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.
To evaluate the differential expression profiles of the lncRNAs, miRNAs, mRNAs and ceRNAs, and their implication in the prognosis in clear cell renal cell carcinoma (CCRCC), the large sample genomics analysis technologies were used in this study. The RNA and miRNA sequencing data of CCRCC were obtained from The Cancer Genome Atlas (TCGA) database, and R software was used for gene expression analysis and survival analysis. Cytoscape software was used to construct the ceRNA network. The results showed that a total of 1 570 lncRNAs, 54 miRNAs, and 17 mRNAs were differentially expressed in CCRCC, and most of their expression levels were up-regulated (false discovery rate < 0.01 and absolute log fold change > 2). The ceRNA regulatory network showed the interaction between 89 differentially expressed lncRNAs and 9 differentially expressed miRNAs. Further survival analysis revealed that 38 lncRNAs (including COL18A1-AS1, TCL6, LINC00475, UCA1, WT1-AS, HOTTIP, PVT1, etc.) and 2 miRNAs (including miR-21 and miR-155) were correlated with the overall survival time of CCRCC (P < 0.05). Together, this study provided us several new evidences for the targeted therapy and prognosis assessment of CCRCC.
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 study value of long noncoding RNA H19 and HOTTIP in plasma in predicting efficacy of neoadjuvant chemotherapy (NAC) for resectable locally advanced gastric cancer. MethodsForty patients with T3–4aN+M0 gastric cancer and 40 patients with benign gastric diseases treated in the Yantai Yuhuangding Hospital Affiliated to Qingdao University from August 2020 to May 2021 were prospectively included. The expressions of H19 and HOTTIP in the plasma of gastric cancer and benign gastric diseases patients without any treatment after admission were detected before treatment (CAPEOX regimen was used in the patients with gastric cancer), then which were detected after 2 NAC courses for patients with gastric cancer. Meanwhile, some clinical items were detected and the efficacy of NAC was evaluated. The complete remission (CR) and partial remission (PR) were classified as objective remission, CR, PR, and disease stability were classified as disease control. The expressions of H19 and HOTTIP between the different patients were compared and the receiver operating characteristic (ROC) curve was used to evaluate their values in the diagnosis of resectable locally advanced gastric cancer. ResultsThere were 13 cases of T downstaging and 27 cases of T non-downstaging and 25 cases of objective remission and 35 disease control after NAC. The median relative expression levels of H19 and HOTTIP before NAC in the patients with gastric cancer were higher than those in the patients with benign gastric diseases (H19: 1.42 versus 0.98, Z=–3.835, P<0.001; HOTTIP: 2.15 versus 1.04, Z=–5.062, P<0.001), and which were in the patients with T downstaging and disease control were lower than those in the patients with T non-downstaging and 5 cases of disease progression (For T staging, H19: 1.12 versus 1.54, Z=–2.960, P=0.002; HOTTIP: 1.49 versus 2.30, Z=–2.310, P=0.019. For efficacy of NAC, H19: 1.39 versus 2.48, Z=–3.211, P<0.001; HOTTIP: 1.96 versus 3.25, Z=–2.393, P=0.014). The median relative expressions of H19 and HOTTIP after NAC were lower than those before NAC in the patients with gastric cancer (H19: 1.12 versus 1.42, Z=–3.965, P<0.001; HOTTIP: 1.30 versus 2.15, Z=–4.839, P<0.001). There were no significant differences in the changes of H19 and HOTTIP before and after NAC between the patients with T downstaging and T non-downstaging, and between disease control and disease progression (P>0.05). The areas of ROC curve of H19, HOTTIP, and combination of H19 and HOTTIP in diagnosis of resectable locally advanced gastric cancer were higher than 0.7. ConclusionsLncRNA H19 and HOTTIP might be potential tumor markers in gastric cancer, and their diagnostic values for resectable locally advanced gastric cancer are higher. Gastric cancer patients with low expressions of H19 and HOTTIP in plasma might be more sensitive to NAC.
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.
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 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.
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 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.