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BACKGROUND: Non-coding RNA is widely distributed in the nervous system in vivo and a significant change in the expression of non-coding RNA has been observed in a neural injury model. This suggests that non-coding RNA may serve as a potential target for resolving the challenges of peripheral nerve repair. OBJECTIVE: To summarize the mechanisms of microRNA, circular RNA and long non-coding RNA in the process of repair after peripheral nerve injury with the attempt to determine the possible treatment of peripheral nerve injury. METHODS: The first author retrieved the relevant literatures in CNKI and PubMed databases published from January 2001 to April 2019. The key words were “non-coding RNA, miRNA, circRNA, IncRNA, peripheral nerve injury” in Chinese and English, respectively. Forty-three literatures were included in accordance with the exclusion and inclusion criteria. RESULTS AND CONCLUSION: (1) MicroRNAs can act on certain signal pathways, regulate the apoptosis, growth, proliferation and differentiation of Schwann cells and participate in the repair of peripheral nerve injury. (2) Circular RNAs act as microRNA sponges to competitively inhibit the transcription in microRNA, and exert corresponding biological functions. (3) A large amount of long non-coding RNAs are expressed after peripheral nerve injury, and play a key role in the peripheral nerve regeneration.
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BACKGROUND: Long non-coding RNA small molecule RNA host gene 1 (SNHG1) was previously identified to be relevant with Parkinson's disease (PD) pathogenesis. This work aims to further elucidate the regulatory networks of SNHG1 involved in PD. Methods: 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-hydrochloride (MPTP)-induced mice and 1-methyl-4-phenylpyridinium (MPP+)-treated SH-SY5Y cells were respectively constructed as the in vivo and in vitro PD models. Expression levels of SNHG1 and miR-153-3p were detected by qRT-PCR. Protein expression levels of phosphate and tension homology deleted on chromosome ten (PTEN) were measured by western blotting assay. Cell viability and apoptosis were determined by MTT and flow cytometry assays. The interactions among SNHG1, miR-153-3p and PTEN were identified by luciferase reporter assay, RNA immunoprecipitation, and/or RNA pull-down analysis. RESULTS: Increased SNHG1 expression was found in midbrain of MPTP-induced PD mice and MPP+-treated SH-SY5Y cells. Overexpression of SNHG1 lowered viability and enhanced apoptosis in MPP+-treated SH-SY5Y cells. Moreover, SNHG1 acted as a molecular sponge to inhibit the expression of miR-153-3p. Furthermore, miR-153-3p-mediated suppression of MPP+-induced cytotoxicity was abated following SNHG1 up-regulation. Additionally, PTEN was identified as a direct target of miR-153-3p, and SNHG1 could serve as a competing endogenous RNA (ceRNA) of miR-153-3p to improve the expression of PTEN. Besides, enforced expression of PTEN displayed the similar functions as SNHG1 overexpression in regulating the viability and apoptosis of MPP+-treated SH-SY5Y cells. Finally, SNHG1 was found to activate PTEN/AKT/mTOR signaling pathway in SH-SY5Y cells by targeting miR-153-3p. CONCLUSION: SNHG1 aggravates MPP+-induced cellular toxicity in SH-SY5Y cells by regulating PTEN/AKT/mTOR signaling via sponging miR-153-3p, indicating the potential of SNHG1 as a promising therapeutic target for PD.
