ObjectiveCombined with long non-coding RNA (lncRNA) to find a regression model that can be used to predict the survival rate of patients with colon cancer before operation.MethodsThe clinical information and gene expression information of patients with colon cancer were downloaded by using TCGA database. The differentially expressed lncRNAs in tumor and paracancerous tissues were screened out, and then combined with the clinical information of patients to construct Cox proportional hazard regression model.ResultsA total of 26 kinds of lncRNAs with statistical difference in gene expression between paracancerous tissues and tumor tissues were selected (P<0.05). Through repeated screening and comparison of prediction efficiency, the prediction model was finally selected, which was constructed by patients’ age, M stage, N stage, and three kinds of lncRNAs (ZFAS1, SNHG25, and SNHG7) gene expression level: age [HR=4.00, 95%CI: (1.48, 10.84), P=0.006], M stage [HR=3.96, 95%CI: (2.23, 7.04), P<0.001], N stage [HR=1.87, 95%CI: (1.24, 2.84), P=0.003], ZFAS1 gene expression level [HR=0.60, 95%CI: (0.41, 0.86), P=0.006], SNHG25 gene expression level [HR=0.85, 95%CI: (0.73, 1.00), P=0.045], and SNHG7 gene expression level [HR=2.32, 95%CI: (1.53, 3.52), P<0.001] were all independent risk factors for postoperative survival of patients with colon cancer. The area under the ROC curves for predicting 1, 3, and 5-year overall survival were 0.802, 0.828, and 0.771, respectiely, which had a good prediction ability.ConclusionThe predictive model constructed by the combination of ZFAS1, SNHG25, SNHG7 genes expression level with M stage, N stage, and age can better predict the overall survival rate of patients before operation, which can effectively guide clinical decision-making and choose the most suitable treatment method for patients.
ObjectiveTo investigate the level of serum long non-coding RNA antisense non-coding RNA INK4 locus (LncRNA ANRIL) in patients with ulcerative colitis (UC), and to analyze the diagnostic value of serum LncRNA ANRIL level in UC. MethodsA total of 143 UC patients admitted to the First Affiliated Hospital of Henan University of Science and Technology from February 2015 to November 2019 were retrospectively analyzed, and 145 healthy people with normal physical examination in the First Affiliated Hospital of Henan University of Science and Technology were selected as the control group. The relationship between serum LncRNA ANRIL level and PCT/IL-17 level was analyzed, the serum levels of LncRNA ANRIL, PCT, and IL-17 were compared between the two groups, and their diagnostic value for UC was explored.ResultsThe disease degree of 143 UC patients: 41 cases were mild, 59 cases were moderate, and 43 cases were severe; endoscopic grade: 38 cases were grade Ⅰ, 65 cases were grade Ⅱ, and 40 cases were grade Ⅲ. Compared with the control group, the serum levels of LncRNA ANRIL, PCT, and IL-17 were increased in the UC group (P<0.05); the levels of serum LncRNA ANRIL, PCT, and IL-17 in the UC group increased gradually with the increase of disease severity and endoscopic grade (P<0.05). The serum levels of LncRNA ANRIL were positively correlated with the levels of PCT and IL-17 in the UC patients (r=0.596, P<0.001; r=0.492, P<0.001). The area under the curve (AUC) of serum LncRNA ANRIL level in the diagnosis of UC was 0.851, the cut-off value was 1.29, the sensitivity and specificity were 75.5% and 83.4%, respectively. The AUC of serum LncRNA ANRIL combined with PCT in the diagnosis of UC was 0.898, the corresponding sensitivity and specificity were 81.8% and 87.6%, respectively. The sensitivity and diagnostic value of combination of LncRNA ANRIL and PCT were higher than that of serum LncRNA ANRIL alone (Z=2.102, P=0.036). ConclusionsThe serum level of LncRNA ANRIL in UC patients is increased, which has a certain diagnostic value, and it combines with PCT can better predict UC.
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.
ObjectiveTo summarize the regulatory role of long non-coding RNA (lncRNA) in peripheral nerve injury (PNI) and neural regeneration.MethodsThe characteristics and mechanisms of lncRNA were summarized and its regulatory role in PNI and neural regeneration were elaborated by referring to relevant domestic and foreign literature in recent years.ResultsNeuropathic pain and denervated muscle atrophy are common complications of PNI, affecting patients’ quality of life. Numerous lncRNAs are upregulated after PNI, which promote the progress of neuropathic pain by regulating nerve excitability and neuroinflammation. Several lncRNAs are found to promote the progress of denervated muscle atrophy. Importantly, peripheral nerve regeneration occurs after PNI. LncRNAs promote peripheral nerve regeneration through promoting neuronal axonal outgrowth and the proliferation and migration of Schwann cells.ConclusionAt present, the research on lncRNA regulating PNI and neural regeneration is still in its infancy. The specific mechanism remains to be further explored. How to achieve clinical translation of experimental results is also a major challenge for future research.
