lncRNA MEG3 Suppresses the Tumorigenesis of Hemangioma by Sponging miR-494 and Regulating PTEN/ PI3K/AKT Pathway

Dai, Yuxin; Wan, Yao; Qiu, Mingke; Wang, Shuqing; Pan, Chang; Wang, Yan; Ou, Jingmin

doi:10.1159/000496040

Cited by 29 publications

(15 citation statements)

References 39 publications

(64 reference statements)

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“…In addition, lncRNAs were also indicated to function as negative regulators on HA proliferation. LncRNA MEG3 (maternally expressed gene 3), a 1.6 kb intergenic lncRNA, can inhibit human HA tumorigenesis by sponging miR‐494 and regulating PTEN/PI3K/AKT pathway . However, the expression of MEG3 was obviously downregulated in proliferating phase human HAs, which eventually promoted the development of HAs.…”

Section: The Critical Role Of Lncrnas In Cutaneous Proliferation‐relamentioning

confidence: 99%

Long non‐coding RNAs in cutaneous biology and proliferative skin diseases: Advances and perspectives

et al. 2019

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Advances in transcriptome sequencing have revealed that the genome fraction largely encodes for thousands of non‐coding RNAs. Long non‐coding RNAs (lncRNAs), which are a class of non–protein‐coding RNAs longer than approximately 200 nucleotides in length, are emerging as key epigenetic regulators of gene expression recently. Intensive studies have characterized their crucial roles in cutaneous biology and diseases. In this review, we address the promotive or suppressive effects of lncRNAs on cutaneous physiological processes. Then, we focus on the pathogenic role of dysfunctional lncRNAs in a variety of proliferative skin diseases. These evidences suggest that lncRNAs have indispensable roles in the processes of skin biology. Additionally, lncRNAs might be promising biomarkers and therapeutic targets for cutaneous disorders.

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Section: The Critical Role Of Lncrnas In Cutaneous Proliferation‐relamentioning

confidence: 99%

Long non‐coding RNAs in cutaneous biology and proliferative skin diseases: Advances and perspectives

et al. 2019

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“…Long non-coding RNAs (lncRNAs) are a set of noncoding transcripts more than 200 nucleotides in length that are often related to proliferation and migration in multiple types of tumours. 4 lncRNAs act as signaling molecules, scaffolds, and instructors, and exert their influence at several levels including transcription, post-transcription, and translation. 5 In recent years, abundant evidence has revealed that anomalous expression of lncRNAs such as HOXD-AS1, H19, CASC9, and NORAD [6][7][8][9] may drive the pathogenesis of breast cancer.…”

Section: Introductionmentioning

confidence: 99%

<p>lncRNA NEAT1 Facilitates Cell Proliferation, Invasion and Migration by Regulating CBX7 and RTCB in Breast Cancer</p>

Yan

Zhang

Yin

et al. 2020

OTT

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To investigate the association between the lncRNA NEAT1 and breast cancer, and to determine the influence of NEAT1 on regulation of other signaling molecules in breast cancer. Methods: In the present study, we measured levels of the lncRNA NEAT1 in 106 breast cancer patients and in a human breast cancer cell line by qRT-PCR. The correlation between NEAT1 expression and patients' clinical characteristics was analyzed with in-house and TCGA data. We used cellular functioning assays and cell immunofluorescence assay to evaluate the role of NEAT1 and its target molecules in proliferation, invasion and migration in breast cancer. We used Western blotting to explore possible targets of NEAT1 and a subcellular fractionation assay to locate NEAT1 expression. Results: NEAT1 was overexpressed in breast cancer tissue and also closely related to advanced clinical stages and positive lymph node metastases. NEAT1 levels were also tightly correlated to prognosis for breast cancer patients in survival analyses. Cellular function assays revealed that downregulation of NEAT1 could inhibit breast cancer cell viability, invasion and migration. Western blotting revealed down-regulation of CBX7 and upregulation of RTCB following NEAT1 inhibition. Based on the cytoplasmic and nuclear expression of NEAT1, we investigated the possible regulation of CBX7 and RTCB by NEAT1. Results showed that NEAT1 regulated the expression of CBX7 and RTCB, possibly by binding of NEAT1 to DNA in the nucleus, which facilitates cell proliferation, invasion and migration. Conclusion: The current results suggest that the lncRNA NEAT1 is upregulated in breast cancer and facilitates tumor cell viability, invasion and migration via CBX7 and RTCB.

