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 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.
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 summarize the research progress of long non-coding RNA (lncRNA) in the regulation of malignant biological behavior of gallbladder cancer so as to provide references for its related research.MethodThe relevant literatures about studies of lncRNA in gallbladder cancer in recent years were reviewed.ResultsThe recent studies had shown that 19 lncRNAs associated with gallbladder cancer had played the important roles in regulating tumor cell proliferation, migration, invasion, apoptosis, “sponge” miRNAs, chemoresistance, and tumor metastasis. Among them, most lncRNAs tended to have carcinogenic properties, only a few had anticarcinogenic effect. Although the research suggested the mechanism and role of lncRNA to promote or inhibit the occurrence and development of gallbladder cancer, the current research on its mechanism was still limited. In addition, some lncRNAs were found to be specifically expressed in the serum of patients with gallbladder cancer, so which were expected to become biomarkers for tumor diagnosis and prognosis.ConclusionslncRNAs associated with gallbladder cancer have carcinogenic or anticarcinogenic effect, or chemoresistance. They play potential roles in diagnosis, prognosis, and (or) treatment of tumors, but molecular mechanisms of their effects are still limited.
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.
ObjectiveTo understand the function of long non-coding RNA (lncRNA) colon cancer associated transcript-1 (CCAT1) and summarize its relationship with gastric cancer.MethodThe published literatures on the studies of lncRNA CCAT1 function and its relationship with gastric cancer were reviewed and analyzed.ResultsThe lncRNA CCAT1 exerted the negative regulation on the genes by binding to microRNAs (miR) as a competitive endogenous RNA, mediating chromatin circulation between the c-MYC promoter and its upstream enhancer, and promoted the expression of c-MYC gene. The recent studies had found that the CCAT1 could bind to the miR-219-1 and miR-490, thereby promoting the progress of gastric cancer. The expression of lncRNA CCAT1 in the gastric cancer tissues increased, which was obviously different from that in the paracancer tissues and normal tissues. The high expression of lncRNA CCAT1 was related to the tumor size, lymphatic metastasis and TNM stage.ConclusionsThe specific mechanism, intracellular signal transduction pathway and interaction mechanism between CCAT1 and other molecules involved in the progress of gastric cancer still need to be further explored. With the in-depth study of lncRNA, especially CCAT1, it may provide a broader prospect for the diagnosis and treatment of gastric cancer as a target of CCAT1.
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.
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 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 investigate the effect of LOC103693069 on hypoxic apoptosis of bone marrow mesenchymal stem cells (BMSCs). Methods BMSCs from 1-week-old Sprague Dawley rat bone marrow were isolated, cultured, and passaged by the whole bone marrow adherent culture method. After identification of adipogenic, chondrogenic, and osteogenic differentiation, the 3rd generation cells were treated with hypoxia under 5%O2, 1%O2, and anaerobic conditions. After 48 hours, the cell viability, apoptosis, and apoptosis-related proteins [hypoxia inducible factor 1α (HIF-1α), Caspase-3, B cell lymphoma/leukemia 2 (Bcl-2)] expressions were detected, and normal BMSCs were used as controls. Based on the research results, the concentration group with the most obvious apoptosis was selected and used for subsequent experiments. After 48 hours of hypoxia treatment, BMSCs were taken and analyzed by gene chip and real-time fluorescence quantitative PCR (qRT-PCR) to screen the most significantly down-regulated gene and construct their high-expression, low-expression, and negative control lentiviruses; BMSCs were transfected with the different lentiviruses, respectively. After qRT-PCR detection confirmed that the transfection was successful, the BMSCs were treated with hypoxia for 48 hours to observe the cell viability and the expressions of apoptosis-related proteins. ResultsAfter cell viability, apoptosis, and apoptosis-related proteins were detected, cell apoptosis was the most significant under anaerobic conditions after 48 hours. The above indicators were significantly different from other groups (P<0.05), and this group was used for treatment conditions for subsequent experiments. Gene chip analysis showed that after 48 hours of hypoxia treatment, AC125847.1, LOC102547753, AABR07017208.2, and LOC103693069 were significantly down-regulated in BMSCs, and the expressions of LOC103693069 was the most significant down-regulation detected by qRT-PCR (P<0.05). It was selected to construct lentivirus and transfect BMSCs. Afterwards, qRT-PCR detection showed the successful transfection into the cells. After hypoxia treatment, the apoptosis rate and the expressions of apoptosis-related proteins of BMSCs overexpressed by the gene were significantly reduced (P<0.05). Conclusion LOC103693069 can relieve the hypoxic apoptosis of BMSCs.