Long noncoding RNA expression profile of infantile hemangioma identified by microarray analysis

Liu, Xiaowen; Lv, Ruihua; Zhang, Linfeng; Xu, Guangqi; Bi, Jianhai; Gao, Feng; Zhang, Jian; Xue, Feng; Wang, Fagang; Wu, Yi-Liang; Fu, Cong; Wang, Qiang; Huo, Ran

doi:10.1007/s13277-016-5434-y

Cited by 30 publications

(44 citation statements)

References 60 publications

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“…Their qRT‐PCR and transwell assay results indicated that the knockdown of linc00152 prevents PDAC cell proliferation and invasion, thereby verifying the oncogenic property of linc00152. The involvement of linc00152 in cell proliferation has also been confirmed in gastric cancer, hepatocellular carcinoma (HCC), pancreatic cancer, clear cell renal cell carcinoma, colorectal cancer, breast cancer, and infantile hemangioma …”

Section: Molecular Functions and Mechanisms Of Linc00152 In Human Tumorsmentioning

confidence: 92%

“…The involvement of linc00152 in cell proliferation has also been confirmed in gastric cancer, [25][26][27][28][29][30][31][32] hepatocellular carcinoma (HCC), 11,20 pancreatic cancer, 33 clear cell renal cell carcinoma, 34 colorectal cancer, 35 breast cancer, 36 and infantile hemangioma. 37 Cao et al 26 applied a cDNA microarray to analyze the profiles of differentially expressed lncRNAs in 88 gastric cancer tissue samples and paired adjacent normal tissues. They detected 80 kinds of differentially expressed lncRNAs, of which the expression levels of linc00152 were particularly significantly different.…”

Section: Overexpression Of Linc00152 Enhances Cell Proliferation Imentioning

confidence: 99%

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Improved characterization of the relationship between long intergenic non‐coding RNA Linc00152 and the occurrence and development of malignancies

Guo

Jiang

et al. 2019

Cancer Medicine

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Linc00152, located on chromosome 2p11.2, is a long intergenic non‐coding RNA molecule with 828 nucleotides that is highly expressed in many types of human tumor tissues, especially in malignant tumors of the digestive system. Linc00152 promotes the occurrence and development of tumors by increasing tumor cell proliferation, invasion, metastasis, and apoptosis. Additionally, linc00152 contributes to the carcinogenesis of several cancers, including gastric cancer, liver cancer, hepatocellular carcinoma, gallbladder cancer, clear cell renal cell carcinoma, and colorectal cancer, by disturbing various signaling pathways (eg PI3K/AKT, mTOR, IL‐1, and NOTCH 1 signaling pathways). High linc00152 expression levels are associated with chemoresistance as well as poor prognosis and shorter survival. Continual advances made in the relevant research have indicated that linc00152 may be useful as a new tumor molecular biomarker, applicable for tumor diagnosis, targeted therapy, and prognosis assessment. This review summarizes the progress in the research into the relationship between linc00152 and the occurrence and development of malignancies based on molecular functions, regulatory mechanisms, and clinical applications.

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Section: Molecular Functions and Mechanisms Of Linc00152 In Human Tumorsmentioning

confidence: 92%

Section: Overexpression Of Linc00152 Enhances Cell Proliferation Imentioning

confidence: 99%

Improved characterization of the relationship between long intergenic non‐coding RNA Linc00152 and the occurrence and development of malignancies

Guo

Jiang

et al. 2019

Cancer Medicine

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“…Abnormal expression of lncRNAs is involved in the pathogenesis of various diseases. In recent years, many studies have used microarray technology to screen for differentially expressed lncRNAs in the occurrence of disease . Exploring the mechanism of disease regulation or new mechanisms have become common practice.…”

Section: Discussionmentioning

confidence: 99%

Aberrant expression of imprinted lncRNA MEG8 causes trophoblast dysfunction and abortion