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“…For example, lncRNA DLX6-AS1 promotes liver cancer by increasing the expression of WEE1 via targeting miR-424-5p [12]; lncRNA MORT overexpression inhibits cancer cell proliferation in oral squamous cell carcinoma by downregulating ROCK1 [13]; lncRNAGIHCG induces cancer progression and chemoresistance and indicates poor prognosis in colorectal cancer [14].It has been found that lncRNA maternally expressed gene 3 (MEG3) with tumor suppressor activity was frequently either lost, mutated or decreased level in many human tumors and tumor derived cell lines [15]. For instance, lncRNA MEG3 inhibits the progression of prostate cancer by modulating miR-9-5p/QKI-5 axis [16]; Down regulation of lncRNA MEG3 promotes colorectal adenocarcinoma cell proliferation and inhibits the apoptosis by up-regulating TGF-β1 and its downstream sphingosine kinase 1 (SPHK1) [17]; lncRNA MEG3 suppresses the tumorigenesis of hemangioma by sponging miR-494 and regulating PTEN/PI3K/ AKT pathway [18]. Additionally, lncRNA MEG3 was also explored in the development of melanoma, e.g., lncRNAMEG3 suppresses the proliferation and invasion of melanoma by regulating CYLD expression mediated by sponging miR-499-5p [19].…”

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confidence: 99%

LncRNA MEG3 promotes melanoma growth, metastasis and formation through modulating miR-21/E-cadherin axis

Zhu

et al. 2020

Cancer Cell Int

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Background: Melanoma is the most aggressive type of skin cancer with high mortality rate and poor prognosis. lncRNA MEG3, a tumor suppressor, is closely related to the development of various cancers. However, the role of lncRNA MEG3 in melanoma has seldom been studied. Methods: RT-PCR was used to examine the expressions of lncRNA MEG3 and E-cadherin in melanoma patients and cell lines. Then, the biological functions of lncRNA MEG3 and E-cadherin were demonstrated by transfecting lncRNA MEG3-siRNA, lncRNA MEG3-overexpression, E-cadherin-siRNA and E-cadherin-overexpression plasmids in melanoma cell lines. Moreover, CCK8 assay and colony formation assay were utilized to assess the cell proliferation; Transwell assay was performed to evaluate the cell invasive ability; and tumor xenografts in nude mice were applied to test the tumor generation. Additionally, the target interactions among lncRNA MEG3, miR-21 and E-cadherin were determined by dual luciferase reporter assay. Finally, RT-PCR and WB were further conducted to verify the regulatory roles among lncRNA MEG3, miR-21 and E-cadherin. Results: The clinical data showed that lncRNA MEG3 and E-cadherin expressions were both declined in carcinoma tissues as compared with their para-carcinoma tissues. Moreover, lncRNA MEG3 and E-cadherin expressions in B16 cells were also higher than those in A375 and A2058 cells. Subsequently, based on the differently expressed lncRNA MEG3 and E-cadherin in these human melanoma cell lines, we chose B16, A375 and A2058 cells for the following experiments. The results demonstrated that lncRNA MEG3 could suppress the tumor growth, tumor metastasis and formation; and meanwhile E-cadherin had the same effects on tumor growth, tumor metastasis and formation. Furthermore, the analysis of Kaplan-Meier curves also confirmed that there was a positive correlation between lncRNA MEG3 and E-cadherin. Ultimately, dual luciferase assays were further used to verify that lncRNA MEG3 could directly target miR-21 which could directly target E-cadherin in turn. Additionally, the data of RT-PCR and WB revealed that knockdown of lncRNA MEG3 in B16 cells inhibited miR-21 expression and promoted E-cadherin expression, but overexpression of lncRNA MEG3 in A375 and A2058 cells presented completely opposite results. Conclusion: Our findings indicated that lncRNA MEG3 might inhibit the tumor growth, tumor metastasis and formation of melanoma by modulating miR-21/E-cadherin axis.

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lncRNA MEG3 Suppresses the Tumorigenesis of Hemangioma by Sponging miR-494 and Regulating PTEN/ PI3K/AKT Pathway

Cited by 29 publications

References 39 publications

Long non‐coding RNAs in cutaneous biology and proliferative skin diseases: Advances and perspectives

Long non‐coding RNAs in cutaneous biology and proliferative skin diseases: Advances and perspectives

<p>lncRNA NEAT1 Facilitates Cell Proliferation, Invasion and Migration by Regulating CBX7 and RTCB in Breast Cancer</p>

LncRNA MEG3 promotes melanoma growth, metastasis and formation through modulating miR-21/E-cadherin axis

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