Distribution characteristics of polymorphism of miRNA-107 gene in Guangxi population and their association with serum lipid levels / 解剖学报

Objective To study the distribution characteristics of single nucleotide polymorphisms (SNP) of miR-107 gene rs2296616 C/T in Guangxi healthy population and comparison with that in different ethnic populations, and further to explore the correlation between rs2296616 C/T SNP and blood lipid level. Methods The polymorphisms of miR-107 gene rs2296616 C/T among 372 Chinese healthy individuals of Guangxi were detected by multiplex SNaPshot and DNA sequencing method, and the blood lipid-related indexes were detected by 7600 biochemical analyzer. The distribution of rs2296616 C/T polymorphism among different ethnic groups and the differences of blood lipid levels among different genotypes were compared by statistical method . Results MiR-107 gene rs2296616 C/T SNP contained TT(91. 1%), CT (8. 9%)genotypes and T(95. 6%), C(4. 4%)alleles in Guangxi healthy population. The frequencies of genotype and allele distribution of rs2296616 C/T were not significantly different among genders in Guangxi population(P>0. 05). However, there were significant differences in the genotype and allele frequency of miR-107 gene rs2296616 C/T in Guangxi healthy population compared with those of Europeans, Japanese, Africans, Mexicans and Indians published in HapMap(P 0. 05). When compared the blood lipid level among two genotypes in rs2296616 C/T, we found that the level of high density lipoprotein cholesterol(HDL-C) with TT genotype was significantly different from that of CT group (P < 0. 05) . Conclusion There are different degrees of variation in the polymorphisms of rs2296616 C / T of miR-107 gene between Guangxi people and other ethnic populations. The polymorphism of rs2296616 C / T locus is related to the level of HDL-C.

MicroRNA-107 is a novel tumor suppressor targeting POU3F2 in melanoma

BACKGROUND: Melanoma is one of the major types of skin cancer. The metastatic melanoma is among the most lethal forms of malignant skin tumors. We hereby aimed to characterize a novel microRNA (miR) in the metastatic melanoma model. METHODS: First, we evaluated the expression of miR-107 in melanoma cells and tumor tissues. The comparison between primary and metastatic cancer tissues was also accessed. Next, we examined the impact of miR-107 on melanoma cell proliferation, cell cycle, colony formation, apoptotic activity, migration and matrix invasion. A downstream target of miR-107 was also predicted and validated functionally in melanoma cells. RESULTS: Our findings showed miR-107 was significantly downregulated in melanoma. Its expression was lowest in metastatic form. Over-expression of miR-107 reduced melanoma cell proliferation, migration and invasion. POU3F2 was identified as the downstream target of miR-107. Over-expression of POU3F2 antagonized miR-107-mediated inhibitory effect on melanoma cells. CONCLUSION: Our study has reported miR-107 as a novel tumor suppressive factor in the metastatic melanoma model. It has provided new avenue to manage melanoma and improve the survival rate in the advanced stage.

Long Noncoding RNA NEAT1 Aggravates Aβ-Induced Neuronal Damage by Targeting miR-107 in Alzheimer's Disease

PURPOSE: Alzheimer's disease (AD) is the most common neurodegenerative disease, with a rising prevalence worldwide. Long noncoding RNAs (lncRNAs) have been found to play important roles in the development and treatment of AD. However, the exact role of lncRNA nuclear enriched abundant transcript 1 (NEAT1) in neuronal damage in AD is largely unknown. MATERIALS AND METHODS: The AD model was established in SH-SY5Y and SK-N-SH cells via treatment with amyloid β1−42 (Aβ). The expression of NEAT1 and microRNA-107 (miR-107) was measured by quantitative real-time polymerase chain reaction. Cell viability and apoptosis were detected by MTT assay, immunocytochemistry, and flow cytometry. The expression of phosphorylated tau protein (p-Tau) was measured by Western blot. The interaction between NEAT1 and miR-107 was explored by bioinformatics analysis, luciferase activity, and RNA immunoprecipitation assays. RESULTS: NEAT1 expression was enhanced in Aβ-treated SH-SY5Y and SK-N-SH cells, and its knockdown attenuated Aβ-induced inhibition of viability and promotion of apoptosis and p-Tau levels. NEAT1 was indicated as a decoy of miR-107. miR-107 abundance was reduced in Aβ-treated cells, and its overexpression reversed Aβ-induced injury. Moreover, interference of miR-107 abated silencing of NEAT1-mediated inhibition of neuronal damage in Aβ-treated SH-SY5Y and SK-N-SH cells. CONCLUSION: LncRNA NEAT1 aggravated Aβ-induced neuronal damage by sponging miR-107, indicating a novel avenue for treatment of AD.

