Long noncoding RNA DANCR regulates proliferation and migration by epigenetically silencing FBP1 in tumorigenesis of cholangiocarcinoma

Wang, Ni; Zhang, Chongguo; Wang, Wulin; Liu, Jie; Yu, Yang; Li, You; Zhang, Mingjiong; Ge, Xianxiu; Li, Quanpeng; Ma, Lin

doi:10.1038/s41419-019-1810-z

Cited by 43 publications

(30 citation statements)

References 54 publications

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“…One of which, the lncRNA ENSG00000226950, that has attracted the attention of several groups had previously been identified as a non-coding RNA associated with enhancer of zeste homolog 2 and was found to repress the runt related transcription factor 2 gene ( 81 ) and was called DANCR (Differentiation Antagonizing Non-Protein Coding RNA). The DANCR gene is bound by MYC when MYC is induced in the P493-6 cells in a time-dependent manner which is consistent with the findings of Hart et al ( 73 ) and other studies that followed DANCR expression in several tumors ( 82 – 89 ). Of interest here is the finding that DANCR plays a role in Acute Myeloid Leukemia (AML) ( 90 ).…”

Section: Myc Regulated Lncrnassupporting

confidence: 90%

Crosstalk Between MYC and lncRNAs in Hematological Malignancies

Arman

Möröy

2020

Front. Oncol.

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The human genome project revealed the existence of many thousands of long non-coding RNAs (lncRNAs). These transcripts that are over 200 nucleotides long were soon recognized for their importance in regulating gene expression. However, their poor conservation among species and their still controversial annotation has limited their study to some extent. Moreover, a generally lower expression of lncRNAs as compared to protein coding genes and their enigmatic biochemical mechanisms have impeded progress in the understanding of their biological roles. It is, however, known that lncRNAs engage in various kinds of interactions and can form complexes with other RNAs, with genomic DNA or proteins rendering their functional regulatory network quite complex. It has emerged from recent studies that lncRNAs exert important roles in gene expression that affect many cellular processes underlying development, cellular differentiation, but also the pathogenesis of blood cancers like leukemia and lymphoma. A number of lncRNAs have been found to be regulated by several well-known transcription factors including Myelocytomatosis viral oncogene homolog ( MYC ). The c-MYC gene is known to be one of the most frequently deregulated oncogenes and a driver for many human cancers. The c- MYC gene is very frequently activated by chromosomal translocations in hematopoietic cancers most prominently in B- or T-cell lymphoma or leukemia and much is already known about its role as a DNA binding transcriptional regulator. Although the understanding of MYC’s regulatory role controlling lncRNA expression and how MYC itself is controlled by lncRNA in blood cancers is still at the beginning, an intriguing picture emerges indicating that c-MYC may execute part of its oncogenic function through lncRNAs. Several studies have identified lncRNAs regulating c- MYC expression and c-MYC regulated lncRNAs in different blood cancers and have unveiled new mechanisms how these RNA molecules act. In this review, we give an overview of lncRNAs that have been recognized as critical in the context of activated c-MYC in leukemia and lymphoma, describe their mechanism of action and their effect on transcriptional reprogramming in cancer cells. Finally, we discuss possible ways how an interference with their molecular function could be exploited for new cancer therapies.

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Section: Myc Regulated Lncrnassupporting

confidence: 90%

Crosstalk Between MYC and lncRNAs in Hematological Malignancies

Arman

Möröy

2020

Front. Oncol.

