PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells

Lemos, Ana Emília Goulart; Ferreira, Luciana Bueno; Batoreu, Nadia Maria; Freitas, Paula Priscilla de; Bonamino, Martín; Gimba, Etel Rodrigues Pereira

doi:10.1007/s13277-016-5012-3

Cited by 72 publications

(61 citation statements)

References 38 publications

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“…Rather, it is involved in several mechanisms, including regulation of cancer genes and AR cofactors as well as partial modulation of EMT [48]. …”

Section: Long Non-coding Rnas and Prostate Cancermentioning

confidence: 99%

“…The experimental knockdown of PCA3 leads to upregulation of epithelial markers E-cadherin, claudin-3, and cytokeratin-18, with consecutive downregulation of the mesenchymal marker vimentin [48]. Of note however, is that the EMT pattern is not completely reversed by PCA3 knockdown; mesenchymal markers zinc finger protein SNAI1 (Snail), Twist-related protein 1 (TWIST1) and Slug are still found upregulated and epithelial markers cytokeratin-8 and claudin-4 downregulated upon PCA3 knockdown [48].…”

Section: Long Non-coding Rnas and Prostate Cancermentioning

confidence: 99%

“…Of note however, is that the EMT pattern is not completely reversed by PCA3 knockdown; mesenchymal markers zinc finger protein SNAI1 (Snail), Twist-related protein 1 (TWIST1) and Slug are still found upregulated and epithelial markers cytokeratin-8 and claudin-4 downregulated upon PCA3 knockdown [48]. …”

Section: Long Non-coding Rnas and Prostate Cancermentioning

confidence: 99%

“…Moreover, PCA3 regulates expression of important cancer genes involved in angiogenesis (vascular endothelial growth factor A (VEGFA), fibrillin-1 (IFNB1)), cell adhesion (metastasis suppressor protein 1 (MTSS1), integrin β-1 (ITGB1)), signal transduction (receptor tyrosine-protein kinase (ERBB2), phosphatidylinositol 3-kinase regulatory subunit α (PIK3R1)), mitogen-activated protein kinase kinase 1 (MAP2K1), and apoptosis (Bcl-2-associated death promoter (BAD), telomerase reverse transcriptase (TERT)) [48]. …”

Section: Long Non-coding Rnas and Prostate Cancermentioning

confidence: 99%

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Current Insights into Long Non-Coding RNAs (LncRNAs) in Prostate Cancer

Smolle

Bauernhofer

Pummer

et al. 2017

IJMS

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The importance of long non-coding RNAs (lncRNAs) in the pathogenesis of various malignancies has been uncovered over the last few years. Their dysregulation often contributes to or is a result of tumour progression. In prostate cancer, the most common malignancy in men, lncRNAs can promote castration resistance, cell proliferation, invasion, and metastatic spread. Expression patterns of lncRNAs often change during tumour progression; their expression levels may constantly rise (e.g., HOX transcript antisense RNA, HOTAIR), or steadily decrease (e.g., downregulated RNA in cancer, DRAIC). In prostate cancer, lncRNAs likewise have diagnostic (e.g., prostate cancer antigen 3, PCA3), prognostic (e.g., second chromosome locus associated with prostate-1, SChLAP1), and predictive (e.g., metastasis-associated lung adenocarcinoma transcript-1, MALAT-1) functions. Considering their dynamic role in prostate cancer, lncRNAs may also serve as therapeutic targets, helping to prevent development of castration resistance, maintain stable disease, and prohibit metastatic spread.

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“…Rather, it is involved in several mechanisms, including regulation of cancer genes and AR cofactors as well as partial modulation of EMT [48]. …”

Section: Long Non-coding Rnas and Prostate Cancermentioning

confidence: 99%

Section: Long Non-coding Rnas and Prostate Cancermentioning

confidence: 99%

Section: Long Non-coding Rnas and Prostate Cancermentioning

confidence: 99%

Section: Long Non-coding Rnas and Prostate Cancermentioning

confidence: 99%

See 2 more Smart Citations

Current Insights into Long Non-Coding RNAs (LncRNAs) in Prostate Cancer

Smolle

Bauernhofer

Pummer

et al. 2017

IJMS

View full text Add to dashboard Cite

show abstract

“…In recent years, many reports have shown that lncRNAs play an oncogenic or tumor suppressive role in various cancers, such as breast, gastric, colorectal cancers and hepatocellular carcinoma [17–19]. Emerging evidences have demonstrated that dysregulation of lncRNAs has been implicated in multiple cellular biological processes, such as cell proliferation, apoptosis, cancer metastasis, as well as tumorigenesis [20, 21]. Furthermore, several lncRNAs were reported to be involved in OS progression and tumorigenesis [22].…”

