英文题目：Ye Y, Shen A, Liu A. Long non-coding RNA H19 and cancer: A competing endogenous RNA.[J]. Bulletin du Cancer, 2019, pii: S0007-4551(19)30327-3.
期 刊 名：Bulletin du Cancer 发表时间：2019.11 IF：0.729
Long non-coding RNA (lncRNA) is a class of non-coding RNA with a length of more than 200 nucleotides, which has become a hotspot in the research of tumorigenesis and development in recent years. Accumulating studies have indicated that H19 is abnormally expressed in human malignant tumors, and regulates cell proliferation, migration, invasion, anti-apoptosis and epithelial-mesenchymal transition through various mechanisms, thus playing a carcinogenic or anti-cancer role. H19 has been found to act as a microRNA sponge to indirectly regulate the expression of microRNA downstream target genes thus mediating cancer progression in several cancer types. Even in the same cancer, H19 also sponges various microRNAs to mediate diverse regulatory mechanisms. Tissue-specific expression of H19 suggests that it may be an early diagnostic marker or prognostic indicator of cancers. In this review, we summarize the latest original researches, mainly focusing on the role of H19 sponging microRNAs in cancers. We hope this article can facilitate readers obtain the molecular mechanisms of H19 sponging miRNAs in cancers and provide a broad perspective for further research on cancer diagnosis and therapy.
英文题目：Hu R, Lu Z. Long non‑coding RNA HCP5 promotes prostate cancer cell proliferation by acting as the sponge of miR-4656 to modulate CEMIP expression[J]. Oncology Reports, 2019.
期 刊 名：Oncology Reports 发表时间：2019.11 IF：3.041
Aberrant expression of long noncoding RNAs (lncRNAs) has been demonstrated in human cancers and regulates the malignant behavior of cancer cells. Previous studies demonstrated the critical involvement of lncRNA histocompatibility leukocyte antigen (HLA) complex P5 (HCP5) in the development of cancers, however, the function of HCP5 in prostate cancer has not been reported. In the present study, we found the overexpressed expression of HCP5 in prostate cancer tissues and cell lines via RT‑qPCR analysis. High expression of HCP5 was positively correlated with the metastasis of prostate cancer. Downregulation of HCP5 inhibited the proliferation, colony formation and induced apoptosis of prostate cancer cells. Functional experiments demonstrated that HCP5 acted as a competing endogenous RNA (ceRNA) to sponge miR‑4656. Ectopic expression of HCP5 decreased the expression of miR‑4656 in prostate cancer cells. MiR‑4656 was found to be decreased in prostate cancer tissues and was negatively correlated with the expression of HCP5. Further luciferase reporter assay revealed that miR‑4656 was able to bind the 3\'‑untranslated region (3\'‑ UTR) of the cell migration inducing hyaluronidase 1 (CEMIP) and suppressed the expression of CEMIP. Consistent with the negative regulation of miR‑4656 by HCP5, western blot analysis uncovered that overexpression of HCP5 upregulated the abundance of CEMIP in prostate cancer cells. The CCK‑8 assay showed that depletion of CEMIP significantly inhibited the HCP5‑promoted proliferation of prostate cancer cells. Collectively, our data provide a novel mechanism by which HCP5 regulates the progression of prostate cancer.
英文题目：Liu J, Li W, Zhang J, Ma Z, Wu X, Tang L. Identification of key genes and long non-coding RNA associated ceRNA networks in hepatocellular carcinoma[J]. PeerJ, 2019, 7:e8021.
期 刊 名：Oncology Reports 发表时间：2019.11 IF：3.041
Background: Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related deaths worldwide. Although multiple efforts have been made to understand the development of HCC, morbidity, and mortality rates remain high. In this study, we aimed to discover the mRNAs and long non-coding RNAs (lncRNAs) that contribute to the progression of HCC. We constructed a lncRNA-related competitive endogenous RNA (ceRNA) network to elucidate the molecular regulatory mechanism underlying HCC.
Methods: A microarray dataset (GSE54238) containing information about both mRNAs and lncRNAs was downloaded from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) and lncRNAs (DElncRNAs) in tumor tissues and non-cancerous tissues were identified using the limma package of the R software. The miRNAs that are targeted by DElncRNAs were predicted using miRcode, while the target mRNAs of miRNAs were retrieved from miRDB, miRTarBas, and TargetScan. Functional annotation and pathway enrichment of DEGs were performed using the EnrichNet website. We constructed a protein-protein interaction (PPI) network of DEGs using STRING, and identified the hub genes using Cytoscape. Survival analysis of the hub genes and DElncRNAs was performed using the gene expression profiling interactive analysis database. The expression of molecules with prognostic values was validated on the UALCAN database. The hepatic expression of hub genes was examined using the Human Protein Atlas. The hub genes and DElncRNAs with prognostic values as well as the predictive miRNAs were selected to construct the ceRNA networks.
