Objective To summarize the latest research progress of tumor energy metabolism regulated by long non-coding RNA (lncRNA). Method Literatures about the recent studies on the bioenergetic metabolic mechanisms regulated by lncRNA in tumor cells were reviewed according to the results searched from PubMed database, Springer database, HighWire database, and so on. Results Aerobic glycolysis (Warburg effect) was regarded as the most important characteristics of energy metabolism in tumor cells. lncRNA could regulate many key progressions involved energy metabolism in tumor cells, such as glucose metabolism, lipid metabolism, and glutamine metabolism, resulting in accelerated uptake of glucose, decomposition of glutamine, and formation of lipid. Conclusions The functions and mechanisms of energy metabolism in tumor cells regulated by lncRNA are entirely unclear. The role of lncRNA played in cancer needs to be understood, which may contribute to new tumor biomarker detection and effective treatment strategies.
Objective The aim of this study is to review the association between long non-coding RNA (lncRNA) and papillary thyroid carcinoma (PTC). Method The relevant literatures about lncRNA associated with PTC were retrospectively analyzed and summarized. Results The expression levels of noncoding RNA associated with MAP kinase pathway and growth arrest (NAMA), PTC susceptibility candidate 3 (PTCSC3), BRAF activated non-coding RNA (BANCR), maternally expressed gene 3 (MEG3), NONHSAT037832, and GAS8-AS1 in PTC tissues were significantly lower than those in non-thyroid carcinoma tissues. The expression levels of ENST00000537266, ENST00000426615, XLOC051122, XLOC006074, HOX transcript antisense RNA (HOTAIR), antisense noncoding RNA in the INK4 locus (ANRIL), and metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in PTC tissues were upregulated in PTC tissues, comparing with the non-thyroid carcinoma tissues. These lncRNAs were possibly involved in cell proliferation, migration, and apoptosis of PTC. Conclusion LncRNAs may provide new insights into the molecular mechanism and gene-targeted therapy of PTC and become new molecular marker for the diagnosis of PTC.
Calcific aortic valve disease has been the most common heart valve disorder in western world, accompanying with the increase of morbidity in our country year by year. Several molecules and mechanisms are involved in the progression of aortic valve calcification, which intensify the complexity of this pathological process. It is known that inflammation, a key factor in many diseases, has its own role in the development of aortic valve calcification. It has been demonstrated that inflammation, one of the most important participants in this disorder, which may accelerate the local lesions in aortic valve via promoting the expression of osteogenic differentiation of associated factors or decreasing the level of protective molecules. Dyslipidemia is a traditional risk factor of cardiovascular events. However, it may induce or enhance the inflammatory response whereby facilitates the calcific lesions in aortic valve. Recently, several researches have illustrated that non-coding RNAs, a stimulative factor in the progression of malignant tumor, might play a role in the development of aortic valve calcification. MiRNA and lncRNA, the non-coding RNAs which regulate the expression of genes involved in inflammatory and osteogenic differentiation, are undeniable regulators of aortic valve calcification.
ObjectivesTo systematically review the association between the expression level of LncRNA and clinicopathological features and prognostic value of gastric cancer.MethodsWe searched PubMed, EMbase, The Cochrane Library, Web of Science, CNKI, VIP, WanFang Data and CBM databases to collect studies on the association between LncRNA overexpression and prognosis for gastric cancer from inception to April 2017. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies, then, meta-analysis was performed by using Stata 12.0 software.ResultsA total of 21 case-control studies were included. The results of meta-analysis showed that: LncRNA overexpression patients had poor TNM stage (OR=0.29, 95%CI 0.24 to 0.35, P<0.001), deeper tumor invasion (OR=0.24, 95%CI 0.12 to 0.49,P<0.001), shorter overall survival (OS) (HR=2.52, 95%CI 2.07 to 3.06,P<0.001) and disease-free survival (DFS) (HR=2.31, 95%CI 1.75 to 3.05,P<0.001).ConclusionsLncRNA overexpression is a poor prognosis risk factor for gastric cancer patients. Due to limited quantity and quality of the included studies, more high quality studies are needed to verify above conclusions.