Effects of miR-107 on proliferation, apoptosis and inflammatory factors of human nasal mucosal epithelial cells induced by LPS and its mechanism / 中国耳鼻咽喉头颈外科

OBJECTIVE To detect the effects of miR-107 on the proliferation, apoptosis and inflammatory factors of human nasal mucosal epithelial cells(HNMECs) induced by Lipopolysaccharides(LPS), and to elucidate the potential molecular mechanism. METHODS The expression changes of miR-107 and HMGBl(High mobility group box 1) in 1 mg/L LPS induced HNMECs before and after LPS induction were detected by using quantitative realtime PCR. LPS induced-HNMECs were transfected with miR-107 agomir and agomir control, and 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide(MTT) assay, flow cytometry and enzyme-linked immunosorbent assay(ELISA) were performed to detect cell proliferation, apoptosis and inflammatory factors. Dual luciferase reporter assay and Western blots were applied to verify whether HMGB1 was a target gene of miR-107. RESULTS The expression of miR-107 in HNMECs after LPS induction was significantly lower than that before induction(t =9.35, P ＜0.05), while the expression of HMGB1 in HNMECs after LPS induction was significantly higher than that before induction(t =13.07, P＜0.05). Compared with transfected agomir control, transfection of miR-107 agomir in HNMECs significantly inhibited cell proliferation (F =17.12, P ＜0.05) and decreased inflammatory factor TNF-α(t =6.11, P ＜0.05). IL-1β(t =6.90, P ＜0.05) and IL-6(t =8.18, P ＜0.05) expression levels, and increased apoptosis rate(t =7.49, P ＜0.05). HMGB1 was a target gene of miR-107, and transfection of miR-107 agomir in HNMECs after LPS induction could significantly reduce the expression of HMGB1 protein (t =28.56, P ＜0.05). CONCLUSION miR-107 is upregulated in HNMECs after LPS induction, while HMGB1 is down-regulated. Overexpression of miR-107 significantly inhibits the proliferation of HNMECs and the expression of inflammatory factors after LPS induction, and promotes apoptosis. HMGB1 is a target gene of miR-107, suggesting that miR-107 may play a regulatory role by regulating HMGB1.

Circular RNA-ZFR Inhibited Cell Proliferation and Promoted Apoptosis in Gastric Cancer by Sponging miR-130a/miR-107 and Modulating PTEN / Journal of the Korean Cancer Association, 대한암학회지

