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Pulpitis and periapical inflammation are two common diseases in stomatology today. Existing treatment options primarily include root canal therapy and pulp revascularization, which can effectively control inflammation and preserve the affected tooth while also causing permanent deactivation of the pulp tissue, structural failure, and secondary infection. In recent years, research on dental pulp regeneration has progressively entered the public consciousness because of tissue engineering technology that combines stem cells and biomaterials. Due to their multi⁃differentiation and high proliferation, dental pulp stem cells (DPSCs) isolated from permanent or deciduous teeth have emerged as a significant stem cell source for dentin or pulp tissue regeneration. However, the number and survival time of live cells in the dam⁃ aged area are impacted, which significantly limits the efficacy of stem cells since they are unable to efficiently be recruited to the injured area. The ability of DPSCs to migrate and multiply must therefore be enhanced. This study sought to determine if miR⁃31 (miR⁃31) may significantly enhance the proliferative and migratory capacities of DPSCs. The tissue block enzyme digestion method was used to successfully separate and culture DPSCs from dental pulp tissues, and the miR⁃31 levels in dental pulp tissues and DPSCs from normal and inflammatory teeth were compared. The results of real⁃time fluorescence quanti⁃ tative PCR (RT⁃qPCR) revealed that the expression level of miR⁃31 in dental pulp tissues and DPSCs from inflammatory teeth was significantly lower when compared to the control group (P<0. 05). Interfer⁃ ence and over⁃expression of miR⁃31 expressions in DPSCs were specifically divided into three groups: the NC group, the miR⁃31 agomir (over⁃expressed) group and the miR⁃31 antagomir (inhibitor) group. RTq⁃PCR results showed that the transfection was successful (P<0. 001). The results of CCK⁃8, wound⁃ healing, and Transwell migration experiments showed that overexpression of miR⁃31 successfully improved the proliferation and migration abilities of DPSCs compared with the control group (P<0. 05). Further⁃ more, Western blotting analysis revealed that miR⁃31 overexpression increased the expression of important migratory proteins, including CXC chemokine receptor type 4 (CXCR4) and matrix metalloproteinase2 (MMP2), as well as key proliferation proteins Ki67 and proliferating cell nuclear antigen (PCNA) (P< 0. 05). This study demonstrates that miR⁃31 can effectively boost the proliferation and migratory ability of DPSCs, providing strong theoretical support for the increased use of DPSCs in regenerative medicine.
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Objective:To investigate the immunoregulatory effects of lentivirus-mediated microRNA (miR)-31-5p overexpression on peripheral blood T helper cell 17 (Th17) in a rabbit model of autoimmune dry eye.Methods:The miR-31-5p recombinant lentiviral vector was constructed.Lentivirus overexpressing miR-31-5p and its control virus were packaged.The concentration measurement and lentiviral titer determination were carried out.A rabbit model of autoimmune dry eye was established and the peripheral blood mononuclear cells (PBMC) of the rabbits were isolated.PBMC infected with miR-31-5p and negative control lentivirus particles were assigned as the miR-31-5p overexpression group and control group, respectively.The miR-31-5p expression level was detected using quantitative real-time PCR (qRT-PCR). Then PBMC in the two groups were co-cultured with γ-ray irradiated lacrimal gland epithelial cells.The expressions of Th17 cell related transcription factor retinoic acid-receptor-related orphan receptor C (RORC) and interleukin-17 (IL-17) mRNA, IL-1β, IL-6 and IL-23 were determined by qRT-PCR.The IL-17 protein expression level was detected by Western blot.The use and care of animals complied with Regulation for the Administration of Affair Concerning Experiment Animals by State Science and Technology Commission.The study protocol was approved by the Ethics Committee of Tianjin Medical University Eye Hospital (No.TJYY20201221036).Results:The construction of the miR-31-5p recombinant lentiviral vector was verified by DNA sequencing.The lentiviral titer of lentivirus overexpressing miR-31-5p and control lentivirus particles was 3.82×10 7 TU/ml and 3.50×10 7 TU/ml, respectively.The miR-31-5p relative expression level of PBMC was significantly increased in miR-31-5p overexpression group in comparison with control group, showing a statistically significant difference ( t=-9.696, P<0.001). When PBMC were co-cultured with lacrimal gland epithelial cells in vitro, the relative expression levels of RORC and IL-17 mRNA in miR-31-5p overexpression group were 0.33±0.03 and 0.28±0.09, which were significantly decreased in comparison with 1.00±0.00 and 1.00±0.00 in control group, with statistically significant differences between them ( t=46.256, 13.810; both at P<0.05). The relative expression level of IL-17 protein in miR-31-5p overexpression group was significantly reduced than control group ( t=4.977, P=0.008). The relative expression levels of IL-1β, IL-6 and IL-23 mRNA were significantly lower in miR-31-5p overexpression group than control group ( t=220.076, 6.641, 13.271; all at P<0.05). Conclusions:The overexpression of miR-31-5p can inhibit the Th17-immune response via down-regulating the expression of IL-6, IL-1β and IL-23.
