Long non-coding RNA MEG3 suppresses migration and invasion of thyroid carcinoma by targeting of Rac1

Wang, C; Yan, Guangqi; Zhang, Y; Jing, Xue; Bu, Pingyuan

doi:10.4149/neo_2015_065

Cited by 104 publications

(77 citation statements)

References 25 publications

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“…For example, maternal expressed gene 3 (MEG3) was the first lncRNA demonstrated to act as a tumor suppressor in melanoma cells (21). In PTC, MEG3 was upregulated in carcinoma tissues compared with normal tissues and suppressed migration and invasion by targeting Ras-related C3 botulinum toxin substrate 1 (22). Papillary thyroid carcinoma susceptibility candidate 3 acts as a tumor suppressor in thyroid cancer cells and leads to marked significant inhibition of proliferation, cell cycle arrest and increased apoptosis (23).…”

Section: Discussionmentioning

confidence: 99%

lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway

Wang

Lin

et al. 2018

Oncol Lett

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Abstract. Thyroid cancer is one of the most common types of cancer in the endocrine system. Among all types of thyroid cancer, papillary thyroid carcinoma (PTC) is the most common type of thyroid cancer. Long non-coding RNA (lncRNA) BRAF-activated non-protein-coding RNA (BANCR) is a 688-bp-long nucleotide transcript, which was first identified in melanoma. The function of BANCR in thyroid cancer remains unclear. The aim of the present study was to investigate whether BANCR is involved in the development of thyroid cancer. The results indicated that BANCR expression was increased in thyroid tumors compared with in adjacent normal tissues. Among cancer cell lines, the expression level of BANCR differed: BANCR expression in BCPAP cell lines was lower compared with that in CAL-62, WRO and FTC-133 cell lines. Overexpression of BANCR promoted the migration and invasion of BCPAP cells. Additionally, BANCR mediated epithelial-mesenchymal transition (EMT) by regulating the expression of epithelial (E)-cadherin, vimentin and neuronal (N)-cadherin. Overexpression of BANCR in BCPAP cells decreased the expression of E-cadherin and increased the expression of vimentin, N-cadherin, phospho (p)-c-Raf, p-extracellular-signal-regulated kinase (ERK)/mitogen activated protein kinase (MEK)1/2 and p-ERK1/2. Administration of U0126 inhibitor inhibited the regulation of phosphorylation levels by MEK1/2 and ERK1/2. Additionally, U0126 upregulated the expression of E-cadherin and downregulated the expression of vimentin. Taken together, the results of the present study suggest that BANCR induces EMT in PTC through the Raf/MEK/ERK signaling pathway.

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Section: Discussionmentioning

confidence: 99%

lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway

Wang

Lin

et al. 2018

Oncol Lett

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“…MEG3 is downregulated in PTC; downregulated MEG3 was significantly associated with lymph node metastasis. MEG3 is an important tumor suppressor in TC which suppresses migration and invasion by targeting Rac1 [48]. …”

Section: Maternally Expressed Genementioning

confidence: 99%

Long Non-Coding RNAs in Thyroid Cancer: Implications for Pathogenesis, Diagnosis, and Therapy

et al. 2019

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Thyroid cancer is a rare malignancy and accounts for less than 1% of malignant neoplasms in humans; however, it is the most common cancer of the endocrine system and responsible for most deaths from endocrine cancer. Long non-coding (Lnc)RNAs are defined as non-coding transcripts that are more than 200 nucleotides in length. Their expression deregulation plays an important role in the progress of cancer. These molecules are involved in physiologic cellular processes, genomic imprinting, inactivation of chromosome X, maintenance of pluripotency, and the formation of different organs via changes in chromatin, transcription, and translation. LncRNAs can act as a tumor suppressor genes or oncogenes. Several studies have shown that these molecules can interact with microRNAs and prevent their binding to messenger RNAs. Research has shown that these molecules play an important role in tumorigenicity, angiogenesis, proliferation, migration, apoptosis, and differentiation. In thyroid cancer, several lncRNAs (MALAT1, H19, BANCR, HOTAIR) have been identified as contributing factors to cancer development, and can be used as novel biomarkers for early diagnosis or even treatment. In this article, we study the newest lncRNAs and their role in thyroid cancer.

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“…A number of studies have demonstrated that lncRNA MEG3, a tumor suppressor gene, was down-regulated in various cancers and was associated with poor prognosis (14)(15)(16)(17)(18). A previous study indicated that the expression of lncRN A MEG3 was clearly lower in osteosarcoma tissues compared with adjacent non-tumor tissues (19).…”

Section: Introductionmentioning

confidence: 99%

“…Zhu et al suggested that MEG3 functions as a tumor suppressor in hepatoma cells through interacting with p53 protein (18). In addition to these studies, the role of MEG3 has been investigated in gallbladder cancer, NSCLC, neuroendocrine tumor, gastric cancer, thyroid carcinoma and so on (25,(14)(15)(16)(17). However, to the best of our knowledge, the potential roles of MEG3 in OS remain largely unknown.…”

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confidence: 99%

MEG3 long non-coding RNA prevents cell growth and metastasis of osteosarcoma

Zhang¹,

Cai²,

Li³

2018

BLL

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OBJECTIVE: This study aimed to investigate the role of long non-coding RNA MEG3 (lncRNA MEG3) in osteosarcoma (OS) and further explore the underlying molecular mechanism. MATERIALS AND METHODS: The expression profi les of MEG3 in OS cell lines and normal osteoblast cell line were detected by qRT-PCR. MEG3 was over-expressed in OS cell line by using LV-MEG3. MTT and colonyformation assays were applied for cell proliferation analysis. Cell migration assay was applied to investigate the cell migration ability. In addition, the expression levels of cell growth and metastasis related factors (Notch1, Hes1, TGF-β, N-cadheren and E-cadheren) were determined to illustrate the mechanisms. RESULTS: We found that compared with normal osteoblast hFOB1.19 cell line, MEG3 was signifi cantly downregulated in MG63 and U2OS cell lines, particularly in MG-63 cells. MEG3 was signifi cantly up-regulated in MG63 cells by LV-MEG3. Cell proliferation and migration ability were obviously repressed by MEG3 over-expression. In addition, MEG3 over-expression markedly inhibited Notch1, Hes1,TGF-β and N-cadheren expression, and the expression level of E-cadheren was improved. CONCLUSIONS: These results indicated that MEG3 could prevent cell growth and metastasis of OS by repressing Notch and TGF-β signaling pathway, thus providing a potential therapeutic target for OS treatment (Tab. 1, Fig. 4, Ref. 30). Text in PDF www.elis.sk.

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Long non-coding RNA MEG3 suppresses migration and invasion of thyroid carcinoma by targeting of Rac1

Cited by 104 publications

References 25 publications

lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway

lncRNA BANCR promotes EMT in PTC via the Raf/MEK/ERK signaling pathway

Long Non-Coding RNAs in Thyroid Cancer: Implications for Pathogenesis, Diagnosis, and Therapy

MEG3 long non-coding RNA prevents cell growth and metastasis of osteosarcoma

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