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“…Recently, lncRNAs have gained great attention as its role in CCA 15 . Several known lncRNAs were reported to be dysregulated in CCA tissues and involved in the CCA development and progression, such as DANCR 16 , PVT1 17 , and RMRP 18 . Recent studies have reported that SNHG6 is highly expressed in variety of cancer tissues (except CCA) and .…”

Section: Discussionmentioning

confidence: 99%

Long noncoding RNA SNHG6 promotes proliferation and angiogenesis of cholangiocarcinoma cells through sponging miR-101-3p and activation of E2F8

Wang¹,

Wang²,

Tang³

et al. 2020

J. Cancer

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Cholangiocarcinoma (CCA) development is an extremely complex process with alterations occurring in numerous genes. SNHG6, a validated lncRNA, has been reported to regulate the expression of multiple tumor-related genes in hepatocellular carcinoma, colorectal cancer and breast cancer. Here, we elucidated the function and possible molecular mechanisms of SNHG6 in human CCA cells. Our results proved that the expression SNHG6 was upregulated in CCA tissues and cell lines. Ectopic expression of SNHG6 promoted cell proliferation, cell cycle progression, migration, and angiogenesis in CCA cells, whereas knockdown of SNHG6 repressed these cellular processes. Further mechanistic studies revealed that SNHG6 could compete with the transcription factor E2F8 to bind with miR-101-3p, thus affecting E2F8 expression. Taken together, these results provided a comprehensive analysis of the role of SNHG6 in CCA cells and offered important clues to understand the key roles of competing endogenous RNA (ceRNA) mechanisms in human cholangiocarcinoma.

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“…lncRNAs are able to regulate the proliferation, apoptosis, migration and invasion of human cancer cells [9,10]. For instance, lncRNA-DANCR regulates proliferation and migration by epigenetically silencing FBP1 in tumourigenesis of cholangiocarcinoma [11]. LncRNA-SNHG6 enhances cell proliferation, migration and invasion by regulating miR-26a-5p/MAPK6 in breast cancer [12].…”

Section: Introductionmentioning

confidence: 99%

Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

Hua

Deng

et al. 2020

J Exp Clin Cancer Res

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Background: Human ovarian cancer specific transcript 2 (HOST2) is a long non-coding RNA (lncRNA) reported to be specifically high expressed in human ovarian cancer. However, the mechanism that how HOST2 regulates triple negative breast cancer (TNBC) need to be explored. Methods: In this study, expression of HOST2 was determined in 40 TNBC patients and matched non-cancerous tissues by qRT-PCR and in situ hybridization (ISH) assay. The biological functions of HOST2 was measured by losing features. The effect of HOST2 on viability, proliferation and migration was evaluated by MTT, colony formation assay, EDU analysis, transwell invasion assay and nude mouse xenograft model. Fluorescence in situ hybridization (FISH), Luciferase report assay, RNA immunoprecipitation (RIP) assay and Western blot were fulfilled to measure molecular mechanisms. Results: The results showed that HOST2 was up-regulated in BC tissues and cell lines. Clinical outcome analysis demonstrated that high expression of HOST2 was associated with poor prognosis of TNBC patients. Functional experiments illustrated that knockdown of HOST2 significantly suppressed TNBC cell proliferation and migration. Western blot assays, qRT-PCR assays, RIP assays and luciferase reporter assays revealed that HOST2 regulated STAT3 via crosstalk with let-7b. Depression of HOST2 suppressed STAT3-mediated proliferation and migration in TNBC cells. HOST2 could function as a decoy of let-7b to depress expression of STAT3. Conclusions: HOST2 could function as a oncogene and promoted STAT3-mediated proliferation and migration through acting as a competing endogenous RNA, which might act as a potential biomarker for TNBC patients.

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Long noncoding RNA DANCR regulates proliferation and migration by epigenetically silencing FBP1 in tumorigenesis of cholangiocarcinoma

Cited by 43 publications

References 54 publications

Crosstalk Between MYC and lncRNAs in Hematological Malignancies

Crosstalk Between MYC and lncRNAs in Hematological Malignancies

Long noncoding RNA SNHG6 promotes proliferation and angiogenesis of cholangiocarcinoma cells through sponging miR-101-3p and activation of E2F8

Long noncoding RNA HOST2, working as a competitive endogenous RNA, promotes STAT3-mediated cell proliferation and migration via decoying of let-7b in triple-negative breast cancer

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