Downregulated long non-coding RNA MEG3 in breast cancer regulates proliferation, migration and invasion by depending on p53’s transcriptional activity

Sun, Li‐Zhong; Li, Yu; Yang, Bangxiang

doi:10.1016/j.bbrc.2016.05.031

Cited by 94 publications

(90 citation statements)

References 24 publications

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“…Re-constitution of MEG3 led to a decrease in cell proliferation and elevated apoptosis of lung cancer cells [23]. Another investigation demonstrated MEG3 suppressed breast cancer cells proliferation, colony formation, migration, and invasion capacities [24]. Further, MEG3 has been found to induce prostate cancer cells apoptosis via reducing the protein expression of Bcl-2, enhancing Bax, and activating caspase-3, as well as to induced cell cycle arrest in G0/G1 phase by suppressing Cyclin D1 [25].…”

Section: Discussionmentioning

confidence: 99%

MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183

Zhang

Feng

2017

Cell Physiol Biochem

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Background/Aims: Pancreatic neuroendocrine tumors (pNETs) are rare neoplasms which arise from pancreatic islet cells. Recently, lncRNA MEG3 has been reported as a tumor suppressor in variety cancers. This study aimed to reveal the functional effects of MEG3 on pNETs which has not been uncovered previously. Methods: The expression of MEG3, miR-183, and BRI3 in BON1 cells were altered by transfection with their specific vectors/shRNA, or mimic/inhibitor. Thereafter, cell viability, apoptosis, the protein expressions of cell cycle related factors, and apoptosis associated factors, as well as cell migration and invasion were respectively assessed by typan blue staining, flow cytometry, western blotting, and transwell assay. Results: MEG3 was low expressed in BON1 and QGP-1 cells, when compared to three normal cell lines (HEK293, CCL-153, and EC-304). MEG3 overexpression decreased BON1 cells viability, invasion, migration, but significantly induced apoptosis. miR-183 was a direct target of MEG3, and miR-183 up-regulation abolished the anti-growth and anti-metastasis effects of MEG3 overexpression on BON1 cells. Moreover, BRI3 was a target of miR-183, and BRI3 exhibited a tumor-promoting role possibly via activation of p38/ERK/AKT and Wnt/β-Catenin signaling in BON1 cells. Conclusion: This study demonstrated a tumor suppressive effect of MEG3 in BON1 cells that suppresses tumor cells growth and metastasis. A novel regulatory mechanism has been revealed that modulation of MEG3/miR-183/BRI3 axis may be pivotal in pNET.

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Section: Discussionmentioning

confidence: 99%

MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183

Zhang

Feng

2017

Cell Physiol Biochem

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“…MEG3 inhibits NSCLC cell proliferation and induces apoptosis by up-regulating TP53 expression [97,98]. As with NSCLC, downregulated MEG3 in breast cancer also regulates proliferation, migration, and invasion by depending on the transcriptional activity of TP53 [99]. …”

Section: Lncrnas and Lung Cancermentioning

confidence: 99%

Major Tumor Suppressor and Oncogenic Non-Coding RNAs: Clinical Relevance in Lung Cancer

Inamura

2017

Cells

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Lung cancer is the leading cause of cancer deaths worldwide, yet there remains a lack of specific and sensitive tools for early diagnosis and targeted therapies. High-throughput sequencing techniques revealed that non-coding RNAs (ncRNAs), e.g., microRNAs and long ncRNAs (lncRNAs), represent more than 80% of the transcribed human genome. Emerging evidence suggests that microRNAs and lncRNAs regulate target genes and play an important role in biological processes and signaling pathways in malignancies, including lung cancer. In lung cancer, several tumor suppressor/oncogenic microRNAs and lncRNAs function as biomarkers for metastasis and prognosis, and thus may serve as therapeutic tools. In this review, recent work on microRNAs and lncRNAs is introduced and briefly summarized with a focus on potential biological and therapeutic applications.

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“…Maternally Expressed Gene 3 (MEG3), a tumor suppressor, is involved in the development and progression of many cancers [47–49]. MEG3 is an imprinted gene located at chromosome 14q32 that encodes a 1.6-kb noncoding RNA from the maternal allele [50].…”

Section: Lncrnas In Hncmentioning

confidence: 99%

“…MEG3 is an imprinted gene located at chromosome 14q32 that encodes a 1.6-kb noncoding RNA from the maternal allele [50]. It is broadly distributed in many normal human tissues; however, MEG3 is not expressed in a series of human tumors and tumor cell lines, such as tongue squamous-cell carcinoma (TSCC), brain cancer, and hepatocellular cancer [47, 48, 51]. One of the main mechanisms of MEG3 silencing is hypermethylation of the MEG3 promoter region [52].…”

Section: Lncrnas In Hncmentioning

confidence: 99%

Long noncoding RNAs in head and neck cancer

Cao

Gong

et al. 2016

Oncotarget

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Head and neck cancers (HNCs) include a series of malignant tumors arising in epithelial tissues, typically oral cancer, laryngeal cancer, nasopharynx cancer and thyroid cancer. HNCs are important contributors to cancer incidence and mortality, leading to approximately 225,100 new patients and 77,500 deaths in China every year. Determination of the mechanisms of HNC carcinogenesis and progression is an urgent priority in HNC treatment. Long noncoding RNAs (lncRNAs) are noncoding RNAs longer than 200 bps. lncRNAs have been reported to participate in a broad scope of biological processes, and lncRNA dysregulation leads to diverse human diseases, including cancer. In this review, we focus on lncRNAs that are dysregulated in HNCs, summarize the latest findings regarding the function and molecular mechanisms of lncRNAs in HNC carcinogenesis and progression, and discuss the clinical application of lncRNAs in HNC diagnosis, prognosis and therapy.

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Downregulated long non-coding RNA MEG3 in breast cancer regulates proliferation, migration and invasion by depending on p53’s transcriptional activity

Cited by 94 publications

References 24 publications

MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183

MEG3 Suppresses Human Pancreatic Neuroendocrine Tumor Cells Growth and Metastasis by Down-Regulation of Mir-183

Major Tumor Suppressor and Oncogenic Non-Coding RNAs: Clinical Relevance in Lung Cancer

Long noncoding RNAs in head and neck cancer

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