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Type 2 diabetes mellitus (T2DM) is a metabolic disease with an increasing incidence worldwide, which leads to damage to various tissues and organs including the liver. MiR-31 is conserved across species and closely associated with metabolic diseases, but its role in type 2 diabetic liver injury has not been elucidated. This study aimed to investigate the effect of miR-31 on liver injury in type 2 diabetes and its underlying mechanism. Four to six weeks old male FVB mice and miR-31-positive transgenic mice were randomly divided into FVB mice control group (C), FVB mice induced diabetes group (DM) and miR-31-overexpression transgenic mice induced diabetes group (31DM). After 1 week of adaptive feeding, the T2DM mouse model was induced by high-fat feeding combined with intraperitoneal injection of streptozotocin (STZ) for 6 weeks. The general condition of mice and related metabolic indicators showed that the increased food and water intake, weight loss and glucose and lipid metabolism disorders could be reversed by miR-31 in T2DM mice. HE staining and liver histological activity index (HAI) scoring results showed that miR-31 improved the inflammatory status in the liver tissue of T2DM mice and decreased the HAI score. RT-qPCR results showed that the high expression of miR-31 was accompanied by a decrease in the expression of activating transcription factor 6 (ATF6) mRNA in the liver of T2DM mice. Furthermore, Western blotting results showed that miR-31 inhibited the expression of endoplasmic reticulum stress-related proteins such as ATF6, glucoregulatory protein 78 (GRP78) and C/EBP homologous protein (CHOP) in the liver of T2DM mice. In conclusion, miR-31 may ameliorate liver injury in T2DM mice by regulating glucose and lipid metabolism disorders and insulin resistance, and inhibiting endoplasmic reticulum stress factors such as ATF6, GRP78, and CHOP.
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To investigate the effects of miR-31 on TLR4/NF-κB signaling pathway and apoptosis-related proteins in dextran sulfate sodium (DSS) induced mouse colon colitis. Methods: ① Mouse model of colon colitis: 1% DSS was used to induce mouse ulcerative colitis (UC). Fourteen FVB non-transgenic mice were randomly divided into control group (n= 6), DSS group (n= 8), and 16 FVB miR-31 transgenic mice were randomly divided into miR-31 overexpression group (n= 8), miR-31 overexpression +DSS group (n= 8). DSS was dissolved in water and administered to mice by drinking water. The DSS group and miR-31+DSS group drank 1% DSS water in the first week, normal sterilized water in the second week, and 1% DSS water in the third week, after 5 weeks, the modeling was completed, then the colon tissues of the mice were collected. Western blot and IHC were used to detect the expressions of NF-κB p65, TLR4, Bax and Bcl-2 proteins in mouse colon tissue, TUNEL was used to detect apoptosis of mouse colon tissues. ② Cell culture experiments: Transfection of miR-31mimic and inhibitor by lipofectamine resulted in overexpression or knockdown of miR-31 in human colon epithelial cell line HCT 116 cells, each group was repeated three times and cells were collected 48 h later, Western blot was used to detect the expressions of NF-κB p65 and TLR4 protein. ① In animal experiments, compared with the control group, the expression levels of NF-κB p65, TLR4 protein and apoptotic cell index in the DSS group and miR-31 overexpression group in mouse colon tissue were significantly increased (P＜0.05 or P＜0.01), and the Bcl-2 / Bax ratio was significantly reduced (P＜0.05 or P＜0.01); and compared with the DSS group, the expression levels of NF-κB p65, TLR4 protein and apoptotic cell index in the miR-31+DSS group were significantly increased (P＜0.01), while the Bcl-2/Bax ratio was significantly decreased (P＜0.01). ② In cell experiments, compared with the control group, the expression levels of NF-κB p65 and TLR4 protein in the over-expressed miR-31 group of HCT 116 cells were significantly increased (P＜0.05 or P＜0.01), the expressions of NF-κB p65 and TLR4 protein in miR-31 knockdown group were decreased (P＜0.05). miR-31 promotes the development of colitis by promoting TLR4/NF-κB signaling pathway and mediating apoptosis of intestinal epithelial cells.
