BC200 RNA in invasive and preinvasive breast cancer

Iacoangeli, Anna; Lin, Yuan; Morley, Eric J.; Muslimov, Ilham A.; Bianchi, R. M.; Reilly, J.J.; Weedon, Jeremy; Diallo, Raihanatou; Böcker, W.; Tiedge, Henri

doi:10.1093/carcin/bgh228

Cited by 136 publications

(115 citation statements)

References 21 publications

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“…BC200 was previously speculated to be associated with invasion and migration in breast cancer. It was reported that BC200 was expressed at high levels in invasive carcinomas of the breast, and may potentially serve as a molecular tool in the diagnosis and/or prognosis of breast cancer (31). However, the results of the present study demonstrated that BC200 has no effect on the migration and invasion ability of ovarian cancer cells.…”

contrasting

confidence: 83%

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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contrasting

confidence: 83%

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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“…Digital images of tissue sections were acquired using a Sony 3CCD DKC-5000 camera (Sony, New York, NY) or a CoolSnap HQ cooled CCD camera mounted on a Microphot-FXA microscope (Nikon, Melville, NY) as described previously (56). …”

Section: Methodsmentioning

confidence: 99%

Dendritic BC200 RNA in aging and in Alzheimer's disease

Mus¹,

Hof

Tiedge

2007

Proc. Natl. Acad. Sci. U.S.A.

280

199

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Small untranslated BC1 and BC200 RNAs are translational regulators that are selectively targeted to somatodendritic domains of neurons. They are thought to operate as modulators of local protein synthesis in postsynaptic dendritic microdomains, in a capacity in which they would contribute to the maintenance of long-term synaptic plasticity. Because plasticity failure has been proposed to be a starting point for the neurodegenerative changes that are seen in Alzheimer's disease (AD), we asked whether somatodendritic levels of human BC200 RNA are deregulated in AD brains. We found that in normal aging, BC200 levels in cortical areas were reduced by >60% between the ages of 49 and 86. In contrast, BC200 RNA was significantly up-regulated in AD brains, in comparison with age-matched normal brains. This up-regulation in AD was specific to brain areas that are involved in the disease. Relative BC200 levels in those areas increased in parallel with the progression of AD, as reflected by Clinical Dementia Rating scores. In more advanced stages of the disease, BC200 RNA often assumed a clustered perikaryal localization, indicating that dendritic loss is accompanied by somatic overexpression. Mislocalization and overexpression of BC200 RNA may be reactive-compensatory to, or causative of, synaptodendritic deterioration in AD neurons.dementia ͉ non-protein-coding RNA ͉ RNA transport

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“…10,11 In breast cancer, invasive carcinoma reportedly expresses BC200 RNA at higher levels than normal tissues or benign tumors. 12 Moreover, overexpression of BC200 RNA in non-small-cell lung and colorectal cancers was recently reported to promote metastasis. 13,14 However, it is still unclear how deregulated BC200 RNA expression influences the metabolism of such cells, and how such changes influence disease.…”

Section: Introductionmentioning

confidence: 99%

Knockdown of BC200 RNA expression reduces cell migration and invasion by destabilizing mRNA for calcium-binding protein S100A11

et al. 2017

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Although BC200 RNA is best known as a neuron-specific non-coding RNA, it is overexpressed in various cancer cells. BC200 RNA was recently shown to contribute to metastasis in several cancer cell lines, but the underlying mechanism was not understood in detail. To examine this mechanism, we knocked down BC200 RNA in cancer cells, which overexpress the RNA, and examined cell motility, profiling of ribosome footprints, and the correlation between cell motility changes and genes exhibiting altered ribosome profiles. We found that BC200 RNA knockdown reduced cell migration and invasion, suggesting that BC200 RNA promotes cell motility. Our ribosome profiling analysis identified 29 genes whose ribosomal occupations were altered more than 2-fold by BC200 RNA knockdown. Many (> 30%) of them were directly or indirectly related to cancer progression. Among them, we focused on S100A11 (which showed a reduced ribosome footprint) because its expression was previously shown to increase cellular motility. S100A11 was decreased at both the mRNA and protein levels following knockdown of BC200 RNA. An actinomycin-chase experiment showed that BC200 RNA knockdown significantly decreased the stability of the S100A11 mRNA without changing its transcription rate, suggesting that the downregulation of S100A11 was mainly caused by destabilization of its mRNA. Finally, we showed that the BC200 RNAknockdown-induced decrease in cell motility was mainly mediated by S100A11. Together, our results show that BC200 RNA promotes cell motility by stabilizing S100A11 transcripts.

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BC200 RNA in invasive and preinvasive breast cancer

Cited by 136 publications

References 21 publications

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

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

Dendritic BC200 RNA in aging and in Alzheimer's disease

Knockdown of BC200 RNA expression reduces cell migration and invasion by destabilizing mRNA for calcium-binding protein S100A11

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