Long non-coding RNA DSCAM-AS1 upregulates USP47 expression through sponging miR-101-3p to accelerate osteosarcoma progression

2020 ◽  
Vol 98 (5) ◽  
pp. 600-611
Author(s):  
Shanyong Zhang ◽  
Lei Ding ◽  
Feng Gao ◽  
Hongwu Fan
Keyword(s):  
Signaling Pathway ◽  
Target Gene ◽  
Molecular Mechanisms ◽  
Negative Relationship ◽  
Non Coding Rna ◽  
Tumorigenesis And Progression ◽  
Tumors Of Bone ◽  
Non Coding Rnas ◽  
Long Non Coding Rna ◽  
Oncogenic Gene

Osteosarcoma (OS) originating from mesenchyme is one of the most common invasive tumors of bone, and has an extremely high mortality rate. Previous studies have reported that long non-coding RNAs (lncRNAs) play essential roles in the tumorigenesis and progression of a multitude of human cancers. The lncRNA DSCAM-AS1 has been reported to be an oncogenic gene in many cancers. However, the roles and regulatory mechanisms of DSCAM-AS1 in OS have not been deeply investigated. In this study, our findings prove that DSCAM-AS1 is highly expressed in OS cells. Knockdown of DSCAM-AS1 suppressed cell proliferation, migration, and invasiveness, and induced cell apoptosis in OS. Additionally, knockdown of DSCAM-AS1 inactivated the Wnt–β-catenin signaling pathway. Moreover, research into its molecular mechanisms confirmed that DSCAM-AS1 functions as a sponge for miR-101-3p, and that ubiquitin-specific peptidase 47 (USP47) is a target gene of miR-101-3p. Furthermore, a negative relationship between miR-101-3p and DSCAM-AS1 or USP47 was discovered. The results from our rescue assays suggest that DSCAM-AS1 regulates the progression of OS through binding with miR-101-3p to control the expression of USP47. Finally, we discovered that AKT–mTOR signaling pathway mediates the activity of DSCAM-AS1 in OS. Taken together, our results show that DSCAM-AS1 accelerates the progression of OS via the miR-101-3p–USP47 axis, which could present a new potential therapeutic treatment for OS.

ADAMTS9-AS2: A functional long non-coding RNA in tumorigenesis

2021 ◽  
Vol 27 ◽  
Author(s):  
Wen Xu ◽  
Bei Wang ◽  
Yuxuan Cai ◽  
Jinlan Chen ◽  
Xing Lv ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Signaling Pathways ◽  
Therapeutic Target ◽  
Molecular Mechanisms ◽  
Human Cancer ◽  
Migration Inhibition ◽  
Cancer Proliferation ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Background: Long non-coding RNAs (lncRNA) have been identified as novel molecular regulators in cancers. LncRNA ADAMTS9-AS2 can mediate the occurrence and development of cancer through various ways such as regulating miRNAs, activating the classical signaling pathways in cancer, and so on, which have been studied by many scholars. In this review, we summarize the molecular mechanisms of ADAMTS9-AS2 in different human cancers. Methods: Through a systematic search of PubMed, lncRNA ADAMTS9-AS2 mediated molecular mechanisms in cancer are summarized inductively. Results: ADAMTS9-AS2 aberrantly expression in different cancers is closely related to cancer proliferation, invasion, migration, inhibition of apoptosis. The involvement of ADAMTS9-AS2 in DNA methylation, mediating PI3K / Akt / mTOR signaling pathways, regulating miRNAs and proteins, and such shows its significant potential as a therapeutic cancer target. Conclusion: LncRNA ADAMTS9-AS2 can become a promising biomolecular marker and a therapeutic target for human cancer.

scholarly journals Long Non-Coding RNA (lncRNA) in Oral Squamous Cell Carcinoma: Biological Function and Clinical Application

Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 5944
Author(s):  
Jianfei Tang ◽  
Xiaodan Fang ◽  
Juan Chen ◽  
Haixia Zhang ◽  
Zhangui Tang
Keyword(s):  
Squamous Cell Carcinoma ◽  
Oral Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Molecular Mechanisms ◽  
Non Coding Rna ◽  
Potential Applications ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Oral squamous cell carcinoma (OSCC) is a type of malignancy with high mortality, leading to poor prognosis worldwide. However, the molecular mechanisms underlying OSCC carcinogenesis have not been fully understood. Recently, the discovery and characterization of long non-coding RNAs (lncRNAs) have revealed their regulatory importance in OSCC. Abnormal expression of lncRNAs has been broadly implicated in the initiation and progress of tumors. In this review, we summarize the functions and molecular mechanisms regarding these lncRNAs in OSCC. In addition, we highlight the crosstalk between lncRNA and tumor microenvironment (TME), and discuss the potential applications of lncRNAs as diagnostic and prognostic tools and therapeutic targets in OSCC. Notably, we also discuss lncRNA-targeted therapeutic techniques including CRISPR-Cas9 as well as immune checkpoint therapies to target lncRNA and the PD-1/PD-L1 axis. Therefore, this review presents the future perspectives of lncRNAs in OSCC therapy, but more research is needed to allow the applications of these findings to the clinic.

scholarly journals Long non-coding RNA CRNDE promote the progression of tongue squamous cell carcinoma through regulating the PI3K/AKT/mTOR signaling pathway

RSC Advances ◽  
2019 ◽  
Vol 9 (37) ◽  
pp. 21381-21390
Author(s):  
Zhongheng Yang ◽  
Weizhi Chen
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Colorectal Neoplasia ◽  
Tongue Squamous Cell Carcinoma ◽  
Mtor Signaling Pathway ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Long non-coding RNAs (lnRNAs) colorectal neoplasia differentially expressed (CRNDE) has been identified as a crucial regulator involved in tongue squamous cell carcinoma (TSCC).

Expression of long non-coding RNAs ROR and MALAT1 in uterine fibroids

2021 ◽  
Vol 20 (4) ◽  
pp. 17-21
Author(s):  
S.A. Levakov ◽  
◽  
G.Ya. Azadova ◽  
A.E. Mamedova ◽  
Kh.R. Movtaeva ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Uterine Fibroids ◽  
Reproductive Age ◽  
Expression Level ◽  
Control Group ◽  
Tissue Samples ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Objective. To study the expression level of long non-coding RNAs ROR and MALAT1 in tissue samples of uterine fibroids. Patients and methods. Samples of myomatous nodes and tissues of normal myometrium in 28 women of reproductive age were examined. The analysis of the expression of long non-coding RNAs was carried out using a real-time reverse-transcription polymerase chain reaction (RT-PCR) with specific primers. Results. There was a significant decrease in the expression level of long non-coding RNA ROR and an increase in the MALAT1 expression in tissue samples of uterine fibroids relative to the control group. Conclusion. The results obtained demonstrate a possible role of long non-coding RNAs in the development of uterine fibroids and correlate with the data which we obtained for patients with endometriosis. Detecting the expression level of long non-coding RNAs can improve the existing methods for diagnosing this disease. However, further research is required to determine the clinical significance of MALAT1 and ROR, and the molecular mechanisms underlying the action of these RNAs in uterine fibroid cells. Key words: long non-coding RNAs, uterine fibroids, myomectomy, lncROR, MALAT1

Long non-coding RNA tumor protein 53 target gene 1 promotes cervical cancer development via regulating microRNA-33a-5p to target forkhead box K2 (Preprint)

2021 ◽  
Author(s):  
Yanyan Liu Sr ◽  
xiaomei Liu ◽  
xiuying Yuan ◽  
poling Feng ◽  
zhiwei Ouyang ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Signaling Pathway ◽  
Target Gene ◽  
Mtor Signaling ◽  
Regulatory Function ◽  
Clinical Samples ◽  
Mtor Signaling Pathway ◽  
Forkhead Box ◽  
Non Coding Rna ◽  
Long Non Coding Rna