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Objective: To detect the effect of over expressed human MIR31HG gene on the proliferation and m grat on of PC9 ce Is, and to clarify the mechan sm of oncogene MIR31 HG Methods: The ful length sequence of ong non coding RNA (LncRNA) MIR31HG was amp fed by RT PGR and cloned nto the pcDNA3 1 ( ) eukaryot c expression vector. The PG9 cells were transfected w th the pcDNA3 1 MIR31HG overexpress on vector and control vector pcDNA3 1. The construction of MIR31HG overexpress on vector was detected by enzymatic digest on identification. The stab e cell 1 nes w th overexpress on of MIR31HG (PC9 pcDNA3 1 MIR31HG∗ stab e transfection group) and control ce 1 1 nes (PC9 pcDNA3 1, empty vector group) were established by G418 drug screen ng. and the express on evel of MIR31 HG gene n stably transfected cell ine was detected by RT PGR CCK 8 method and scratch heal ng assay were used to detect the proliferation act vities and m gration ab 1 ties of PC9 eel s. Results: The agarose gel e ectrophoresis resu ts showed that the spec f c gene fragment of MIR31HG was obta ned by amplif cation successfu ly. The gene fragments of target gene and vector were produced by double enzyme digest on of MIR31HG eukaryotic expression vector. The RT PGR resu ts showed that the MIR31HG RNA expression leve in the cells n stable transfect on group was sign ficantly h gher than that in empty vector group (P< 0 05). The results of CGK 8 test showed that the pro iferat on act vities of the eels in stable transfection group were s gnif cant y higher than those in empty vector group at 24, 36 and 48 h after culture ( P<0 01). The results of scratch healing assay showed that the scratch heal ng rate of ce Is n stable transfect on group was sign ficantly h gher than that in empty vector group at 48 h after culture ( P<0 05). Conclusion: The eukaryotic overexpression vector and the PG9 eel line stably transfected w th human LncRNA MIR31 HG gene are constructed successfully, and M1R31 HG overexpression can promote the pro iferat on and m grat on of ung cancer PG9 cells.
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To explore the role of miR-31-5p/STAT3 in the pathogenesis of colitis-assosiated cancer (CAC) and the intervention mechanism of Huangqi Baizhu decoction. Methods The CAC model of C57BL/6 mice was established by AOM/DSS method. The differential expression of MicroRNA in control and CAC mice was detected. qPCR was used to screen differential MicroRNAs; Western blot was used to detect the expression levels of STAT3 , p-STAT3 and IL-6Ra. Results AOM was injected into abdominal cavity once, combined with 3% DSS free drinking for three cycles to establish model. After eight weeks, moderate and/or severe dysplasia of colonic mucosa appeared in model mice. After detection, the expression of miR-31-5p and STAT3 and p-STAT3 proteins significantly increased. After intervention with Huangqi Baizhu decoction, the expressions of miR-31-5p and STAT3 and p-STAT3 proteins were down-regulated. In vitro, miR-31-5p over-expression in RAW264. 7 by transfect method, and the expression of STAT3 protein increased significantly compared with that of control. On the other hand, stimulated by IL-6 or TNF-a for 24 h, miR-31-5p levels were up-regulated significantly, suggesting that inflammatory factors could cause a positive correlation between miR-31-5p/STAT3. At the same time, ATRII + AST (atractylodesin II + astragaloside) mixture significantly down-regulated miR-31-5p, STAT3, IL-6Ra increase induced by IL-6 stimulation. Conclusions miR-31-5p/STAT3 forms a positive feedback loop, which plays an important role in the pathogenesis of CAC. miR-31-5p/STAT3 may continue to amplify the inflammation effect and eventually lead to the dysplasia of colonic epithelium and even tumorigenesis.