ObjectiveBy detecting the expression of the long non-coding RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in myocardial tissue under different hypoxia patterns, to explore the possible mechanism of obstructive sleep apnea (OSA)-induced cardiovascular diseases.MethodsSD rats were randomly and equally divided into 4 groups namely a normal (N) group, a continuous hypoxia (CH) group, an intermittent hypoxia (IH) group and an intermittent hypoxia with hypercapnia (IHH) group, and were treated for 1, 2, and 3 weeks. The expression of MALAT1 and associated immune factors of the myocardial tissue were examined by qRT-PCR.ResultsAn elevation without significance was observed in those three hypoxia groups in contrast with N group after 1 week’s treatment. However, in 2 and 3 weeks’ groups, the mRNA expression of MALAT1 was significantly higher in IHH group than the other three groups (all P<0.01), while there was no significant difference among IH, CH or N groups despite an increasing tendency in IH and CH groups against N group were observed. Additionally, the expressions of hypoxia inducible factor-1α (P<0.05), Toll-like receptor 4 (P<0.01) and interleukin-6 (P<0.05) mRNA were also increased significantly in IHH group compared with IH, CH and IHH groups in 3 weeks’ treatment respectively, which were coordinated with the change of MALAT1 mRNA.ConclusionsThe expression of MALAT1 in myocardial tissue is elevated by intermittent hypoxia with hypercapnia, and the tendency is similar with hypoxia-induced inflammation factors. These findings indicate that MALAT1 is probably a regulatory factor of OSA induced myocardial immune injury.
ObjectiveTo evaluate the expression level and diagnostic value of lnc-PAPSS2-2 (lnc-PA) in peripheral blood of active pulmonary tuberculosis (PTB) patients.MethodsFrom January 2011 to January 2018, 798 patients with active PTB and 1 650 healthy people undergoing health examination in West China Hospital of Sichuan University and their electronic health records (EHR) were collected. Peripheral blood lnc-PA levels were quantified by quantitative real-time polymerase chain reaction method. The data of lnc-PA and EHR were modeled using nomogram, and the receiver operating characteristic (ROC) curves of lnc-PA, EHR and the combination of lnc-PA and EHR were compared to evaluate the diagnostic value of lnc-PA for active PTB.ResultsThe level of lnc-PA was lower in active PTB patients than that in healthy controls (P<0.001). The areas under ROC curve of lnc-PA, EHR and their combination were 0.619, 0.962, and 0.964 in the training set and 0.626, 0.950, and 0.950 in the validation set, respectively.ConclusionThe diagnostic ability of lnc-PA is poor and that of EHR is good, which indicates that the clinical value of lnc-PA as a biomarker of active PTB remains to be further explored.
Objective To explore relationship between long non-coding RNA maternally expressed gene 3 (MEG3) polymorphisms and risk of gastric cancer. Methods One hundred and seventy-two Han patients with gastric cancer (gastric cancer group) and 224 Han individuals for physical examination (control group) in the Yunnan Cancer Hospital from March 2013 to October 2017 were selected as subjects. The rs7158663 and rs4081134 polymorphisms of the MEG3 were genotyped by using a TaqMan technique. The associations between the 2 polymorphisms and the risk of the gastric cancer and its clinical features were analyzed using the SPSS software. Results The frequencies of the AG+AA genotype and the A allele of the MEG3 rs7158663 in the gastric cancer group were significantly higher than those in the control group using the GG genotype and G allele as a reference respectively ［adjusted OR=1.71, 95%CI (1.14, 2.56), P=0.010; adjusted OR=1.58, 95%CI (1.15, 2.19), P=0.005］ after the Chi-square test and the adjustment of age and gender. The frequencies of the AG+AA genotype and the A allele of the MEG3 rs4081134 had no significant differences between the gastric cancer group and the control group (P>0.017). Moreover, the polymorphisms of the MEG3 rs7158663 and rs4081134 were not associated with the clinical features of the gastric cancer (P>0.017). Conclusion MEG3 rs7158663 AG+AA genotype might be one of susceptibility gene of gastric cancer in Chinese Han population.
