LncRNA LINC00844 regulates prostste cancer cell migration and invasion through AR signaling
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ABSTRACT:
PROVIDER: PRJNA430460 | ENA |
REPOSITORIES: ENA
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Project description:The majority of the human genome is transcribed, yielding a rich repository of non-coding transcripts that are involved in a myriad of biological processes including cancer. However, how non-coding transcripts such as Long Non-coding RNAs (lncRNAs) function in prostate cancer is still unclear. In this study, we have identified a novel set of clinically relevant androgen-regulated lncRNAs in prostate cancer. Among this group, we found LINC00844 is a direct androgen regulated target that is actively transcribed in AR-dependent prostate cancer cells. In clinical analysis, the expression of LINC00844 is higher in normal prostate compared to malignant and metastatic prostate cancer samples and patients with low expression demonstrate poor prognosis and significantly increased biochemical recurrence suggesting LINC00844 may function in suppressing tumor progression and metastasis. From in-vitro loss-of-function studies, we showed LINC00844 prevents prostate cancer cell migration and invasion. Moreover, in gene expression studies we demonstrate LINC00844 functions in trans, affecting global androgen-regulated gene transcription. Mechanistically, we provide evidence to show LINC00844 is important in facilitating AR binding to the chromatin. Finally, we showed LINC00844 mediates its phenotypic effects in part by activating the expression of NDRG1, a crucial cancer metastasis suppressor. Collectively, our findings indicate LINC00844 is a novel coregulator of AR that plays an important role in the androgen transcriptional network and the development and progression of prostate cancer.
2019-01-01 | GSE109336 | GEO
Project description:The majority of the human genome is transcribed, yielding a rich repository of non-coding transcripts that are involved in a myriad of biological processes including cancer. However, how non-coding transcripts such as Long Non-coding RNAs (lncRNAs) function in prostate cancer is still unclear. In this study, we have identified a novel set of clinically relevant androgen-regulated lncRNAs in prostate cancer. Among this group, we found LINC00844 is a direct androgen regulated target that is actively transcribed in AR-dependent prostate cancer cells. In clinical analysis, the expression of LINC00844 is higher in normal prostate compared to malignant and metastatic prostate cancer samples and patients with low expression demonstrate poor prognosis and significantly increased biochemical recurrence suggesting LINC00844 may function in suppressing tumor progression and metastasis. From in-vitro loss-of-function studies, we showed LINC00844 prevents prostate cancer cell migration and invasion. Moreover, in gene expression studies we demonstrate LINC00844 functions in trans, affecting global androgen-regulated gene transcription. Mechanistically, we provide evidence to show LINC00844 is important in facilitating AR binding to the chromatin. Finally, we showed LINC00844 mediates its phenotypic effects in part by activating the expression of NDRG1, a crucial cancer metastasis suppressor. Collectively, our findings indicate LINC00844 is a novel coregulator of AR that plays an important role in the androgen transcriptional network and the development and progression of prostate cancer.
2019-01-01 | GSE108704 | GEO
Project description:<p>Hepatocellular carcinoma (HCC), a prevalent malignant neoplasm, presents significant therapeutic challenges. However, the key factors and mechanisms driving HCC metastasis remain incompletely understood. This study aimed to elucidate the mechanism through which CHML regulates the migration and invasion of HCC cells. Following CHML knockout or overexpression, we assessed the proliferative capacity of HCC cells using the Cell Counting Kit-8 (CCK-8) assay, 5-ethynyl-2′-deoxyuridine (EdU) incorporation, colony formation assay, and subcutaneous xenograft tumor models in nude mice. Cell migration and invasion were evaluated using wound healing and Transwell assays. Results demonstrated that CHML knockout significantly inhibited the migration and invasion of HCC cells in vitro, whereas CHML overexpression promoted these phenotypes. Transcriptomic sequencing revealed CHML-mediated regulation of migration-associated pathways, whereas untargeted metabolomics identified choline metabolism as a key significantly altered pathway. Notably, the integration of transcriptomics and untargeted metabolomics identified choline metabolism as a pivotal pathway in CHML-regulated migration and invasion. The subsequent mechanistic analysis demonstrated that CHML upregulated the Solute carrier family 44 member 3 (SLC44A3) to enhance choline uptake, thereby increasing phosphatidic acid (PA) production. This metabolic shift activated MAPK and PI3K-AKT signaling cascades, ultimately driving HCC cell migration and invasion. Our findings provide novel insights into metabolic dependencies in HCC metastasis and position CHML as a promising therapeutic target.</p>
2025-07-28 | MTBLS12789 | MetaboLights
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Project description:Long noncoding RNAs (lncRNAs) are emerging as important regulators in cellular processes. In the present study, the effects of the long non-coding RNA, SNHG5 was investigated in lung adenocarcinoma (LAD) and we also revealed the underlying mechanisms of it. Overexpressed SNHG5 suppressed migration and invasion of LAD cell line A549 in vitro. Transcriptome sequencing analysis supported the inhibitory effects of SNHG5 were associated with cell adhesion molecules. In addition, western blot and immunofluorescence showed that the expression of SNHG5 was associated with epithelial-mesenchymal transition (EMT) markers. Furthermore, we determined the effects of SNHG5 in EMT procession of A549 induced by TGF-β1. Consistent with previous results, overexpression of SNHG5 suppressed the migration and invasion, and also the expression of EMT-related transcription factors including Snail, SLUG and ZEB1 in EMT of A549 reduced by TGF-β1. Moreover, qRT-PCR demonstrated expression of SNHG5 was positively correlated with E-cadherin protein expression, but negatively correlated with N-cadherin and Vimentin in LAD tissues. In summary, our study demonstrated that lncRNA SNHG5 could suppress cell migration and invasion of LAD cancer by inhibiting EMT procession, highlighting the potential of SNHG5 as a therapy strategy for lung adenocarcinoma.
2020-01-17 | GSE143766 | GEO
Project description:The Androgen Receptor (AR) is the master regulator of Prostate Cancer (PCa) development, and inhibition of AR signalling is the most effective PCa treatment. AR is expressed in PCa cells and also in the PCa-associated stroma, including infiltrating macrophages ). Macrophages play a decisive role in PCa initiation and progression, however, the role of AR in these cells remains largely unexplored. Here we show that AR signalling in macrophage-like THP-1 cell line supports PCa cell line migration and invasion in culture via increased Triggering REceptor of Macrophage-1 (TREM-1) signalling and expression of its downstream cytokines.
2019-05-18 | GSE131381 | GEO
Project description:TCF7L1 regulates colorectal cancer cell migration and invasion by repressing GAS1 expression (ChIP-Seq)
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Project description:TCF7L1 regulates colorectal cancer cell migration and invasion by repressing GAS1 expression (RNA-Seq)
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