The functions of long noncoding RNAs in development and stem cells

Perry, Rotem Ben-Tov; Ulitsky, Igor

doi:10.1242/dev.140962

Cited by 180 publications

(133 citation statements)

References 139 publications

(185 reference statements)

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“…Moreover, lncRNAs have been identified as new modulators in the origination and progression of glioma [6]. Mounting evidence has also demonstrated that lncRNAs involved in the regulation of gene expression in stem cell biology and in tumorigenesis [7]. …”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway

et al. 2017

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BackgroundGlioma is one of the most frequent intracranial malignant tumors. LncRNAs have been identified as new modulators in the origination and progression of glioma.MethodsQuantitative real-time PCR were conducted to evaluate the expression of linc00152 and miRNA-103a-3p in glioma tissues and cells. Western blot were used to determine the expression of FEZF1 and CDC25A in glioma tissues and cells. Stable knockdown of linc00152 or over-expression of miR-103a-3p in glioma stem cells (GSCs) were established to explore the function of linc00152 and miR-103a-3p in GSCs. Further, luciferase reports were used to investigate the correlation between linc00152 and miR-103a-3p. Cell Counting Kit-8, transwell assays, and flow cytometry were used to investigate the function of linc00152 and miR-103a-3p in GSC malignant biological behaviors. ChIP assays were employed to ascertain the correlations between FEZF1 and CDC25A.ResultsLinc00152 was up-regulated in glioma tissues as well as in GSCs. Knockdown of linc00152 inhibited cell proliferation, migration and invasion, while promoted GSC apoptosis. Linc00152 regulated the malignant behavior of GSCs by binding to miR-103a-3p, which functions as a tumor suppressor. In addition, knockdown of linc00152 down-regulated forebrain embryonic zinc finger protein 1 (FEZF1), a direct target of miR-103a-3p which played an oncogenic role in GSCs. FEZF1 elevated promoter activities and up-regulated expression of the oncogenic gene cell division cycle 25A (CDC25A). CDC25A over-expression activated the PI3K/AKT pathways, which regulated the malignant behavior of GSCs.ConclusionsLinc00152/miR-103a-3p/FEZF1/CDC25A axis plays a novel role in regulating the malignant behavior of GSCs, which may be a new potential therapeutic strategy for glioma therapy.Electronic supplementary materialThe online version of this article (doi:10.1186/s12943-017-0677-9) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway

et al. 2017

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“…LncRNAs are very abundant with estimates of 430 000 lncRNAs transcripts in the human genome. [71][72][73][74][75][76][77] One group of investigators estimated that there were close to 60 000 lncRNAs including 8000 oncologic lncRNAs. 74 A growing number of these lncRNAs are being isolated and characterized from thyroid and other cancers.…”

Section: Non-coding Rnas and Emt Micrornas And Emtmentioning

confidence: 99%

The evolving concept of cancer stem-like cells in thyroid cancer and other solid tumors

Hardin

Zhang

Helein

et al. 2017

Laboratory Investigation

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The cancer stem-like cell (CSC) hypothesis postulates that a small population of cells in a cancer has self-renewal and clonal tumor initiation properties. These cells are responsible for tumor initiation, growth, recurrence and for resistance to chemotherapy and radiation therapy. CSCs can be characterized using markers such as SSEA-1, SSEA-4, CD44, CD24, ALDEFLUOR and others. CSCs form spheres when they are cultured in serum-free condition in low attachment plates and can generate tumors when injected into immune-deficient mice. During epithelial to mesenchymal transition (EMT), cells lose cellular adhesion and polarity and acquire an invasive phenotype. Recent studies have established a relationship between EMT and increased numbers of CSCs in some solid malignancies. Non-coding RNAs such as microRNAs and long non-coding RNAs (lncRNAs) have been shown to have important roles during EMT and some of these molecules also have regulatory roles in the proliferation of CSCs. Specific lncRNAs enhanced cell migration and invasion in breast carcinomas, which was associated with the generation of stem cell properties. The tumor microenvironment of CSCs also has an important role in tumor progression. Recent studies have shown that the interaction between tumor cells and the local microenvironment at the metastatic site leads to the development of premetastatic niche(s) and allows for the proliferation of the metastatic cells during colonization. The role of exosomes in the microenvironment during the EMT program is currently a major area of research. This review examines CSCs and the relationship between EMT and CSCs in solid tumors with emphasis on thyroid CSCs. The role of non-coding RNAs and of the microenvironment in EMT and in tumor progression are also examined. This review also highlights the growing number of studies that show the close association of EMT and CSCs and the role of exosomes and other elements of the tissue microenvironment in CSC metastasis. A better understanding of these mechanisms will lead to more effective targeting of primary and metastatic malignancies.

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“…They have critical roles in several cellular processes, including gene expression regulation, chromatin remodeling, post-transcriptional regulation, and translational control. 3 The discovery of lncRNAs has dramatically altered the understanding of cell biology, especially the biology of diseases such as cancer. The identity, function, and dysregulation of lncRNAs as the leading edge of cancer research are only beginning to be understood, and recent data suggest that they may serve as important regulators of different pathways in cancer cells.…”

Section: Introductionmentioning

confidence: 99%

MIAT lncRNA is overexpressed in breast cancer and its inhibition triggers senescence and G1 arrest in MCF7 cell line

Alipoor

Asadi²,

Torkzadeh‐Mahani³

2018

J of Cellular Biochemistry

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Long non-coding RNAs are known as key regulators in the progression and metastasis of breast cancer. MIAT originally has been considered as an lncRNA to be associated with a susceptibility to myocardial infarction. Here, we have detected the expression of MIAT in different cancer cells and a series of breast tumor tissue. MIAT expression was much higher in high-grade tumors compared to low-grade ones. Unlike P53 positive tumors, MIAT expression was upregulated in ER, PR, Her2 positive tumor tissues. Knockdown MIAT suppressed breast cancer cell proliferation and caused G1 arrest in cell cycle. Furthermore, downregulation of MIAT promoted apoptosis and significantly decreased migration of breast cancer cells. An increase in the expression of mir-302, mir-150, and a decrease in the expression of mir-29c were detected following MIAT silencing. More importantly, knockdown MIAT significantly elevated the expression of p16 and Cox2, which commitment cellular senescence in breast cancer cells. Altogether, our results suggest that MIAT involved in breast cancer progression and could be candidate as a novel tumor marker for diagnosis and treatment of breast cancer.

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The functions of long noncoding RNAs in development and stem cells

Cited by 180 publications

References 139 publications

RETRACTED ARTICLE: Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway

RETRACTED ARTICLE: Linc00152 promotes malignant progression of glioma stem cells by regulating miR-103a-3p/FEZF1/CDC25A pathway

The evolving concept of cancer stem-like cells in thyroid cancer and other solid tumors

MIAT lncRNA is overexpressed in breast cancer and its inhibition triggers senescence and G1 arrest in MCF7 cell line

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