Section: Introductionmentioning

confidence: 99%

LncRNA SNHG15 contributes to proliferation, invasion and autophagy in osteosarcoma cells by sponging miR-141

et al. 2017

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BackgroundLncRNA small nucleolar RNA host gene 15 (SNHG15) was reported to play an oncogenic role in tumors. However, the role of SNHG15 and its molecular mechanism in osteosarcoma (OS) cells are largely unknown.MethodsqRT-PCR was performed to evaluate the expression levels of SNHG15 and miR-141 in OS tissues and cells. Cell transfection with different siRNAs, miRNAs or pcDNAs into U2OS and MG63 cells were carried out by Lipofectamine 2000. The effects of SNHG15 and miR-141 on OS cell proliferation, invasion and the levels of autophagy-related proteins were analyzed by MTT assay, Transwell invasion/migration assay and western blot, respectively. Luciferase reporter assay was used to confirm whether SNHG15 could directly interact with miR-141.ResultsWe found that up-regulation of SNHG15 was inversely correlated with miR-141 expression in OS tissues. SNHG15 knockdown and miR-141 overexpression significantly suppressed cell proliferation, invasion, migration and autophagy while SNHG15 overexpression and miR-141 repression exhibited the opposite effects on OS cells. Besides, SNHG15 could directly interact with miR-141 and regulate its expression. Furthermore, miR-141 suppressing significantly overturned the inhibition on proliferation, invasion, migration and autophagy mediated by SNHG15 knockdown while miR-141 overexpression remarkably attenuated SNHG15 overexpression-induced proliferation, invasion, migration and autophagy in OS cells.ConclusionOur data showed that SNHG15 contributes to proliferation, invasion, migration and autophagy in OS by negatively regulating miR-141, providing a new potential target and prognostic biomarker for the treatment of OS.

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Revealing metastatic castration‐resistant prostate cancer master regulator through lncRNAs‐centered regulatory network

Ferraz,

Cavalcante,

Magalhães

et al. 2023

Cancer Medicine

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BackgroundMetastatic castration‐resistant prostate cancer (mCRPC) is an aggressive form of cancer unresponsive to androgen deprivation therapy (ADT) that spreads quickly to other organs. Despite reduced androgen levels after ADT, mCRPC development and lethality continues to be conducted by the androgen receptor (AR) axis. The maintenance of AR signaling in mCRPC is a result of AR alterations, androgen intratumoral production, and the action of regulatory elements, such as noncoding RNAs (ncRNAs). ncRNAs are key elements in cancer signaling, acting in tumor growth, metabolic reprogramming, and tumor progression. In prostate cancer (PCa), the ncRNAs have been reported to be associated with AR expression, PCa proliferation, and castration resistance. In this study, we aimed to reconstruct the lncRNA‐centered regulatory network of mCRPC and identify the lncRNAs which act as master regulators (MRs).MethodsWe used publicly available RNA‐sequencing to infer the regulatory network of lncRNAs in mCRPC. Five gene signatures were employed to conduct the master regulator analysis. Inferred MRs were then subjected to functional enrichment and symbolic regression modeling. The latter approach was applied to identify the lncRNAs with greater predictive capacity and potential as a biomarker in mCRPC.ResultsWe identified 31 lncRNAs involved in cellular proliferation, tumor metabolism, and invasion‐metastasis cascade. SNHG18 and HELLPAR were the highlights of our results. SNHG18 was downregulated in mCRPC and enriched to metastasis signatures. It accurately distinguished both mCRPC and primary CRPC from normal tissue and was associated with epithelial–mesenchymal transition (EMT) and cell‐matrix adhesion pathways. HELLPAR consistently distinguished mCRPC from primary CRPC and normal tissue using only its expression.ConclusionOur results contribute to understanding the regulatory behavior of lncRNAs in mCRPC and indicate SNHG18 and HELLPAR as master regulators and potential new diagnostic targets in this tumor.

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PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells

Cited by 72 publications

References 38 publications

Current Insights into Long Non-Coding RNAs (LncRNAs) in Prostate Cancer

Current Insights into Long Non-Coding RNAs (LncRNAs) in Prostate Cancer

LncRNA SNHG15 contributes to proliferation, invasion and autophagy in osteosarcoma cells by sponging miR-141

Revealing metastatic castration‐resistant prostate cancer master regulator through lncRNAs‐centered regulatory network

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