Subject(s)
Animals , Male , Mice , Parkinson Disease/metabolism , 1-Methyl-4-phenylpyridinium/toxicity , PTEN Phosphohydrolase/metabolism , Proto-Oncogene Proteins c-akt/metabolism , TOR Serine-Threonine Kinases/metabolism , RNA, Long Noncoding/metabolism , Parkinson Disease/genetics , Transfection , Signal Transduction , Cells, Cultured , Gene Expression Regulation , Blotting, Western , Apoptosis , MicroRNAs , Disease Models, Animal , Real-Time Polymerase Chain Reaction , RNA, Long Noncoding/genetics , Mice, Inbred C57BLABSTRACT
Objective@#To investigate the regulatory mechanism of long non-coding RNA (lncRNA) 53106 in the apoptosis model of MIN6 cells stimulated by cytokines.@*Methods@#The stimulation model of cytokines 10 ng/ml interleukin-1β, 50 ng/ml tumor necrosis factor-α, 50 ng/ml interferon-γ in MIN6 islet cell lines were established. The apoptosis rate was measured by flow cytometry and the expression levels of lncRNA53106 and (C-X-C motif) ligand (CXCL)10 were detected by realtime quantitative PCR (qPCR). LncRNA53106 smart silencer and CXCL10 siRNA were constructed, and lncRNA53106 and CXCL10 were knocked down respectively. Then inflammatory cytokines were combined to stimulate, and their roles in the apoptosis of min6 cells were detected by flow cytometry, qPCR, and Western blotting.@*Results@#In the apoptosis model of MIN6 cells stimulated by cytokines, the apoptosis rate of cytokines group was significantly increased and reached statistical significance. The apoptosis rate of the knocked down lncRNA53106 group was significantly lower than that of the control group (P<0.05). The expression of CXCL10 was also decreased in the knockdown group by qPCR and Western blotting, the expressions of the apoptosis-related factors Bax and Caspase3 mRNA were decreased. The apoptosis rate in the knocked down CXCL10 group was significantly lower than that in the control group (P<0.05), and the expression of lncRNA53106 was slightly increased, but the difference was not significant (P=0.61).@*Conclusion@#LncRNA53106 may promote the expression of apoptosis factor by upregulation of CXCL10, and promote the apoptosis of β cells of the pancreas, which may lead to the occurrence of type 1 diabetes.
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Aim To investigate the protective effect of resveratrol( Rev) on atherosclerosis( AS) , and clarify the rolcof Rev in regulating IncRNA MALATi (MALAT1) and the role of MALATI in AS. Methods ApoE'/ mice were randomly divided into two groups-, the high-fat diet(HFD) group, the HFD plus Rev treatment group, and the atherosclerosis model was established for 16 weeks. Hematoxylin-eosin( HE) staining was used to detect the area of aortic plaques in mice. And electron microscopy was performed to measure the formation of foam cells. The effects of Rev on MALATI, inflammatory cytokine ( 1L-6, 1L-1(3 and TNF-a) were examined using real time PCR. In addition, the roles of MALATI on inflammatory cytokine, and the influence of free cholesterol (FC) on the ex pression of MALATI were measured by real time PCR. Results The Rev treatment group significantly reduced arterial plaque areas and foam cell formation. In normal peritoneal macrophages, Rev could increase the expression of MALATI, and FC could down-regulate MALATI. Furthermore, Rev could decrease the expression of IL-6, 11,-1(3 and TNF-a in a dose-dependent manner. Knockdown of MALATI promoted the mRNA expression of IL-6 and TNF-a. Conclusions Rev may modulate the expression of inflammatory cytokine IL-6, lL-lp and TNF-a by affecting the level of MALAT, thereby exerting the anti-atherogenic effects.
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Objective To investigate the regulatory mechanism of long non-coding RNA ( lncRNA) 53106 in the apoptosis model of MIN6 cells stimulated by cytokines. Methods The stimulation model of cytokines 10 ng/ml interleukin-1β, 50 ng/ml tumor necrosis factor-α, 50 ng/ml interferon-γin MIN6 islet cell lines were established. The apoptosis rate was measured by flow cytometry and the expression levels of lncRNA53106 and ( C-X-C motif) ligand (CXCL)10 were detected by realtime quantitative PCR (qPCR). LncRNA53106 smart silencer and CXCL10 siRNA were constructed, and lncRNA53106 and CXCL10 were knocked down respectively. Then inflammatory cytokines were combined to stimulate, and their roles in the apoptosis of min6 cells were detected by flow cytometry, qPCR, and Western blotting. Results In the apoptosis model of MIN6 cells stimulated by cytokines, the apoptosis rate of cytokines group was significantly increased and reached statistical significance. The apoptosis rate of the knocked down lncRNA53106 group was significantly lower than that of the control group ( P<0.05) . The expression of CXCL10 was also decreased in the knockdown group by qPCR and Western blotting, the expressions of the apoptosis-related factors Bax and Caspase3 mRNA were decreased. The apoptosis rate in the knocked down CXCL10 group was significantly lower than that in the control group (P<0.05), and the expression of lncRNA53106 was slightly increased, but the difference was not significant ( P=0.61) . Conclusion LncRNA53106 may promote the expression of apoptosis factor by upregulation of CXCL10, and promote the apoptosis ofβcells of the pancreas, which may lead to the occurrence of type 1 diabetes.
