Targeting LncRNA-MALAT1 suppresses the progression of osteosarcoma by altering the expression and localization of β-catenin

Zhang, Zhichang; Tang, Cheng-Wei; Dong, Yang; Zhang, Jing; Yuan, Ting; Li, Xin

doi:10.7150/jca.22113

Cited by 42 publications

(30 citation statements)

References 75 publications

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“…This would enable clearance of osteosarcoma cells from the body by the immune system. Therefore, lncMALAT1 was individually correlated with immune system activity and overall survival [ 56 ]. LncRNAs cannot encode proteins but do regulate gene expression at different levels, including through epigenetic, transcriptional or posttranscriptional regulation [ 57 ].…”

Section: Discussionmentioning

confidence: 99%

Molecular characterization of breast cancer: a potential novel immune-related lncRNAs signature

et al. 2020

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Background Accumulating evidence has demonstrated that immune-related lncRNAs (IRLs) are commonly aberrantly expressed in breast cancer (BC). Thus, we aimed to establish an IRL-based tool to improve prognosis prediction in BC patients. Methods We obtained IRL expression profiles in large BC cohorts (N = 911) from The Cancer Genome Atlas (TCGA) database. Then, in light of the correlation between each IRL and recurrence-free survival (RFS), we screened prognostic IRL signatures to construct a novel RFS nomogram via a Cox regression model. Subsequently, the performance of the IRL-based model was evaluated through discrimination, calibration ability, risk stratification ability and decision curve analysis (DCA). Results A total of 52 IRLs were obtained from TCGA. Based on multivariate Cox regression analyses, four IRLs (A1BG-AS1, AC004477.3, AC004585.1 and AC004854.2) and two risk parameters (tumor subtype and TNM stage) were utilized as independent indicators to develop a novel prognostic model. In terms of predictive accuracy, the IRL-based model was distinctly superior to the TNM staging system (AUC: 0.728 VS 0.673, P = 0.010). DCA indicated that our nomogram had favorable clinical practicability. In addition, risk stratification analysis showed that the IRL-based tool efficiently divided BC patients into high- and low-risk groups (P < 0.001). Conclusions A novel IRL-based model was constructed to predict the risk of 5-year RFS in BC. Our model can improve the predictive power of the TNM staging system and identify high-risk patients with tumor recurrence to implement more appropriate treatment strategies.

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Section: Discussionmentioning

confidence: 99%

Molecular characterization of breast cancer: a potential novel immune-related lncRNAs signature

et al. 2020

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“…In recent years, accumulating evidence has suggested a positive association between MALAT1 and the progres-sion of OS ( 33 ). For instance, MALAT1 silencing delayed the progression of OS by altering the expression and localization of β-catenin ( 34 ). Additionally, high serum levels of MALAT1 predicted poor survival in OS patients; overexpression of MALAT1 promoted cell metastasis and decreased E-cadherin levels by associating with enhancer of zeste homolog 2 ( 35 ).…”

Section: Discussionmentioning

confidence: 99%

Knockdown of MALAT1 inhibits osteosarcoma progression via regulating the miR‑34a/cyclin D1 axis

Duan

Zhang

et al. 2018

Int J Oncol

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Long non-coding (lnc)RNAs have been demonstrated to be involved in the development of various types of cancers, such as osteosarcoma (OS). Long non-coding (lnc) RNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) expression was reported to be highly expressed in OS and promoted the development of this disease; however, the underlying molecular mechanism by which MALAT1 promotes the progression of OS requires further investigation. In the present study, the expression of MALAT1 and miR-34a was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). The abundance of cyclin D1 (CCND1) was detected by RT-qPCR and western blotting. Cell viability, migration and invasion were examined by MTT and Transwell assays. The interaction between miR-34a and MALAT1 or CCND1 was probed by a dual luciferase reporter assay and RNA immunoprecipitation. Xenograft tumor assay was performed to verify the roles of MALAT1 and miR-34a in tumor growth in vivo. The results demonstrated that MALAT1 and CCND1 mRNA expression levels were upregulated and miR-34a was downregulated in OS tissues and cells. Additionally, MALAT1 expression was correlated with tumor size, clinical stage and distant metastasis in patients with OS. In addition, MALAT1 promoted OS cell viability, invasion and migration, while MALAT1 silencing exhibited opposing effects. Moreover, MALAT1 functioned as a ceRNA to suppress miR-34a expression and in turn upregulate CCND1 in OS cells. Rescue experiments further demonstrated that MALAT1 knockdown partially reversed anti-miR-34a-mediated promotion on OS cell viability, migration and invasion; overexpression of CCND1 partially reversed the effects of MALAT1 silencing on OS progression. Furthermore, in vivo experiments also revealed that MALAT1 promoted OS tumor growth via miR-34a inhibition and upregulating the expression of CCND1. In conclusion, the present study suggested that MALAT1 exerted its oncogenic function in OS by regulating the miR-34a/CCND1 axis in OS, which may provide novel insight into the diagnosis and therapy for OS.

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“…For example, MALAT-1 can act as a competing endogenous RNA (ceRNA) for various miRNAs including miR-1, miR-200c, miRNA-204, and miR-205 resulting in the subsequent promotion of EMT [ 103 , 104 , 105 , 106 ]. Another mechanism by which MALAT-1 induces EMT is via the recruitment of the PRC2 components Suz12 and EZH2 to regulate E-Cadherin [ 105 , 107 ] and β-catenin [ 108 , 109 ].…”

Section: Resultsmentioning

confidence: 99%

In Silico and In Vitro Analyses of LncRNAs as Potential Regulators in the Transition from the Epithelioid to Sarcomatoid Histotype of Malignant Pleural Mesothelioma (MPM)

Singh

Heery

Gray

2018

IJMS

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Malignant pleural mesothelioma (MPM) is a rare malignancy, with extremely poor survival rates. At present, treatment options are limited, with no second line chemotherapy for those who fail first line therapy. Extensive efforts are ongoing in a bid to characterise the underlying molecular mechanisms of mesothelioma. Recent research has determined that between 70–90% of our genome is transcribed. As only 2% of our genome is protein coding, the roles of the remaining proportion of non-coding RNA in biological processes has many applications, including roles in carcinogenesis and epithelial–mesenchymal transition (EMT), a process thought to play important roles in MPM pathogenesis. Non-coding RNAs can be separated loosely into two subtypes, short non-coding RNAs (<200 nucleotides) or long (>200 nucleotides). A significant body of evidence has emerged for the roles of short non-coding RNAs in MPM. Less is known about the roles of long non-coding RNAs (lncRNAs) in this disease setting. LncRNAs have been shown to play diverse roles in EMT, and it has been suggested that EMT may play a role in the aggressiveness of MPM histological subsets. In this report, using both in vitro analyses on mesothelioma patient material and in silico analyses of existing RNA datasets, we posit that various lncRNAs may play important roles in EMT within MPM, and we review the current literature regarding these lncRNAs with respect to both EMT and MPM.

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Targeting LncRNA-MALAT1 suppresses the progression of osteosarcoma by altering the expression and localization of β-catenin

Cited by 42 publications

References 75 publications

Molecular characterization of breast cancer: a potential novel immune-related lncRNAs signature

Molecular characterization of breast cancer: a potential novel immune-related lncRNAs signature

Knockdown of MALAT1 inhibits osteosarcoma progression via regulating the miR‑34a/cyclin D1 axis

In Silico and In Vitro Analyses of LncRNAs as Potential Regulators in the Transition from the Epithelioid to Sarcomatoid Histotype of Malignant Pleural Mesothelioma (MPM)

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