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 investigate the expression level of long non-coding RNA Down’s syndrome critical region 8 (LncRNA DSCR8) in gastric cancer and its clinical significance.MethodsEighty-six patients with gastric cancer who were hospitalized in our hospital from August 2014 to August 2015 were selected as the research object. Real-time quantitative PCR (qRT-PCR) was used to detect the expression level of LncRNA DSCR8 mRNA in gastric cancer tissues and its adjacent tissues. The relationship between the expression level of LncRNA DSCR8 mRNA and clinicopathological features of gastric cancer was analyzed. Kaplan-Meier method was used to analyze the relationship between the expression of LncRNA DSCR8 mRNA and the survival rate of patients, and multivariate Cox proportional hazards regression analysis was used to analyze the prognostic factors of gastric cancer.ResultsThe expression level of LncRNA DSCR8 mRNA in gastric cancer tissues was higher than that in the paracancerous tissues (P<0.001). The expression levels of LncRNA DSCR8 mRNA in patients with poorly differentiated, TNM Ⅲ–Ⅳ and lymph node metastasis were higher than those in patients with well/moderately differentiated, TNM Ⅰ–Ⅱ and no lymph node metastasis (P<0.05). The 1, 3 and 5-year survival rate of patients with low LncRNA DSCR8 mRNA expression (97.62%, 92.86%, 83.33%, respectively) were higher than those of patients with high LncRNA DSCR8 mRNA expression (63.64%, 38.64%, 31.82%, respectively), P<0.05. LncRNA DSCR8 mRNA and TNM stage were independent risk factors of death in patients with gastric cancer (P<0.05).ConclusionsLncRNA DSCR8 is associated with the occurrence, development and prognosis of gastric cancer. It may be an important molecular marker of tumor stage and lymph node metastasis in patients with gastric cancer.
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.
Objective To investigate the role of long non-coding RNA metastasis-associated in colon cancer 1-antisense RNA （MACC1-AS1）in cisplatin resistant gastric cancer and its possible mechanism. Methods Human gastric cancer cell line BGC823 and cisplatin resistant gastric cancer cell line (BGC823/DDP) were selected as the research objects. BGC823/DDP cells were transfected and divided into negative control group (si-NC group, transfected with si-NC empty plasmid) and MACC1-AS1 gene silencing group (si-MACC1-AS1 group, transfected with si-MACC1-AS1 plasmid). The BGC823 cells were transfected and divided into positive control group (pcDNA-NC group, transfected with pcDNA-NC empty plasmid) and MACC1-AS1 gene overexpression group (pcDNA-MACC1-AS1 group, transfected with pcDNA-MACC1-AS1 plasmid). MTT was used to detect the inhibition and 50% inhibition concentration (IC50). Flow cytometry was used to detect apoptosis. Real-time fluorescence quantitative PCR was used to detect the mRNA expression levels of MACC1-AS1, B-lymphoma-2 gene (Bcl-2), Bcl-2 related X gene (Bax), mammalian target of rapamycin (mTOR), phosphorylated mTOR (p-mTOR), protein kinase B (AKT), and phosphorylated AKT (p-AKT). Western blot was used to detect the protein expression levels of Bax, Bcl-2, p-mTOR, mTOR, AKT, and p-AKT. Results The relative expression level of MACC1-AS1 mRNA in BGC823/DDP cells was higher than that in BGC823 gastric cancer cells (P<0.01). The relative expression level of MACC1-AS1 mRNA in the si-MACC1-AS1 group cells was lower than that in the si-NC group cells (P<0.01). The relative expression level of MACC1-AS1 mRNA in the pcDNA-MACC1-AS1 group cells was higher than that in the pcDNA-NC group cells (P<0.01). The cell growth inhibition rate and IC50 of the si-MACC1-AS1 group were higher than those of the si-NC group (P<0.01). The cell growth inhibition rate and IC50 of the pcDNA-MACC1-AS1 group were lower than those of the pcDNA-NC group (P<0.01). The mRNA and protein relative expression levels of Bcl-2, p-AKT/AKT and p-mTOR/mTOR in the pcDNA-MACC1-AS1 group were significantly higher than those in the pcDNA-NC group (P<0.01). The relative expression levels of Bax protein and mRNA in the pcDNA-MACC1-AS1 group were significantly lower than those in the pcDNA-NC group (P<0.01). The apoptosis rate of the pcDNA-MACC1-AS1 group was significantly lower than that of the pcDNA-NC group (P<0.01). The mRNA and protein relative expression levels of Bcl-2, p-AKT/AKT and p-mTOR/mTOR in the si-MACC1-AS1 group were significantly lower than those in the si-NC group (P<0.01). The relative expression levels of Bax protein and mRNA in the si-MACC1-AS1 group were significantly higher than those in the si-NC group (P<0.01). The apoptosis rate of the si-MACC1-AS1 group was significantly higher than that of the si-NC group (P<0.01). Conclusions MACC1-AS1 highly expresses in cisplatin resistant gastric cancer cells. Overexpression of MACC1-AS1 regulates AKT/mTOR pathway mediated apoptosis and enhances cisplatin resistance of gastric cancer cells.
ObjectiveTo summarize research progress of non-coding RNAs (ncRNAs) in acute pancreatitis (AP), so as to provide new ideas for pathogenesis, diagnosis, and therapy of AP.MethodThe literatures on studies of ncRNAs in AP in recent years were read and reviewed.ResultsThe incidence of AP was currently increasing, but its etiology was diverse, and its pathogenesis was still fully unclear. In recent years, a large number of studies had confirmed that the ncRNA played an important role in the occurrence of many cellulars and diseases processes. Through continuous exploration for potential mechanisms of AP based on ncRNA (including long non-coding RNA and microRNA) function, it was found that the specificity and sensitivity of ncRNAs in the diagnosis of AP were better than of the traditional biomarkers. Meanwhile, ncRNAs were involved in the regulation of inflammatory response through a variety of ways.ConclusionsncRNAs are involved in altering gene expression (including up-regulation or down-regulation) in the key physiological functions of AP through a variety of ways, it might provide new ideas for understanding pathogenesis of AP and help to find new therapeutic targets. A variety of ncRNAs closely related to AP are expected to become biomarkers and molecular targets for early diagnosis and treatment of AP, so as to achieve early diagnosis and targeted treatment of AP.
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.