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Colon cancer associated transcript 1 (CCAT1) is a kind of long non-coding RNA (IncRNA) found re-cently, which is aberrant overexpression in colorectal cancer, and it can promote cancer cell proliferation, invasion and metastasis. CCAT1 involves in the regulation of multiple pathophysiological processes, especially the formation and progression of gastrointestinal cancer, through the interaction with microRNA (miRNA) or protein by regulation mechanism like endogenous competition, and it is expected to serve as a valuable biomarker and therapeutic target.
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Objective To explore the effect and mechanism of IncRNA EVADR on the proliferation and migration in human colorectal cancer cell lines HCT116 and LOVO. Methods HCT116 and LOVO cell lines were transfected with IncRNA EVADR by overexpressing lentivirus system. CCK8 assay was performed to measure the growth of HCT116 and LOVO cells after overexpression of EVADR. Transwell migration was performed to determine if EVADR promote HCT116 and LOVO cells migration. Finally, the expression of Ecadherin and transcription factor Snail, Slug, ZEB1 and ZEB2 were detected by Western blot and realtime quantitative PCR respectively. Results We successfully established colorectal cancer cells strains HCT116, LOVO which can stably overexpress IncRNA EVADR and the capacity of proliferation and migration in overexpression group was significantly improved (P＜0.05). The expression of Ecadherin was decreased while mesenchymal markers Snail, Slug, ZEB1 and ZEB2 were increased in EVADR overexpression HCT116 and LOVO cells. Conclusions Overexpression of IncRNA EVADR in HCT116 and LOVO cells can significantly promote the proliferation and migration of HCT116 and LOVO cells which may play an important role in regulating epithelial-mesenchymal transition in colorectal cancer cells.
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Objective To investigate the mechanism of lnc-AC079612.1-1∶1 in the metastasis of colorectal cancer by regulating miR-1915 expression and provide a theoretical basis for new therapeutic targets of colon cancer.Methods Continuously harvested 3 pairs of primary tumor and hepatic metastases of patients with synchronous colon cancer with liver metastasis.LncRNA + mRNA Human Gene Expression Microarray V4.0 and 4 × 180K Expression Microarray were used to detect the Expression profile of LncRNA in primary colon cancer and matched liver metastases.The detection of expression profile chip was used to find some lncRNAs that may be closely associated with colon cancer liver metastasis,and through the literature retrieval,the author preliminarily analyzed the co-expression encoding genes of lncRNAs,in order to find lncRNAs that may play key roles in the process of colon cancer liver metastasis.The effect of lnc-AC079612.1.1-1∶1 on the proliferation capacity of colon cancer cell lines was detected in SW480 cell lines and SW620 cell lines of colon cancer through CCK-8 experiment.Effects of lnc-AC079612.1.1-1∶1 on the migration and invasion of colon cancer cells were examined by Transwell cell invasion assay.Through TargetScan,Miranda,LNCipedia and other web tools,miRNAs that may bind to lncRNA and o-6-methylguanine-DNA methyl transferase (MGMT) were predicted.Double luciferase reporter gene assay was used to detect the interaction between miR-1915 andlnc-AC079612.1.1-1 ∶ 1.SPSS 22.0 statistical software was used to analyze the data.The measurement data were expressed as ((x) ± s).T test was compared between the two groups,and multiple groups were compared with F test.Results The expression of lnc-AC079612.1-1 ∶ 1 was 3.94 times higher in the liver metastases than in the primary tumor,and expression of MGMT was 3.74 times higher in the liver metastases than in the primary tumor.The results showed that there was a significant co-expression relationship between the lncRNA and o-6-methylguanine DNA transferase (MGMT) gene,and the co-expression correlation coefficient was 0.994 (P ＜ 0.001).The over expression of lnc-ac079612.1.1-1∶1 could significantly enhance the proliferation capacity of SW480 and SW620 cell lines of colon cancer through the CCK-8 experiment.The over expression of lnc-ac079612.1.1-1:1 could promote the invasion and metastasis of SW480 and SW620 cell lines of colon cancer through Transwell cell invasion experiment.MirR-1915-3p was the only miRNA that predicted to be combined with lnc-ac079612.1-1∶1 and MGMT through TargetScan,Miranda,LNCipedia and other web tools.Lnc-ac079612.1.1-1∶1 was found to bind to miR-1915 by double luciferase assay.Conclusion Lnc-ac079612.1.1-1∶ 1 may participate in the liver metastasis process of colon cancer by regulating MGMT,and may play a role in the liver metastasis of colon cancer through the action of mir-1915 on MGMT.