PURPOSE: This study aimed to probe into the associations among circular RNA ZFR (circ-ZFR), miR-130a/miR-107, and PTEN, and to investigate the regulatory mechanism of circ-ZFR–miR-130a/miR-107–PTEN axis in gastric cancer (GC). MATERIALS AND METHODS: GSE89143 microarray data used in the study were acquired from publicly available Gene Expression Omnibus database to identify differentially expressed circular RNAs inGC tissues. The expressions of circ-ZFR, miR-130a, miR-107, and PTEN were examined by real-time reverse transcription polymerase chain reaction, while PTEN protein expression was measured by western blot. The variation of GC cell proliferation and apoptosis was confirmed by cell counting kit-8 assay and flow cytometry analysis. The targeted relationships among circZFR, miR-130a/miR-107, and PTEN were predicted via bioinformatics analysis and demonstrated by dual-luciferase reporter assay and RNA immunoprecipitation assay. The impact of ZFR on gastric tumor was further verified in xenograft mice model experiment. RESULTS: Circ-ZFR and PTEN were low-expressed whereas miR-107 and miR-130a were highexpressed in GC tissues and cells. There existed targeted relationships and interactions between miR-130a/miR-107 and ZFR/PTEN. Circ-ZFR inhibited GC cell propagation, cell cycle and promoted apoptosis by sponging miR-107/miR-130a, while miR-107/miR-130a promoted GC cell propagation and impeded apoptosis through targeting PTEN. Circ-ZFR inhibited cell proliferation and facilitated apoptosis in GC by sponging miR-130a/miR-107 and modulating PTEN. Circ-ZFR curbed GC tumor growth and affected p53 protein expression in vivo. CONCLUSION: Circ-ZFR restrained GC cell proliferation, induced cell cycle arrest and promoted apoptosis by sponging miR-130a/miR-107 and regulating PTEN.

Study on effect of miR-107 targeting CCNE1 on function of human non-small cell lung cancer cell line A549 / 重庆医学

Objective To investigate the effect of miR-107 on the function of human non-small cell lung cancer cell line A549 and its possible target genes.Methods The experiment was divided into the liposome+miR-107 mimics overexpression group(OV-miR-107 group),liposome+miR-107 inhibiting mimics downregulation group(KD-miR-107 group)and liposome+ negative control mimics group(NC group).The cell transfections of siRNA were siRNA-1,siRNA-2 and siRNA-3 respectively.The cellular prolifer-ation capacity was detected by MTT assay.The cellular cycle was detected by flow cytometry.The dual luciferase reporter gene as-say was performed to detect the downstream target gene of miR-107.The real time quantitative reverse transcription PCR and Western blot were respectively employed to examine mRNA and protein expression levels of downstream target gene.Results miR-107 inhibited the proliferation of A549 cells in a time-and dose-dependent manner(P<0.05).miR-107 arrested more A549 cells at the G0G1phase,and the proportions of S phase and G2M phase were decreased(P<0.05).miR-107 combinded with the 246 bp-253 bp of CCNE1 3′-untranslated region,and decreased mRNA and protein expression of CCNE1(P<0.05);after down-regulating CC-NE1 in A549 cells,siRNA-2 inhibited cellular proliferation(P<0.05)and blocked the cells to stay at G0G1phase(P<0.05).Con-clusion miR-107 inhibits the proliferation of human non-small cell lung cancer cell line A549 and regulates the cellular cycle by tar-geting CCNE1.

The effects of miRNAs-107 on cell proliferation, senescence and invasion of pancreatic cancer PANC-1 cells / 中华肝胆外科杂志

Objective To investigate the effects of miRNAs-107 (miR-107) on pancreatic cancer proliferation,senescence and invasion.Methods MiR-107 expression levels in 3 pancreatic cancer cell lines PANC-1,ASPC-1,BXPC-3 and normal pancreatic HTERT-HPNE cells were studied by quantitative reverse transcription-polymerase chain reaction (qRT-PCR).PANC-1 cells were transfected with 50 nmol/L anti-miR-107 or negative control using Lipofectamine 2000.After transfection,the miR-107 expression was measured by qRT-PCR.Cell proliferation was tested by methylthiazol tetrazolium (MTT) assay.Cell senescence was detected by β-galactosidase staining.The expression levels of PCNA,P16INK4A and MMP2 were measured by qRT-PCR.Results Compared with the HTERT-HPNE cells,the expression level of miR-107 in 3 pancreatic cancer cell lines was significantly increased (P ＜ 0.01).After transfected with 50 nmol/L anti-miR-107,cell proliferation was inhibited,and cell senescence were increased in PANC-1 cells (P ＜ 0.05),and there was no obvious change in cell invasion.Compared with the HTERT-HPNE cells,after transfected with anti-miR-107,the PCNA expression was significantly decreased and P16INK4A was significantly increased,but expression of M MP2 didn't change significantly.Conclusions These results demonstrate that miR-107 promotes the proliferation and escapes cell senescence in PANC-1 cells by targeting PCNA and P16INK4A.But it has no obvious effects on cell invasion.Therefore,it may be a new target for the biologic therapy for pancreatic cancer.