BACKGROUND Long non-coding RNA tumor protein 53 target gene 1 (TP53TG1) has been studied in multiple diseases, while the regulatory function of TP53TG1 on cervical cancer (CC) via regulating microRNA (miR)-33a-5p to target Forkhead box K2 (FOXK2) remains limited. This study aims to unearth the effects of TP53TG1/miR-33a-5p/FOXK2 axis on CC. OBJECTIVE This study aims to unearth the effects of TP53TG1/miR-33a-5p/FOXK2 axis on CC. METHODS The clinical samples were collected and TP53TG1, miR-33a-5p and FOXK2 levels were examined in CC tissues. The CC cells were transfected with high- or low-expressed TP53TG1, FOXK2 and miR-33a-5p to determine the change of CC cell biological activities and the status of phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) pathway. The tumorigenesis in nude mice was conducted. The relationship among TP53TG1, miR-33a-5p and FOXK2 was validated. RESULTS TP53TG1 and FOXK2 were enriched and miR-33a-5p was inhibited in CC. The reduced TP53TG1 or FOXK2 or elevated miR-33a-5p decelerated the CC cell development and the activation of PI3K/AKT/mTOR signaling pathway. The depleted FOXK2 or enriched miR-33a-5p reversed the effects of decreased TP53TG1. TP53TG1 sponged miR-33a-5p which targeted FOXK2. The experiment in vivo validated the outcomes of the experiment in vitro. CONCLUSIONS TP53TG1 accelerates the CC development via regulating miR-33a-5p to target FOXK2 with the involvement of PI3K/AKT/mTOR signaling pathway. This study provides novel theory references and a distinct direction for the therapy strategies of CC.

scholarly journals The Combined Regulation of Long Non-coding RNA and RNA-Binding Proteins in Atherosclerosis

2021 ◽  
Vol 8 ◽  
Author(s):  
Yuanyuan Ding ◽  
Ruihua Yin ◽  
Shuai Zhang ◽  
Qi Xiao ◽  
Hongqin Zhao ◽  
...  
Keyword(s):  
Binding Proteins ◽  
Molecular Mechanisms ◽  
Complex Disease ◽  
Rna Binding ◽  
Rna Binding Proteins ◽  
Specific Interaction ◽  
Clinical Issue ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Atherosclerosis is a complex disease closely related to the function of endothelial cells (ECs), monocytes/macrophages, and vascular smooth muscle cells (VSMCs). Despite a good understanding of the pathogenesis of atherosclerosis, the underlying molecular mechanisms are still only poorly understood. Therefore, atherosclerosis continues to be an important clinical issue worthy of further research. Recent evidence has shown that long non-coding RNAs (lncRNAs) and RNA-binding proteins (RBPs) can serve as important regulators of cellular function in atherosclerosis. Besides, several studies have shown that lncRNAs are partly dependent on the specific interaction with RBPs to exert their function. This review summarizes the important contributions of lncRNAs and RBPs in atherosclerosis and provides novel and comprehensible interaction models of lncRNAs and RBPs.

scholarly journals Autophagy‐related Long Non-coding RNA Signature Associated with Prognosis of Lung Adenocarcinoma

2021 ◽  
Author(s):  
Guofei Zhang ◽  
Jiayi Shen ◽  
Zipu Yu ◽  
Gang Shen ◽  
Chengxiao Liang
Keyword(s):  
Lung Adenocarcinoma ◽  
Molecular Mechanisms ◽  
Cox Regression ◽  
Microarray Dataset ◽  
Risk Groups ◽  
The Cancer Genome Atlas ◽  
Non Coding Rna ◽  
Cancer Genome Atlas ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Abstract BackgroundEvidence suggests that long non-coding RNAs (lncRNAs) are involved in various cancers. Here, we developed and evaluated an autophagy-related prognostic lncRNA signature for lung adenocarcinoma (LUAD). ResultsUsing a publicly available microarray dataset from The Cancer Genome Atlas, we analyzed the lncRNA expression profile in a cohort of 439 LUAD patients. The lncRNA-mRNA co-expression network along with univariate and multivariate Cox regression analyses were used to determine 15 autophagy-related lncRNA signatures that were significantly correlated with patient overall survival. Autophagy-related lncRNA signatures stratified patients into high- and low-risk groups with significantly different survival (hazard ratio = 3.256, 95% confidence interval = 2.858–4.101, P < 0.001). The lncRNA signature was further confirmed in other independent datasets. Moreover, the lncRNA signature had prognostic value independent of routine clinical factors. Functional analysis indicated that autophagy-related lncRNA signatures may be involved in LUAD via known autophagy-related pathways. ConclusionsThis newly identified autophagy-related lncRNA signature is a more powerful prognostic tool than the clinicopathological factors routinely used to predict patient survival, and can provide further insights into the molecular mechanisms underlying LUAD.