Sheng

Sun

et al. 2019

J of Cellular Biochemistry

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Long noncoding RNAs (lncRNAs) are a group of noncoding RNAs whose nucleotides are longer than 200 bp. Previous studies have shown that they play an important regulatory role in many developmental processes and biological pathways. However, the contributions of lncRNAs to placental development are largely unknown. Here, our study aimed to investigate the lncRNA expression signatures in placental development by performing a microarray lncRNA screen. Placental samples were obtained from pregnant C57BL/6 female mice at three key developmental time points (embryonic day E7.5, E13.5, and E19.5). Microarrays were used to analyze the differential expression of lncRNAs during placental development. In addition to the genomic imprinting region and the dynamic DNA methylation status during placental development, we screened imprinted lncRNAs whose expression was controlled by DNA methylation during placental development. We found that the imprinted lncRNA Rian may play an important role during placental development. Its homologous sequence lncRNA MEG8 (RIAN) was abnormally highly expressed in human spontaneous abortion villi. Upregulation of MEG8 expression in trophoblast cell lines decreased cell proliferation and invasion, whereas downregulation of MEG8 expression had the opposite effect. Furthermore, DNA methylation results showed that the methylation of the MEG8 promoter region was increased in spontaneous abortion villi. There was dynamic spatiotemporal expression of imprinted lncRNAs during placental development. The imprinted lncRNA MEG8 is involved in the regulation of early trophoblast cell function. Promoter methylation abnormalities can cause trophoblastic cell defects, which may be one of the factors that occurs in early unexplained spontaneous abortion.

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“…Low expression of MEG3 acts as an independent factor for predicting poor prognosis in cancer patients [12,15,25,26], and the downregulation of MEG3 is attributed to its promoter hypermethylation in cancer [27][28][29], and the negative modulation by DNMT1 in glioma [30]. MEG3 and VEGF have the differential expression levels in HAs [5,18]. In the present study, we found that, MEG3 expression was decreased and harbored the negative association with VEGF expression in proliferating phase HAs rather than in the involuting phase HAs, suggesting that MEG3 might be a negative regulator of HAs proliferation.…”

Section: Discussionmentioning

confidence: 99%

“…LncRNA expression profiles have been used to identify the involvement of MEG3 in the pathogenesis of Infantile HAs [18]. In addition to the lncRNAs, microRNAs (miRNAs), a subgroup of ncRNAs with about 20 nucleotides that inhibit their target gene are differentially expressed in different phase HAs [19].…”

Section: Introductionmentioning

confidence: 99%

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

Dai

Wan

Qiu

et al. 2018

Cell Physiol Biochem

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Background/Aims: Dysregulation of long noncoding RNAs (lncRNAs) is associated with the proliferation and metastasis in a variety of cancers, of which lncRNA maternally expressed gene 3 (MEG3) has been indicated as a tumor suppressor in multiple malignancies. However, the underlying mechanisms by which MEG3 contributes to human hemangiomas (HAs) remain undetermined. Methods: qRT-PCR analysis was performed to examine the expression levels of MEG3 and VEGF in proliferating or involuting phase HAs. MTT, colony formation assay, flow cytometry analysis and a subcutaneous xenograft tumor model were conducted to assess the effects of MEG3 on the HAs tumorigenesis. The interaction between MEG3 and miRNAs or their downstream pathways was evidenced by bioinformatic analysis, luciferase report assays, RNA immunoprecipitation (RIP) assay. and Western blot analysis. Results: The expression of MEG3 was substantially decreased and had a negative correlation with VEGF expression in proliferating phase HAs, as compared with the involuting phase HAs and normal skin tissues. Ectopic expression of MEG3 suppressed cell proliferation, colony formation and induced cycle arrest in vitro and in vivo, followed by the downregulation of VEGF and cyclinD1, but knockdown of MEG3 reversed these effects. Furthermore, MEG3 was verified to act as a sponge of miR-494 in HAs cells, and miR-494 counteracted MEG3-caused anti-proliferative effects by regulating PTEN/PI3K/AKT pathway, and exhibited the negative correlation with MEG3 and PTEN expression in proliferating phase HAs. Conclusion: Our findings suggested that lncRNA MEG3 inhibited HAs tumorigenesis by sponging miR-494 and regulating PTEN/PI3K/AKT pathway.

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Long noncoding RNA expression profile of infantile hemangioma identified by microarray analysis

Cited by 30 publications

References 60 publications

Improved characterization of the relationship between long intergenic non‐coding RNA Linc00152 and the occurrence and development of malignancies

Improved characterization of the relationship between long intergenic non‐coding RNA Linc00152 and the occurrence and development of malignancies

Aberrant expression of imprinted lncRNA MEG8 causes trophoblast dysfunction and abortion

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

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