SWI/SNF remains localized to chromatin in the presence of SCHLAP1

AbstractSCHLAP1 is a long-noncoding RNA that is prognostic for progression to metastatic prostate cancer and promotes an invasive phenotype. SCHLAP1 is reported to function by depleting the core SWI/SNF subunit, SMARCB1, from the genome. SWI/SNF is a large, multi-subunit, chromatin remodeling complex that can be combinatorially assembled to yield hundreds to thousands of distinct complexes. Here, we investigated the hypothesis that SCHLAP1 affects only specific forms of SWI/SNF and that the remaining SWI/SNF complexes were important for the increased invasion in SCHLAP1 expressing prostate cells. Using several assays we found that SWI/SNF is not depleted from the genome by SCHLAP1 expression. We find that SCHLAP1 induces changes to chromatin openness but is not sufficient to drive changes in histone modifications. Additionally, we show that SWI/SNF binds many coding and non-coding RNAs. Together these results suggest that SCHLAP1 has roles independent of canonical SWI/SNF and that SWI/SNF broadly interacts with RNA.

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Retraction: Long noncoding RNA PCA3 regulates glycolysis, viability and apoptosis by mediating the miR-1/CDK4 axis in prostate cancer

RSC Advances ◽

10.1039/d1ra90066h ◽

2021 ◽

Vol 11 (11) ◽

pp. 5894-5894

Author(s):

Laura Fisher

Keyword(s):

Prostate Cancer ◽

Long Noncoding Rna ◽

Noncoding Rna

Retraction of ‘Long noncoding RNA PCA3 regulates glycolysis, viability and apoptosis by mediating the miR-1/CDK4 axis in prostate cancer’ by Shuo Gu et al., RSC Adv., 2018, 8, 37564–37572, DOI: 10.1039/C8RA08083F

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The function of long noncoding RNA HOTAIRM1 in the progression of prostate cancer cells

Andrologia ◽

10.1111/and.13897 ◽

2020 ◽

Author(s):

Lei Wang ◽

Longning Wang ◽

Qingfen Wang ◽

Bahman Yosefi ◽

Sen Wei ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Prostate Cancer Cells

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Discovery of a novel long noncoding RNA overlapping the LCK gene that regulates prostate cancer cell growth

Molecular Cancer ◽

10.1186/s12943-019-1039-6 ◽

2019 ◽

Vol 18 (1) ◽

Cited By ~ 5

Author(s):

Huy Q. Ta ◽

Hilary Whitworth ◽

Yi Yin ◽

Mark Conaway ◽

Henry F. Frierson ◽

...

Keyword(s):

Prostate Cancer ◽

Cell Growth ◽

Cancer Cell ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Prostate Cancer Cell ◽

Cancer Cell Growth

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Transcriptional Gene Silencing of the Autism-Associated Long Noncoding RNA MSNP1AS in Human Neural Progenitor Cells

Developmental Neuroscience ◽

10.1159/000453258 ◽

2016 ◽

Vol 38 (5) ◽

pp. 375-383 ◽

Cited By ~ 13

Author(s):

Jessica J. DeWitt ◽

Patrick M. Hecht ◽

Nicole Grepo ◽

Brent Wilkinson ◽

Oleg V. Evgrafov ◽

...

Keyword(s):

Immune Response ◽

Chromatin Remodeling ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Multiple Comparisons ◽

Neural Progenitor ◽

Autism Spectrum ◽

Biological Processes ◽

Altered Expression ◽

Genome Wide

The long noncoding RNA MSNP1AS (moesin pseudogene 1, antisense) is a functional element that was previously associated with autism spectrum disorder (ASD) with genome-wide significance. Expression of MSNP1AS was increased 12-fold in the cerebral cortex of individuals with ASD and 22-fold in individuals with a genome-wide significantly associated ASD genetic marker on chromosome 5p14.1. Overexpression of MSNP1AS in human neuronal cells caused decreased expression of moesin protein, which is involved in neuronal process stability. In this study, we hypothesize that MSNP1AS knockdown impacts global transcriptome levels. We transfected the human neural progenitor cell line SK- N-SH with constructs that caused a 50% suppression of MSNP1AS expression. After 24 h, cells were harvested for total RNA isolation. Strand-specific RNA sequencing analysis indicated altered expression of 1,352 genes, including altered expression of 318 genes following correction for multiple comparisons. Expression of the OAS2 gene was increased >150-fold, a result that was validated by quantitative PCR. Gene ontology analysis of the 318 genes with altered expression following correction for multiple comparisons indicated that upregulated genes were significantly enriched for genes involved in immune response, and downregulated genes were significantly enriched for genes involved in chromatin remodeling. These data indicate multiple transcriptional and translational functions of MSNP1AS that impact ASD-relevant biological processes. Chromatin remodeling and immune response are biological processes implicated by genes with rare mutations associated with ASD. Our data suggest that the functional elements implicated by association of common genetic variants impact the same biological processes, suggesting a possible shared common molecular pathway of ASD.