scholarly journals Long Non-coding RNA: An Emerging Contributor and Potential Therapeutic Target in Renal Fibrosis

2021 ◽  
Vol 12 ◽  
Author(s):  
Weiping Xia ◽  
Yao He ◽  
Yu Gan ◽  
Bo Zhang ◽  
Guoyu Dai ◽  
...  
Keyword(s):  
Renal Fibrosis ◽  
Molecular Mechanisms ◽  
Pathological Process ◽  
Major Type ◽  
Future Research ◽  
Non Coding Rna ◽  
Future Research Directions ◽  
Non Coding Rnas ◽  
Long Non Coding Rna

Renal fibrosis (RF) is a pathological process that culminates in terminal renal failure in chronic kidney disease (CKD). Fibrosis contributes to progressive and irreversible decline in renal function. However, the molecular mechanisms involved in RF are complex and remain poorly understood. Long non-coding RNAs (lncRNAs) are a major type of non-coding RNAs, which significantly affect various disease processes, cellular homeostasis, and development through multiple mechanisms. Recent investigations have implicated aberrantly expressed lncRNA in RF development and progression, suggesting that lncRNAs play a crucial role in determining the clinical manifestation of RF. In this review, we comprehensively evaluated the recently published articles on lncRNAs in RF, discussed the potential application of lncRNAs as diagnostic and/or prognostic biomarkers, proposed therapeutic targets for treating RF-associated diseases and subsequent CKD transition, and highlight future research directions in the context of the role of lncRNAs in the development and treatment of RF.

scholarly journals Long Non-Coding RNA and Breast Cancer

2019 ◽  
Vol 18 ◽  
pp. 153303381984388 ◽  
Author(s):  
Tianzhu Zhang ◽  
Hui Hu ◽  
Ge Yan ◽  
Tangwei Wu ◽  
Shuiyi Liu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Molecular Mechanisms ◽  
Biological Function ◽  
Tumor Development ◽  
Health Concern ◽  
Sequencing Technologies ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Long Non Coding Rna ◽  
Generation Sequencing

Breast cancer, one of the most common diseases among women, is regarded as a heterogeneous and complicated disease that remains a major public health concern. Recently, owing to the development of next-generation sequencing technologies, long non-coding RNAs have received extensive attention. Numerous studies reveal that long non-coding RNAs are playing important roles in tumor development. Although the biological function and molecular mechanisms of long non-coding RNAs remain enigmatic, recent researchers have demonstrated that an array of long non-coding RNAs express abnormally in cancers, including breast cancer. Herein, we summarized the latest literature about long non-coding RNAs in breast cancer, with a particular focus on the multiple molecular roles of regulatory long non-coding RNAs that regulate cell proliferation, invasion, metastasis, and apoptosis.

scholarly journals Long Non-Coding RNA H19 Promotes Porcine Satellite Cell Differentiation by Interacting with TDP43

Genes ◽  
2020 ◽  
Vol 11 (3) ◽  
pp. 259
Author(s):  
Jingxuan Li ◽  
Wenjuan Zhao ◽  
Qianqian Li ◽  
Ziying Huang ◽  
Gaoli Shi ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Molecular Mechanisms ◽  
Rna Binding ◽  
Rna Binding Protein ◽  
Biological Processes ◽  
Non Coding Rna ◽  
Non Coding Rnas ◽  
Functional Analyses ◽  
Long Non Coding Rna

Long non-coding RNAs (lncRNAs) have been implicated in fundamental and diverse biological processes, including myogenesis. However, the molecular mechanisms involved in this process remain largely unexplored. This study found that H19 affected the differentiation of porcine satellite cells (PSCs) by directly binding to the DNA/RNA-binding protein TDP43. Functional analyses showed that TDP43 knockdown decreased PSC differentiation, whereas TDP43 overexpression exerted opposite effects in vitro. Furthermore, rescue experiments demonstrated that TDP43 can rescue the decrease in PSC differentiation caused by H19 knockdown. Mechanistically, H19 may act as a scaffold to recruit TDP43 to the promoters of MYOD and thereby activate the transcription of MYOD, leading to PSC differentiation. In summary, we elucidate the molecular mechanism by which H19 and TDP43 regulate myogenesis.

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