A long non-coding RNA, PTCSC3, as a tumor suppressor and a target of miRNAs in thyroid cancer cells

Fan, Min; Li, Xinying; Jiang, Wei; Huang, Yun; Li, Jingdong; Wang, Zhiming

doi:10.3892/etm.2013.933

Cited by 141 publications

(118 citation statements)

References 22 publications

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“…Moreover, PTCSC3 stable overexpression also downregulated the expression of S100A4 in BCPAP cells . Furthermore, PTCSC3 was shown to counteract miR-574-5p and inhibit significant cell growth, arrest cell cycle and enhance apoptosis in thyroid cancer cells (Fan et al 2013). In support of this idea, recently, PTCSC3 was identified to be significantly downregulated in PTCs .…”

Section: Ptcsc3 (Papillary Thyroid Carcinoma Susceptibility Candidate 3)supporting

confidence: 56%

Long noncoding RNAs: emerging players in thyroid cancer pathogenesis

Murugan

Munirajan

Alzahrani

2018

Endocrine-Related Cancer

111

103

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Thyroid cancer continues to be the most common malignancy of endocrine glands. The incidence of thyroid cancer has risen significantly over the past 4 decades and has emerged as a major health issue. In recent years, significant progress has been achieved in our understanding of the molecular mechanisms of thyroid carcinogenesis, resulting in significant diagnostic, prognostic and therapeutic implications; yet, it has not reached a satisfactory level. Identifying novel molecular therapeutic targets and molecules for diagnosis and prognosis is expected to advance the overall management of this common malignancy. Long noncoding RNAs (lncRNAs) are implicated in the regulation of various key cellular genes involved in cell differentiation, proliferation, cell cycle, apoptosis, migration and invasion mainly through modulation of gene expression. Recent studies have established that lncRNAs are deregulated in thyroid cancer. In this review, we discuss extensively the tumor-suppressive (for example, LINC00271, MEG3, NAMA, PTCSC1/2/3, etc.) and oncogenic (for example, ANRIL, FAL1, H19, PVT1, etc.) roles of various lncRNAs and their possible disease associations implicated in thyroid carcinogenesis. We briefly summarize the strategies and mechanisms of lncRNA-targeting agents. We also describe the potential role of lncRNAs as prospective novel therapeutic targets, and diagnostic and prognostic markers in thyroid cancer.

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Section: Ptcsc3 (Papillary Thyroid Carcinoma Susceptibility Candidate 3)supporting

confidence: 56%

Long noncoding RNAs: emerging players in thyroid cancer pathogenesis

Murugan

Munirajan

Alzahrani

2018

Endocrine-Related Cancer

111

103

View full text Add to dashboard Cite

show abstract

“…Both computational and experimental evidence support the extensive targeting of lncRNAs by miRNAs (Paraskevopoulou et al 2013). While a small number of lncRNAs are currently known to function as ceRNAs (Cesana et al 2011;Fan et al 2013;Wang et al 2013;Tan et al 2014), the full extent of lncRNAs possessing miRNA-dependent regulatory roles remains to be determined (Ulitsky and Bartel 2013).…”

mentioning

confidence: 99%

Extensive microRNA-mediated crosstalk between lncRNAs and mRNAs in mouse embryonic stem cells

et al. 2015

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Recently, a handful of intergenic long noncoding RNAs (lncRNAs) have been shown to compete with mRNAs for binding to miRNAs and to contribute to development and disease. Beyond these reports, little is yet known of the extent and functional consequences of miRNA-mediated regulation of mRNA levels by lncRNAs. To gain further insight into lncRNA-mRNA miRNA-mediated crosstalk, we reanalyzed transcriptome-wide changes induced by the targeted knockdown of over 100 lncRNA transcripts in mouse embryonic stem cells (mESCs). We predicted that, on average, almost one-fifth of the transcript level changes induced by lncRNAs are dependent on miRNAs that are highly abundant in mESCs. We validated these findings experimentally by temporally profiling transcriptome-wide changes in gene expression following the loss of miRNA biogenesis in mESCs. Following the depletion of miRNAs, we found that >50% of lncRNAs and their miRNA-dependent mRNA targets were up-regulated coordinately, consistent with their interaction being miRNA-mediated. These lncRNAs are preferentially located in the cytoplasm, and the response elements for miRNAs they share with their targets have been preserved in mammals by purifying selection. Lastly, miRNA-dependent mRNA targets of each lncRNA tended to share common biological functions. Post-transcriptional miRNA-mediated crosstalk between lncRNAs and mRNA, in mESCs, is thus surprisingly prevalent, conserved in mammals, and likely to contribute to critical developmental processes.

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“…PTCSC3 is a newly identified, thyroid-specific lncRNA that is significantly downregulated in thyroid cancer. PTCSC3 can induce growth inhibition, cell cycle arrest and increased apoptosis (29,30). BC200 was previously speculated to be associated with invasion and migration in breast cancer.…”

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confidence: 99%

Downregulation of BC200 in ovarian cancer contributes to cancer cell proliferation and chemoresistance to carboplatin

Wang

Ren

et al. 2015

Oncology Letters

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Abstract. Previous studies have demonstrated that long non-coding RNAs (lncRNAs) serve an important role in carcinogenesis. BC200 is a lncRNA that is reportedly associated with ovarian cancer. The aim of the present study was to investigate this potential association between BC200 and ovarian cancer, and to subsequently analyze the biological function of BC200 in the disease. BC200 expression was compared in ovarian cancer tissue and normal ovarian tissue samples through the use of quantitative polymerase chain reaction. To allow the biological function of BC200 in ovarian cancer to be analyzed, small interfering RNA was used to knock down the expression of BC200 in SKOV3 and A2780 ovarian cancer cells. The proliferative, invasive and migratory abilities of the cells were identified by means of cell counting kits and Transwell assays. Carboplatin was also used to treat the ovarian cancer cells, and a luminescent cell viability assay was subsequently used to detect the sensitivity of the cells to the carboplatin. The results demonstrated that BC200 expression was reduced in ovarian cancer compared with normal ovarian tissue samples. In the SKOV3 and A2780 cells, BC200 exerted no effect on invasive or migratory ability, however, the inhibition of BC200 was demonstrated to promote cell proliferation. Additionally, it was observed that carboplatin induced BC200 expression in the cell lines, and that the inhibition of BC200 decreased the sensitivity of the cells to the drug. BC200 is therefore likely to have a tumor suppressive function in ovarian cancer by affecting cell proliferation. Furthermore, BC200 appears to serve a role in the mediation of carboplatin-induced ovarian cancer cell death.

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A long non-coding RNA, PTCSC3, as a tumor suppressor and a target of miRNAs in thyroid cancer cells

Cited by 141 publications

References 22 publications

Long noncoding RNAs: emerging players in thyroid cancer pathogenesis

Long noncoding RNAs: emerging players in thyroid cancer pathogenesis

Extensive microRNA-mediated crosstalk between lncRNAs and mRNAs in mouse embryonic stem cells

Downregulation of BC200 in ovarian cancer contributes to cancer cell proliferation and chemoresistance to carboplatin

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