Long noncoding RNA MEG3 plays a promoting role in the proliferation, invasion, and angiogenesis of lung adenocarcinoma cells through the AKT pathway

Li, Hui; Wang, Jue; Liu, Shuang; Zhang, Ying; Zhang, Cuiying; Lige, Baya; Su, Dan; Sun, Yanyan

doi:10.1002/jcb.28895

Cited by 12 publications

(8 citation statements)

References 28 publications

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“…Guan et al [ 25 ] reported that LINC00673-v4 apparently enhanced cell migration, invasiveness and metastasis in LUAD. Li et al [ 26 ] reported that lncRNA MEG3 showed a high expression profile in LUAD tissues and some specific cell lines, which predicted lower survival probabilities in LUAD patients. In addition, entopic expression of MEG3 significantly promoted cell proliferation, invasion and angiogenesis.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of LINC00665 suppresses the progression of lung adenocarcinoma via regulating miR-181c-5p/ZIC2 axis

Wei

Zhao

Liu

et al. 2021

Aging

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Long non-coding RNA (lncRNA) LINC00665 was demonstrated to be upregulated in lung adenocarcinoma (LUAD) and target miR-181c-5p. ZIC2, which is upregulated in LUAD, serves as a putative target of miR-181c-5p. In this study, we aimed to reveal whether LINC00665 regulates miR-181c-5p/ZIC2 axis to promote LUAD progression. The results showed that LINC00665, HOXA1, ZIC2, and HOXA11 levels were increased in LUAD tissues, while miR-181c-5p level was decreased when compared to the adjacent normal tissues. High expression levels of LINC00665, ZIC2, HOXA1 and HOXA11, and low expression of miR-181c-5p were closely linked to poor prognosis of LUAD patients. Knockdown of LINC00665 induced obvious inhibitions in cell viability, clone formation, invasion and tumorigenesis in LUAD cells, whereas miR-181c-5p downregulation significantly neutralized these effects. In addition, downregulation of ZIC2 obviously reversed the enhancements of cell viability, clone formation, invasion and tumorigenesis induced by miR-181c-5p knockdown. In summary, the present study reveals that silencing of LINC00665 suppresses LUAD progression through targeting miR-181c-5p/ZIC2 axis.

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Section: Discussionmentioning

confidence: 99%

Downregulation of LINC00665 suppresses the progression of lung adenocarcinoma via regulating miR-181c-5p/ZIC2 axis

Wei

Zhao

Liu

et al. 2021

Aging

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“…MiR-137 acts as a negative regulator of the C-X-C motif chemokine, which participates in gastric cancer progression [109]. The loss of maternally expressed gene 3 (MEG3), which encodes a tumor-suppressive lncRNA, is associated with tumorigenesis in many cancer types as it mediates various cellular factors and pathways, such as p53, proangiogenic genes, or miRNAs [4,105]. Ye and colleagues [106] investigated a regulatory axis of lncRNA MEG3, miR-421, and the growth factor platelet-derived growth factor receptor α (PDGFRA) by binding to each other.…”

Section: Reproductive System Cancermentioning

confidence: 99%

“…Mechanistically, linc00665 stabilizes YB-1 protein from degradation, hence activating VEGF expression, leading to increased angiogenesis in vitro and in vivo [44]. In contrast to the detected downregulation of MEG3 in lung cancer, Li et al [105] published data detecting an enhanced expression of MEG3 in lung adenocarcinoma, promoting VEGF-mediated angiogenesis by activating Akt signaling. This hypothesis proposes MEG3 as a cell-specific angiogenesis promotor, as Lui and colleagues [115] detected a significant downregulation of MEG3 in lung adenocarcinoma.…”

