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.
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.
Pulmonary fibrosis is a kind of chronic and fibrotic lung disease caused by a variety of reasons, and its main pathological characteristic is excessive scar formation after the destruction of normal lung tissue structure, which eventually leads to respiratory insufficiency. Although the research on the pathophysiological mechanism of pulmonary fibrosis has made great progress, its pathogenesis has not been fully elucidated, and it is still clinically incurable. In recent years, studies have shown that non-coding RNAs are involved in the pathogenesis of pulmonary fibrosis, therefore, this article summarizes the related research progress of non-coding RNA in regulation of pulmonary fibrosis by affecting epithelial-mesenchymal transition, fibroblast activation and function of macrophages, in order to provide new ideas for the treatment of pulmonary fibrosis.
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 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 investigate the regulatory effect of long chain non-coding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) adsorbing microRNA-124 (miR-124) on osteogenic differentiation of mesenchymal stem cells (MSCs).MethodsC3H10T1/2 cells derived from mouse embryos were cultured in vitro, then randomly divided into control group (group A), lncRNA MALAT1 no-load plasmid group (group B), lncRNA MALAT1 overexpression plasmid group (group C), lncRNA MALAT1 small interfering RNA (siRNA) group (group D), and lncRNA MALAT1 siRNA negative control group (group E). The cells were transfected into plasmids and siRNA, then induced to differentiate into osteoblasts. Alkaline phosphatase (ALP) and alizarin red staining were used to detect the osteogenic differentiation of cells in each group, real-time fluorescence quantitative (qRT-PCR) analysis was used to detect the expressions of lncRNA MALAT, miR-124, and osteogenesis-related genes such as Runt-related transcription factor 2 (Runx2), osteopontin (OPN), and osteocalcin (OCN) in each group. Double luciferase reporter gene was used to detect the targeting regulation of lncRNA MALAT1 to miR-124.ResultsThe relative contents of ALP positive cells, mineralized nodule, and the relative mRNA expressions of lncRNA MALAT1, Runx2, OPN, and OCN in group C were significantly higher than those in other groups (P<0.05), while in group D significantly lower than in other groups (P<0.05); the relative expression of miR-124 in group C was significantly lower than that in other groups(P<0.05), while in group D significantly higher than in other groups (P<0.05). There was no significant difference in these indexes between groups A, B, and E (P>0.05). The results of double luciferase reporter gene assay showed that lncRNA MALAT1 targeting down-regulated the expression of miR-124.ConclusionLncRNA MALAT1 can targeting down-regulate the expression of miR-124 and promote the osteogenic differentiation of MSCs.
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.
Aortic dissection is a catastrophic emergency with a high mortality rate, and its full pathogenesis remains unknown to researchers, which brings a heavy burden to the individuals, society and family because of its poor prognosis. Improving the efficiency of its diagnosis and treatment and defining the pathogenic mechanism clearly is a research hotspot. Recently, utilizing bioinformatics to find diagnostic biomarker of aortic dissection has attracted the attention of many researchers. Besides, exploring the relationship between pathogenic mechanism and inflammatory process, extracellular matrix degradation, elastic fiber fracture and the phenotypic transformation of vascular smooth muscle cells is also a hot topic. We summarize recent progress made in the pathogenesis of aortic dissection. We hope to identify key molecules driving aortic dissection and provide reliable reference for the diagnosis, medical treatment and prevention of aortic dissection.
The pathogenesis of diabetic retinopathy (DR) is complex. Antisense non-coding RNA (ANRIL) in the INK4 locus in long-chain non-coding RNA (lncRNA) is closely related to cell proliferation, differentiation, and individual development. It plays an important role in the dysplasia of retinal vascular endothelial cells and is a new field in the study of the pathogenesis of DR. According to the researches at present, ANRIL may plays its role in the occurrence and development of DR through the signal pathway of nuclear factor-κB and ROS/polyadenylation diphosphate ribose polymerase, and interact with p300, miR-200b, and EZH2 to regulating the expression and function of VEGF. Specific blocking ANRIL and its related pathways may become a new target in the treatment of DR.
Objective To investigate the expression and clinical value of long chain non-coding RNA nicotinamide nucleotide hydrogenase antisense RNA1 (LncRNA NNT-AS1), motor neuron and pancreas homeobox protein 1 antisense RNA1 (MNX1-AS1) in lung cancer patients. Methods This study selected 128 patients diagnosed with lung cancer admitted to The Third Medical Center of the General Hospital of the People’s Liberation Army from April 2020 to April 2021 as a cancer group. During the same period, 128 patients with benign pulmonary nodules were regarded as a benign group, and 128 healthy individuals who underwent physical examination were selected as a control group. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to detect the levels of LncRNA NNT-AS1 and MNX1-AS1 in serum. A three-year follow-up was conducted on all lung cancer patients, with 52 patients in the death group and 76 patients in the survival group. Receiver operator characteristic (ROC) curve was applied to analyze the diagnostic value of serum LncRNA NNT-AS1 and MNX1-AS1 for the occurrence of lung cancer and their predictive value for prognosis. Results Compared with the control group, the serum levels of LncRNA NNT-AS1 and MNX1-AS1 were obviously increased in the benign group and the cancer group (P<0.05). Compared with the benign group, the levels of LncRNA NNT-AS1 and MNX1-AS1 in serum of the cancer patients were obviously increased (P<0.05). The area under ROC curve (AUC) of serum LncRNA NNT-AS1 combined with MNX1-AS1 for the diagnosis of lung cancer was higher than that of LncRNA NNT-AS1 and MNX1-AS1 alone (ZLncRNA NNT-AS1~LncRNA NNT-AS1+MNX1-AS1=2.496, P=0.013; ZMNX1-AS1~LncRNA NNT-AS1+MNX1-AS1=2.831, P=0.007). The levels of LncRNA NNT-AS1 and MNX1-AS1 were related to tumor differentiation, clinical stage, and lymph node metastasis (P<0.05). Compared with the survival group, the serum levels of LncRNA NNT-AS1 and MNX1-AS1 in the death group were obviously increased (P<0.05). The AUC of combined prediction for lung cancer prognosis by serum LncRNA NNT-AS1 and MNX1-AS1 was higher than that predicted by LncRNA NNT-AS1 and MNX1-AS1 alone (ZLncRNA NNT-AS1~LncRNA NNT-AS1+MNX1-AS1=2.539, P=0.011; ZMNX1-AS1~LncRNA NNT-AS1+MNX1-AS1=3.377, P=0.001). Conclusion LncRNA NNT-AS1 and MNX1-AS1 are highly expressed in serum of lung cancer patients, and both have certain value in diagnosis and prognosis evaluation of lung cancer.