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Atorvastatin is proven to ameliorate cardiac hypertrophy induced by chronic intermittent hypoxia (CIH).However,little is known about the mechanism by which atorvastatin modulates CIH-induced cardiac hypertrophy,and whether specific hypertrophyrelated microRNAs are involved in the modulation.MiR-31 plays key roles in the development of cardiac hypertrophy induced by ischemia/hypoxia.This study examined whether miR-31 was involved in the protective role of atorvastatin against CIH-induced myocardial hypertrophy.H9c2 cells were subjected to 8-h intermittent hypoxia per day in the presence or absence of atorvastatin for 5 days.The size of cardiomyocytes,and the expression of caspase 3 and miR-31 were determined by Western blotting and RT-PCR,respectively.MiR-31 mimic or Ro 31-8220,a specific inhibitor of protein kinase C epsilon (PKCε),was used to determine the role of miR-31 in the anti-hypertrophic effect of atorvastatin on cardiomyocytes.PKCε in the cardiomyocytes with miR-31 upregulation or downregulation was detected using RT-PCR and Western blotting.The results showed that CIH induced obvious enlargement of cardiomyocytes,which was paralleled with increased atrial natriuretic peptide (ANP),brain natriuretic peptide (BNP),and slow/beta cardiac myosin heavy-chain (MYH7) mRNA levels.All these changes were reversed by the treatment with atorvastatin.Meanwhile,miR-31 was increased by CIH in vitro.Of note,the atorvastatin pretreatment significantly increased the mRNA and protein expression of PKCε and decreased that of miR-31.Moreover,overexpression of miR-31 abolished the anti-hypertrophic effect of atorvastatin on cardiomyocytes.Upregulation and downregulation of miR-31 respectively decreased and increased the mRNA and protein expression of PKCε.These results suggest that atorvastatin provides the cardioprotective effects against CIH probably via up-regulating PKCε and down-regulating miR-31.
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Atorvastatin is proven to ameliorate cardiac hypertrophy induced by chronic intermittent hypoxia (CIH).However,little is known about the mechanism by which atorvastatin modulates CIH-induced cardiac hypertrophy,and whether specific hypertrophyrelated microRNAs are involved in the modulation.MiR-31 plays key roles in the development of cardiac hypertrophy induced by ischemia/hypoxia.This study examined whether miR-31 was involved in the protective role of atorvastatin against CIH-induced myocardial hypertrophy.H9c2 cells were subjected to 8-h intermittent hypoxia per day in the presence or absence of atorvastatin for 5 days.The size of cardiomyocytes,and the expression of caspase 3 and miR-31 were determined by Western blotting and RT-PCR,respectively.MiR-31 mimic or Ro 31-8220,a specific inhibitor of protein kinase C epsilon (PKCε),was used to determine the role of miR-31 in the anti-hypertrophic effect of atorvastatin on cardiomyocytes.PKCε in the cardiomyocytes with miR-31 upregulation or downregulation was detected using RT-PCR and Western blotting.The results showed that CIH induced obvious enlargement of cardiomyocytes,which was paralleled with increased atrial natriuretic peptide (ANP),brain natriuretic peptide (BNP),and slow/beta cardiac myosin heavy-chain (MYH7) mRNA levels.All these changes were reversed by the treatment with atorvastatin.Meanwhile,miR-31 was increased by CIH in vitro.Of note,the atorvastatin pretreatment significantly increased the mRNA and protein expression of PKCε and decreased that of miR-31.Moreover,overexpression of miR-31 abolished the anti-hypertrophic effect of atorvastatin on cardiomyocytes.Upregulation and downregulation of miR-31 respectively decreased and increased the mRNA and protein expression of PKCε.These results suggest that atorvastatin provides the cardioprotective effects against CIH probably via up-regulating PKCε and down-regulating miR-31.