ObjectiveTo investigate the expression of growth arrest-specific 5 (GAS5) mRNA and its clinical significance in hepatocellular carcinoma.MethodsThe expression of GAS5 mRNA in the hepatocellular carcinoma tissues and corresponding adjacent tissues were detected by real time-PCR. The relationship between the expression of GAS5 mRNA and clinicopathological characteristics were analyzed by SPSS 19.0 software.ResultsThe expression of GAS5 mRNA in hepatocellular carcinoma tissues was significantly lower than that of the adjacent tissues (P<0.01). The expression of GAS5 mRNA was related to tumor size, tumor number, lymph node metastasis, clinical TNM stage, alpha fetoprotein level, and tumor differentiation (P<0.05). Cox hazard model results showed that low expression of GAS5 mRNA was associated with poor prognosis (P<0.05).ConclusionGAS5 mRNA is expected to be a diagnostic and prognostic marker for patients with hepatocellular carcinoma.
ObjectiveTo summarize the recent advances in the relationship between long non-coding RNA (LncRNA) and tumor autophagy, autophagy and drug resistance regulation.MethodsReviewed the relevant literatures at home and abroad, and reviewed the recent research progress of LncRNA regulation of autophagy to affect tumor resistance.ResultsDrug resistance was a common problem in the process of anti-tumor therapy. Autophagy played an important role in the process of tumor resistance as an important mechanism to maintain cell homeostasis. Abnormal regulation of LncRNA could contribute to the occurrence and development of tumors, and could also mediate the resistance of tumor cells to anti-tumor drugs by promoting or inhibiting autophagy.ConclusionsLncRNA can mediate tumor autophagy in a positive or negative direction, and autophagy is a " double-edged sword” for tumor resistance. LncRNA may improve tumor resistance to drugs by regulating autophagy.
ObjectiveTo explore the differential expressed lncRNA genes associated with formation of cholesterol gallstone, and analyze the biological functions of differential expressed lncRNA through bioinformatics.MethodsA total of 24 C57BL/6 mice were randomly divided into normal control group (n=8) and lithogenic group (n=16), which were treated with chow diets and lithogenic diets respectively for 5 weeks. After 5 weeks, mice of the lithogenic group were randomly divided into model control group (n=8) and ursodeoxycholic acid treatment group (n=8). Afterwards, mice of the normal control group were still fed with chow diets, mice of the model control group were fed with lithogenic diets, mice of the ursodeoxycholic acid treatment group were fed with ursodeoxycholic acid. After 2 weeks, collected liver tissues and gallbladder bile from the three groups, and observed gallbladder gross sample and analyzed lipids component of gallbladder bile, meanwhile detected the differential expressed lncRNA and analyzed the biological functions of differential expressed lncRNA through bioinformatics, including Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) pathway analysis.ResultsWe successfully constructed the mice model of cholesterol gallstone. Total cholesterol level of gallbladder in the model control group had significantly higher than those of the normal control group and ursodeoxycholic acid treatment group (P<0.05), yet there was no significant difference between the normal control group and ursodeoxycholic acid treatment group (P=0.59). The levels of total bile acid, total bilirubin, and direct bilirubin had no significant difference among the three groups (P>0.05). There were 49 kinds of common overlapped difference lncRNA between the ursodeoxycholic acid treatment group and the model control group through differential expression analysis of lncRNA in liver tissues of the mice in three groups. GO and KEGG path analysis were performed separately by differential expressed lncRNA, and 88 kinds of GO terms and 18 kinds of pathways were significantly enriched from the model control group and the normal control group, 205 kinds of GO terms and 20 kinds of pathways were significantly enriched from the ursodeoxycholic acid treatment group and the normal control group.ConclusionsUrsodeoxycholic acid has therapeutic effect for cholesterol gallstone. Differential expressed lncRNAs play an important regulatory role in the formation of cholesterol gallstone and the prevention of gallstone formation by ursodeoxycholic acid treatment, which further lay the foundation in discussing specific mechanism regulated by lncRNA.