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Knockdown of long noncoding RNA AC245100.4 inhibits the tumorigenesis of prostate cancer cells via the STAT3/NR4A3 axis

Epigenomics ◽

10.2217/epi-2021-0293 ◽

2021 ◽

Author(s):

Chi Liu ◽

Ping Lin ◽

Jiabin Zhao ◽

Hui Xie ◽

Rou Li ◽

...

Keyword(s):

Prostate Cancer ◽

Cancer Cells ◽

Rna Sequencing ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Transcriptional Repressor ◽

Sequencing Analysis ◽

Loss Of Function ◽

Prostate Cancer Cells ◽

Rna Immunoprecipitation

Aim: To explore the role and mechanism of long noncoding RNA AC245100.4 and NR4A3 in prostate cancer (PCa). Methods: RNA-sequencing analysis was used to detect the downstream genes of AC245100.4. A series of gain- and loss-of-function approaches were used to investigate the roles of AC245100.4 and NR4A3. RNA immunoprecipitation was performed to examine the interaction between AC245100.4 and STAT3. Results: AC245100.4 was significantly upregulated in PCa cells and tissues. Knockdown of AC21500.4 significantly inhibited the tumorigenesis of PCa cells. Mechanistically, AC245100.4 deregulated the transcription of NR4A3 via increasing p-STAT3, which acted as a transcriptional repressor of NR4A3. Conclusion: Knockdown of lncRNA AC245100.4 inhibits the tumorigenesis of PCa cells via the STAT3/ NR4A3 axis.

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Corrigendum to: The long noncoding RNA HORAS5 mediates castration‐resistant prostate cancer survival by activating the androgen receptor transcriptional program

Molecular Oncology ◽

10.1002/1878-0261.12618 ◽

2020 ◽

Vol 14 (2) ◽

pp. 484-484

Keyword(s):

Prostate Cancer ◽

Androgen Receptor ◽

Long Noncoding Rna ◽

Noncoding Rna ◽

Cancer Survival ◽

Castration Resistant Prostate Cancer ◽

Transcriptional Program ◽

Castration Resistant

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Role of specialized composition of SWI/SNF complexes in prostate cancer lineage plasticity

Nature Communications ◽

10.1038/s41467-020-19328-1 ◽

2020 ◽

Vol 11 (1) ◽

Cited By ~ 1

Author(s):

Joanna Cyrta ◽

Anke Augspach ◽

Maria Rosaria De Filippo ◽

Davide Prandi ◽

Phillip Thienger ◽

...

Keyword(s):

Prostate Cancer ◽

Chromatin Remodeling ◽

Hormonal Treatment ◽

Prostate Adenocarcinoma ◽

Aggressive Disease ◽

Chromatin Remodeling Complex ◽

Large Patient ◽

Neuroendocrine Prostate Cancer ◽

Specific Factors

Abstract Advanced prostate cancer initially responds to hormonal treatment, but ultimately becomes resistant and requires more potent therapies. One mechanism of resistance observed in around 10–20% of these patients is lineage plasticity, which manifests in a partial or complete small cell or neuroendocrine prostate cancer (NEPC) phenotype. Here, we investigate the role of the mammalian SWI/SNF (mSWI/SNF) chromatin remodeling complex in NEPC. Using large patient datasets, patient-derived organoids and cancer cell lines, we identify mSWI/SNF subunits that are deregulated in NEPC and demonstrate that SMARCA4 (BRG1) overexpression is associated with aggressive disease. We also show that SWI/SNF complexes interact with different lineage-specific factors in NEPC compared to prostate adenocarcinoma. These data point to a role for mSWI/SNF complexes in therapy-related lineage plasticity, which may also be relevant for other solid tumors.

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