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@#Objective: To investigate the mechanism of miR-31-5p/tension protein 1 gene (TNS1) axis modulating radiotherapy resistance in breast cancer. Methods: The breast cancer tissues and corresponding para-cancerous tissues of 21 patients with breast cancer, who underwent surgical resection at Department of Cancer Radiotherapy of Nanyang Central Hospital from July 2017 to December 2017, were collected for this study; breast cancer cell lines (MCF-7，MDA-MB-23 and SKBR-3) were also collected; qPCR was applied to detect the expression level of miR-31-5p in breast cancer tissues and cell lines. The radiation resistant cell line MCF-7R was constructed by using 6 MV-X ray radiotherapy treatment. Subsequently, the influence of over-expression/kockdown of miR-31-5p on radiation sensitivity of MCF-7 and MCF-7R cells were detected by colony formation assay, Transwell assay and Annexin V-FITC/PI double staining flow cytometry assay, respectively. Moreover, luciferase reporter assay was used to verify whether TNS1 was a target gene of miR-31-5p. Results: Compared with para-cancerous tissues, normal mammary epithelial MCF-10A cells and MCF-7 cells, miR-31-5p was low-expressed in breast cancer, cell lines and MCF-7R (all P<0.01). Over-expression of miR-31-5p resulted in inhibited invasion and promoted apoptosis of MCF-7R cells (P<0.01), whereas miR-31-5p knockdown got opposite results in MCF-7 cells. Moreover, luciferase reporter assay confirmed that TNS1 was a target gene of miR-31-5p. Over-expression of miR-31-5p inhibited invasion and increased radio-sensitivity, apoptosis of MCF-7R cell via targeting TNS1 (P<0.01), whereas knockdown of miR-31-5p significantly promoted the invasion but reduced apoptosis of MCF-7R cells (all P<0.01), and further up-regulated the radio-sensitivity of MCF-7R cells. Conclusion: miR-31-5p/TNS1 axis regulates the radiotherapy resistance of breast cancer, and over-expression of miR-31-5p may reverse the resistance of MCF-7R to radiotherapy.
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Objective To establish a stably overexpressing miR-31 transgenic mouse and detect the expression of miR-31 in the organs and tissues,and to provide qualified tool mice with overexpression of miR-31 in vivo. Methods The miR-31 overexpression vector was constructed by Gateway cloning technology. The vector was injected into fertilized ovum by DNA microinjection technology,then transferred to the pseudopregnant mice and waited for eutocia. Newborn mouse tail DNA was extracted and PCR and agarose gel electrophoresis were performed to identify the positive miR-31 transgenic mice. microRNA was extracted from the organs and tissues of miR-31 transgenic mice and the expression of miR-31 was de-tected by RT-PCR. The expression of Nestin and number of neural stem cells in the nervous system were compared in the positive and WT mice. Results The miR-31 transgenic mice were constructed successfully and bred more than 14 genera-tions in barrier environment. Expression of miR-31 was increased in major organs and tissues. The expression of Nestin and the number of neural stem cells in the positive mice were higher than those in the wild type mice. Conclusions MiR-31 overexpressing transgenic mice are constructed by Gateway cloning technology and the expression of miR-31 is stable in sub-sequent generations. The number of neural stem cells in the nervous system is higher than that in wild-type mice. The miR-31 overexpressing transgenic mice can be a good tool for experimental research of the function of overexpressed miR-31 in vivo and the treatment of nervous system diseases.