MiR-107 target NID2 regulating invasion and proliferation of lung cancer by JAK/STAT signaling pathway / 中国免疫学杂志

Objective:To investigate the effect of miR-107 targeting NID2 on Notch signaling pathway on invasion and proliferation of lung cancer.Methods: The expression of NID2 in lung cancer and normal tissues was detected by immunohistochemistry.The expression of miR-107 in lung cancer cell line was detected by PCR.The effect of miR-107 on the expression of NID2 was examined by the dual luciferase gene system.Effect of miR-26 on the proliferation ability of H1650 were detected by tumor in ball assays.Transwell invasion assay was used to detect the ability of invasion in the lung cancer cell line A549 after overexpression the miR-107.Scratch test was used to detect the ability of migration in the lung cancer cell line A549 after overex-pression the miR-107.Western blot was used to detect the protein expression of Notch signal pathway after overexpression miR-107.Results:The expression of NID2 in lung cancer tissues was significantly higher than that in normal lung tissues.The expression of miR-107 in lung cancer tissues was significantly lower than that in normal lung tissues.The dual luciferase reporter gene system showed that miR-107 could directly regulate the transcriptional activity of NID2.After miR-107 overexpression,the proliferation,invasion and migration ability of lung cancer cell A549 were significantly decreased.The expression of miR-107 protein could down-regulate the expression of Notch1,hes-1 and presenilin1 protein.Conclusion: miR-107 targets the expression of NID2 and regulates the invasion and proliferation of lung cancer cells by Notch pathway.

Long non-coding RNA H19 promoted lung cancer cells migration and invasion through miR-107 / 中国免疫学杂志

Objective:To investigate the effect and the related mechanism of H19 on the invasion and migration ability of pancreatic cancer cells.Methods: The expression of H19 in tissues of pancreatic carcinoma and non-carcinoma adjacent tissues of pancreatic carcinoma were detected.qPCR was used to detect the expression of H19 in different pancreatic cancer cells.The migration and invasion ability of pancreatic cancer cells was detected after silencing H19 using wound healing assays and Transwell matrigel invasion assays.Dual-Luciferase Reporter Assay System was used to detect miR-107regulating H19.The expression of miR-107 in tissues of pancreatic carcinoma and non-carcinoma adjacent tissues of pancreatic carcinoma were detected.The regulation of miR-107 on the migration and invasion ability of pancreatic cancer cells were detected after silencing H19 using wound healing assays and Transwell matrigel invasion assays.Subcutaneous tumor was used to detect the size and volume of the tumor after inject the tumor cells.Immunohistochemistry was used to detect the expression of Ki67 and PCNA.Results: Compared with non-carcinoma adjacent tissues of pancreatic carcinoma,the expression of H19 of tissues of pancreatic carcinoma was significantly increased.The expression of H19 in pancreatic cancer cell A549 was highest.Silencing H19 could inhibit the migration of human pancreatic cancer A549 cells.miR-107 was the direct target of H19.Compared with non-carcinoma adjacent tissues of pancreatic carcinoma,the expression of H19 of tissues of pancreatic carcinoma was significantly decreased.After silencing H19,inhibiting the expression of miR107 could inhibit the migration of human pancreatic cancer A549 cells.Compared with the group of H19-siRNA,H19-siRNA+miR-107-inhibitor group mice tumor volume and weight were significantly bigger.Immunohistochemistry showed that compared with H19-siRNA group,the expression Ki67 and PCNA expression in H19-siRNA+miR-107-inhibitor group increased.Conclusion: H19 plays the role of tumor promotor factor in pancreatic cancer.H19 can affect the invasion and migration ability of pancreatic carcinoma cells by regulating miR-107.