec. 2017. The expression of SNHG3 was examined in breast cancer and paracancerous tissues by qRT-PCR. Correlations between the expression of SNHG3 and clinicopathological parameters were analyzed.Results SNHG3 expression was significantly downregulated in breast cancer tissues compared to paracancerous tissues, and the difference was of statistical significance (P<0.000). Low expression of SNHG3 was in negative correlation to Ki-67 (rs=-0.296, P=0.013).ConclusionThe expression of SNHG3 downregulated in breast cancer tissues, and its expression level is related to Ki-67, which may serve as a potential diagnostic molecular marker.

Noncoding RNA small nucleolar RNA host gene 1 promote cell proliferation in nonsmall cell lung cancer.

BACKGROUND: Nonsmall cell lung cancer (NSCLC) is the major cause of cancer death worldwide. Increasing evidence shows that noncoding RNAs (ncRNAs) are widely involved in the development and progression of NSCLC. ncRNA small nucleolar RNA host gene 1 (SNHG1) has not been studied in cancer, especially its role in lung cancer remains unknown. Our studies were designed to investigate the expression and biological significance of SNHG1 in lung cancer. SNHG1 may be a novel ncRNA in early diagnosis in lung cancer. METHODS: Noncoding RNA SNHG1 expression in 7 lung cancer cell lines was measured by quantitative real‑time polymerase chain reaction. RNA interference approaches were used to find the biological functions of SNHG1. The effect of SNHG1 on proliferation was evaluated by cell count and crystal violet stains. RESULTS: Noncoding RNA SNHG1 expression was significantly upregulated in lung cancer cells when compared with normal bronchial epithelial cells. In addition, in vitro assays our results indicated that knockdown of SNHG1 inhibited cell proliferation. CONCLUSIONS: Our data indicated that ncRNA SNHG1 is significantly upregulated in NSCLC cell lines and may represent a new biomarker and a potential therapeutic target for NSCLC intervention.

Identification of the N-terminal Glycine-arginine Rich (GAR) Domain in Giardia lamblia Fibrillarin and Evidence of its Essentiality for snoRNA Binding.

Aims: Study the role of glycine-arginine rich (GAR) domain of fibrillarin in Giardia lamblia. Study Design: Identifying a specific glycine arginine rich (GAR) sequence of Giardia fibrillarin which plays an important role in ribonucleoprotein particles complex formation with snoRNA during post transcriptional modifications of rRNA. The present study uses Electrophoretic Mobiliy Shift Assay (EMSA) to detect protein-RNA interactions. 32P labeled snoRNA incubated with purified fibrillarin or GAR domain truncated fibrillarin protein were separated by a non denaturing polyacrylamide gel where the band patterns suggested the interaction of the RNAs with both proteins. Place and Duration of Study: Department of Parasitology, National Institute of Cholera and Enteric Diseases, Indian Council of Medical Research, Kolkata, between January 2011 and July 2012. Methodology: Homology analysis of G. lamblia fibrillarin was performed with fibrillarins from Homo sapiens, Mus musculus and Arabidopsis thaliana to determine the conserved domain by ClustalW analysis. Cloning, expression and purification of fibrillarin and GAR domain truncated fibrillarin were done to study the role of GAR domain in snoRNA-fibrillarin binding by EMSA and Gradient EMSA. Immunoblot assay of purified GAR domain truncated fibrillarin was performed by using polyclonal antibody of purified recombinant giardia fibrillarin protein. Results: Gel retardation assay showed that snoRNA does not bind with GAR domain truncated fibrillarin to form any RNP complex. Similarly in gradient EMSA the GAR domain truncated fibrillarin does not bind with any of the in vitro transcribed snoRNA even at much higher concentration than they do for full length purified recombinant fibrillarin. Conclusion: The amino terminal conserved glycine arginine rich (GAR) domain is present in Giardia lamblia fibrillarin and is essential for binding with snoRNA of this protein.