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BACKGROUND: Psoriasis is a complex, chronic inflammatory skin disease with substantial negative effects on patient quality of life. Long non-coding RNAs (lncRNAs) are able to be involved in multitudes of cellular processes in diverse human diseases. This study aimed to investigate the potential involvement of lncRNA MIR31HG in HaCaT keratinocytes proliferation. RESULTS: The study showed that MIR31HG was significantly elevated in the lesional psoriatic skin compared with normal individuals' skin. Knockdown of MIR31HG inhibited HaCaT keratinocytes proliferation. Flow cytometry analysis showed that siRNA-mediated MIR31HG depletion induced cell cycle arrest in the G2/M phase. In addition, MIR31HG expression was found to be dependent on NF-κB activation. CONCLUSIONS: NF-κB activation mediated MIR31HG upregulation plays an important role in the regulation of HaCaT keratinocytes proliferation. It could be a potential diagnostic biomarker and therapeutic target for psoriasis.
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Humanos , Psoriasis/metabolismo , Queratinocitos/metabolismo , ARN Largo no Codificante/fisiología , Psoriasis/genética , Psoriasis/patología , Biomarcadores , Transducción de Señal , Estudios de Casos y Controles , Queratinocitos/patología , Regulación hacia Arriba , Regulación de la Expresión Génica , Proliferación CelularRESUMEN
Purpose To investigate the correlation of Dock180 and miR-31 expression in breast cancer cells,and to observe the effect of miR-31 on the invasion of breast cancer cells by Dock180.Methods MiR-31 was transfected into breast cancer cells by liposome transfection technique.The actual binding site of miR-31 to the 3'-untranslated region of Dock180 was confirmed through luciferase assay.Western blot was performed to detect the expression of Dockl80 and other related proteins.Real-time PCR was used to measure the expression of Dock180.Matrigel invasion were performed to detect the invasion of breast cancer cell lines with miR-31 increased.Resuits The protein levels of Dock180 in breast cancer cell lines negatively correlated with miR-31 expression,and Dock180 was directly targeted by miR-31.Dock180 downregulation and miR-31 overexpression reduced breast cancer cells invasion.Conclusion Dock180 modulated by miR-31 plays an important function in breast cancer cell lines invasion.
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Objective To study the expression and roles of miR-31-5p in acute myeloid leukemia (AML).Methods miR-31-5p in AML patients were evaluated by real-time PCR;THP-1 cells were transfected with the miR-31-5p mimic and control, respectively.The effects of over-expression of miR-31-5p were examined by CCK-8 and FACS analysis;Dual-luciferase and Western blot were performed to detect target gene HuR expression.The effects of knock-down of HUR were also examined by CCK-8 and FACS analysis.Results miR-31-5p was down-regulated in AML patients compared to the normal control.Over-expression of miR-31-5p in THP-1 cells reduces cell proliferation and accelerates monocytic differentiation.miR-31-5p could target HuR, and knock-down of HuR inhibits cell proliferation and attenuates monocytic differentiation in THP-1 cells.Conclusions miR-31-5p may regulate AML cell proliferation and monocytic differentiation by targeting HuR.
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Background and purpose:miRNA plays important roles in tumorigenesis. It has been reported that many kinds of serum miRNA serve as markers for tumor diagnosis and screening. This study aimed to detect the expression of serum miRNA-31 (miR-31) in colorectal cancer patients and to explore the effect of miR-31 on cell proliferation, apoptosis and cell cycle distribution. Methods: The expressions of miR-31 in 40 cases of colorectal cancer serum and 35 cases of the healthy control were examined by real-time lfuorescent quantitative polymerase chain reaction (RTFQ-PCR). The correlation between miR-31 expression and clinicopathological features of colorectal cancer (including age, gender, depth of inifltration, lymph node metastasis, clinical stage) were further analyzed. The miR-31 mimics, inhibitor and miR-control (negative control) were transfected into HCT116 cells. The effect of miR-31 on cell proliferation was evaluated by CCK-8 method. Flow cytometry was used to examine the change of cell apoptosis and cell cycle. Results:Relative expression of serum miR-31 was signiifcantly increased in cancer patients compared with healthy controls (P<0.01). Expression of serum miR-31 was higher in poorly differentiated carcinoma than that in well or moderately differentiated carcinoma (P<0.05). No correlation was found between serum miR-31 expression and other clinicopathological variables. CCK-8 assay showed that after transfection with miR-31 mimics, the cell proliferation was increased, compared with miR-31 inhibitor and negative control group. Meantime, the apoptotic cell number was signiifcantly decreased, particularly in late apoptosis. The cell number of G1 stage was remarkably increased in miR-31 inhibitor group, compared with miR-31mimics and negative control group. Conclusion:The expression of serum miR-31 is higher in colorectal cancer. miR-31 can promote cell proliferation and inhibit the apoptosis of HCT116 cells. It might be a potential biomarker for colorectal cancer.