Section: Lung Cancermentioning

confidence: 99%

Involvement of Long Non-Coding RNAs (lncRNAs) in Tumor Angiogenesis

Teppan

Barth

Prinz

et al. 2020

ncRNA

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Long non-coding RNAs (lncRNAs) are defined as non-protein coding transcripts with a minimal length of 200 nucleotides. They are involved in various biological processes such as cell differentiation, apoptosis, as well as in pathophysiological processes. Numerous studies considered that frequently deregulated lncRNAs contribute to all hallmarks of cancer including metastasis, drug resistance, and angiogenesis. Angiogenesis, the formation of new blood vessels, is crucial for a tumor to receive sufficient amounts of nutrients and oxygen and therefore, to grow and exceed in its size over the diameter of 2 mm. In this review, the regulatory mechanisms of lncRNAs are described, which influence tumor angiogenesis by directly or indirectly regulating oncogenic pathways, interacting with other transcripts such as microRNAs (miRNAs) or modulating the tumor microenvironment. Further, angiogenic lncRNAs occurring in several cancer types such as liver, gastrointestinal cancer, or brain tumors are summarized. Growing evidence on the influence of lncRNAs on tumor angiogenesis verified these transcripts as potential predictive or diagnostic biomarkers or therapeutic targets of anti-angiogenesis treatment. However, there are many unsolved questions left which are pointed out in this review, hence driving comprehensive research in this area is necessary to enable an effective use of lncRNAs as either therapeutic molecules or diagnostic targets in cancer.

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“…Tano et al suggested that MALAT1 enhances cell motility of lung adenocarcinoma cells by influencing the expression of motility-related genes [40]. Li et al confirmed that MEG3 plays a promoting role in the proliferation, invasion, and angiogenesis of lung adenocarcinoma cells through the AKT pathway [41]. Liu et al reasoned that H19 promotes viability and epithelial-mesenchymal transition of lung adenocarcinoma cells by targeting miR-29b-3p and modifying STAT3 [42].…”

Section: Case Studiesmentioning

confidence: 99%

IDSSIM: an lncRNA functional similarity calculation model based on an improved disease semantic similarity method

et al. 2020

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Background: It has been widely accepted that long non-coding RNAs (lncRNAs) play important roles in the development and progression of human diseases. Many association prediction models have been proposed for predicting lncRNA functions and identifying potential lncRNA-disease associations. Nevertheless, among them, little effort has been attempted to measure lncRNA functional similarity, which is an essential part of association prediction models. Results: In this study, we presented an lncRNA functional similarity calculation model, IDSSIM for short, based on an improved disease semantic similarity method, highlight of which is the introduction of information content contribution factor into the semantic value calculation to take into account both the hierarchical structures of disease directed acyclic graphs and the disease specificities. IDSSIM and three state-of-the-art models, i.e., LNCSIM1, LNCSIM2, and ILNCSIM, were evaluated by applying their disease semantic similarity matrices and the lncRNA functional similarity matrices, as well as corresponding matrices of human lncRNA-disease associations coming from either lncRNADisease database or MNDR database, into an association prediction method WKNKN for lncRNA-disease association prediction. In addition, case studies of breast cancer and adenocarcinoma were also performed to validate the effectiveness of IDSSIM. Conclusions: Results demonstrated that in terms of ROC curves and AUC values, IDSSIM is superior to compared models, and can improve accuracy of disease semantic similarity effectively, leading to increase the association prediction ability of the IDSSIM-WKNKN model; in terms of case studies, most of potential diseaseassociated lncRNAs predicted by IDSSIM can be confirmed by databases and literatures, implying that IDSSIM can serve as a promising tool for predicting lncRNA functions, identifying potential lncRNA-disease associations, and pre-screening candidate lncRNAs to perform biological experiments. The IDSSIM code, all experimental data and prediction results are available online at https://github.com/ CDMB-lab/IDSSIM.

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Long noncoding RNA MEG3 plays a promoting role in the proliferation, invasion, and angiogenesis of lung adenocarcinoma cells through the AKT pathway

Cited by 12 publications

References 28 publications

Downregulation of LINC00665 suppresses the progression of lung adenocarcinoma via regulating miR-181c-5p/ZIC2 axis

Downregulation of LINC00665 suppresses the progression of lung adenocarcinoma via regulating miR-181c-5p/ZIC2 axis

Involvement of Long Non-Coding RNAs (lncRNAs) in Tumor Angiogenesis

IDSSIM: an lncRNA functional similarity calculation model based on an improved disease semantic similarity method

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