Results: We found that 10 hub genes (KPNA2, MCM7, CKS2, KIF23, HMGB2, ZWINT, E2F1, MCM4, H2AFX, and EZH2) and four lncRNAs (FAM182B, SNHG6, SNHG1, and SNHG3) with prognostic values were overexpressed in the hepatic tumor samples。 We also constructed a network containing 10 lncRNA-miRNA-mRNA pathways, which might be responsible for regulating the biological mechanisms underlying HCC。
Conclusion: We found that the 10 significantly overexpressed hub genes and four lncRNAs were negatively correlated with the prognosis of HCC. Further, we suggest that lncRNA SNHG1 and the SNHG3-related ceRNAs can be potential research targets for exploring the molecular mechanisms of HCC.
英文题目：Lin , Li Q, Hao W, Zhang Y, Zhao L Han W. Upregulation of LncRNA Malat1 Induced Proliferation and Migration of Airway Smooth Muscle Cells via miR-150-eIF4E/Akt Signaling[J]. Frontiers in Physiology, 2019, 10:1337.
期 刊 名：Frontiers in Physiology 发表时间：2019.10 IF：3.201
The increased proliferation and migration of airway smooth muscle cells (ASMCs) are critical processes in the formation of airway remodeling in asthma. Long non-coding RNAs (lncRNAs) have emerged as key mediators of diverse physiological and pathological processes, and are involved in the pathogenesis of various diseases, including asthma. LncRNA Malat1 has been widely reported to regulate the proliferation and migration of multiple cell types and be involved in the pathogenesis of various human diseases. However, it remains unknown whether Malat1 regulates ASMC proliferation and migration. Here, we explored the function of Malat1 in ASMC proliferation and migration in vitro stimulated by platelet-derived growth factor BB (PDGF-BB), and the underlying molecular mechanism involved. The results showed that Malat1 was significantly upregulated in ASMCs treated with PDGF-BB, and knockdown of Malat1 effectively inhibited ASMC proliferation and migration induced by PDGF-BB. Our data also showed that miR-150 was a target of Malat1 in ASMCs, and inhibited PDGF-BB-induced ASMC proliferation and migration, whereas the inhibition effect was effectively reversed by Malat1 overexpression. Additionally, translation initiation factor 4E (eIF4E), an important regulator of Akt signaling, was identified to be a target of miR-150, and both eIF4E knockdown and Akt inhibitor GSK690693 inhibited PDGF-BB-induced ASMC proliferation and migration. Collectively, these data indicate that Malat1, as a competing endogenous RNA (ceRNA) for miR-150, derepresses eIF4E expression and activates Akt signaling, thereby being involved in PDGF-BB-induced ASMC proliferation and migration. These findings suggest that Malat1 knockdown may present a new target to limit airway remodeling in asthma.
英文题目：Cao M, Zhang L, Wang JH, Zeng H, Peng Y, Zou J, Shi J, Zhang L, Li Y, Yoshida S, Tang L, Zhou Y. Identifying circRNA-associated-ceRNA networks in retinal neovascularization in mice[J]. International Journal of Medical Sciences, 2019, 16(10):1356-1365.
期 刊 名：International Journal of Medical Sciences 发表时间：2019.9 IF：2.333
Retinal neovascularization is a complication which caused human vision loss severely. It has been shown that circular RNAs (circRNAs) play essential roles in gene regulation. However, circRNA expression profile and the underlying mechanisms in retinal neovascular diseases remain unclear. In the present study, we identified altered circRNAs in the retinas of oxygen-induced retinopathy (OIR) mouse model by microarray profiling. Microarray analysis revealed that 539 circRNAs were significantly altered in OIR retinas compared with controls. Among them, 185 up-regulated and 354 down-regulated circRNAs were identified. The expression levels of 4 altered circRNAs including mmu_circRNA_002573, mmu_circRNA_011180, mmu_circRNA_016108 and mmu_circRNA_22546 were validated by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR). Bioinformatic analysis with validated circRNAs such as competing endogenous RNA (ceRNA) regulatory networks with Gene Ontology (GO) enrichment analysis demonstrated that qRT-PCR validated circRNAs were associated with cellular process, cell part and phosphoric ester hydrolase activity. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis demonstrated that MAPK signaling pathway and renin-angiotensin system were related to validated circRNAs, suggesting these pathways may participate in pathological angiogenesis. The results together suggested that circRNAs were aberrantly expressed in OIR retinas and may play potential roles in retinal neovascular diseases.