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Objective To analyze the correlation between miR-31 and ESCC in expression of miR-31 in the plasma of ESCC in Xinjiang Kazak and Han nationality patients. Methods The plasma samples were collected respectively from patients with ESCC in 20 cases and healthy subjects in 20 cases. The relatively expression of miR-31 was detected by real-time Q-PCR. Results The expression of miR-31 with ESCC were higher than those of the normal control group, which related to the degree of tumor differentiation in Kazak ESCC patients (P < 0.01); the levels of miR-31 relative expression in Kazak were higher than that of Han (P = 0.008, P = 0.027). Conclusion miR-31 may be involved in the occurrence of ESCC in Han and Kazak nationality. miR-31 might be another risk factor in high incidence of ESCC in Kazak than Han nationality.
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Objective To synthetically evaluate the relationship between miR-31 and the prognosis of carcinoma and to investi-gate its related mechanism.Methods The correlative literatures of tumor prognosis were retrieved from the electronic databases PubMed,EMBASE and ISI Web of Science.The pooled hazard ratios (HRs)and 95% confidence interval(95%CI )were extracted. The prognostic data were performed the synthesis analysis.Results A total of 7 trials conformed to the inclusion criteria including accumulated 2 012 cases of carcinoma.Meta-analysis revealed that the decrease of miR-31 expression in the tumor patients had the poor prognosis (HR=0.784,95%CI :0.630-0.974);in the subgroup analysis,the synthesis results adopting the multivariable a-nalysis and China subjects were 3.512 (95%CI :1.797-6.865)and 1.574 (95%CI :1.062-2.333),which indicating that the in-crease of miR-31 expression predicted the poor prognosis;miR-31 had no statistical significance in the digestive system (P >0.05). Conclusion The prognostic role of miR-31 may possess the histological and regional specificity and has the potential as a novel marker.
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Background and purpose:It was reported that many microRNAs (miRNAs) have close relation with carcinomas. miR-31 (microRNA-31) shows abnormal change in numerous cancers. China is one of the most high-risk areas of esophageal squamous cell carcinoma (ESCC). The aim of the present study was to investigate the expression of miR-31 in ESCC, and analyze the relationship of its expression with clinicopathological features and prognosis. Methods:The expression of miR-31 in KYSE410, EC1 and EC9706 cell lines, as well as 81 cases of ESCC tissues and adjacent normal esophageal tissues were detected by real-time reverse transcription-polymerase chain reaction (RT-PCR). The result was combined with clinical and follow-up data and statistical analysis was conducted. Results: MiR-31 was up-expression in 3 cell lines and 75.31% of the ESCC tissues. miR-31 up-expression was positively related to severer lymph node metastasis (P=0.043), deeper invasion of tumors (P=0.002) and advanced pathological stage (P=0.027). There was no relationship of miR-31 with other clinicopathological features (P>0.05). Furthermore, high expression of miR-31 was associated with poor progression-free survival (PFS) in 81 ESCC patients by Kaplan-Meier analysis (P=0.014) and by multivariate Cox analysis (P=0.021). Conclusion:Our results identiifed miR-31 may be a new diagnostic criteria and prognostic biomarker for ESCC.