Author | Lemos, Ana Emília Goulart | |
Author | Ferreira, Luciana Bueno | |
Author | Batoreu, Nadia Maria | |
Author | Freitas, Paula Priscilla de | |
Author | Bonamino, Martin Hernan | |
Author | Gimba, Etel Rodrigues Pereira | |
Access date | 2016-04-11T17:08:09Z | |
Available date | 2016-04-11T17:08:09Z | |
Document date | 2016 | |
Citation | LEMOS, Ana Emília Goulart et al. PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells.Tumor Biology, p. 1-10, mar. 2016. | pt_BR |
ISSN | 1010-4283 | |
URI | https://www.arca.fiocruz.br/handle/icict/13673 | |
Language | eng | pt_BR |
Publisher | Springer | pt_BR |
Rights | open access | pt_BR |
Subject in Portuguese | Expressão Gênica | pt_BR |
Subject in Portuguese | Neoplasias da Próstata | pt_BR |
Title | PCA3 long noncoding RNA modulates the expression of key cancer-related genes in LNCaP prostate cancer cells | pt_BR |
Type | Article | pt_BR |
Abstract | Prostate cancer antigen 3 (PCA3)is a prostate-specific long noncoding RNA (lncRNA) involved in the control of prostate cancer (PCa) cell survival, through modulating androgen receptor (AR) signaling.To furthercomprehendthemechanisms by which PCA3 modulates LNCaP cell survival, we characterized the expression patterns of several cancer-related genes, including those involved in epithelial-mesenchymal transition (EMT) and AR cofactors in response to PCA3 silencing. We also aimed to develop a strategyto stably silence PCA3. SmallinterferingRNA (siRNA) or short hairpinRNA (shRNA) was usedto knock down PCA3inLNCaP cells.The expression of 84cancer-related genes, as well as those coding for AR cofactors and EMT markers, was analyzed by quantitative real-time PCR (qRT-PCR). LNCaPPCA3 silenced cells differentially expressed 16 of the 84 cancer genes tested, mainly those involved in gene expression control and cell signaling. PCA3 knockdown also induced the upregulation of severaltranscripts coding for AR cofactors and modulated the expression of EMT markers. LNCaP cells transduced with lentivirus vectors carrying an shRNA sequence targeting PCA3 stably downregulated PCA3 expression, causing a significant drop (60 %) in the proportion of LNCaP cells expressing the transgene. In conclusion, our data provide evidence that PCA3 silencing modulates the expression of key cancer-related genes, including those coding for AR cofactors and EMT markers. Transducing LNCaP cells with an shRNA sequence targeting PCA3 led to loss of viability of the cells, supporting the proposal of PCA3 knockdown as a putativetherapeutic approachtoinhibit PCa growth. | pt_BR |
Affilliation | Fundação Oswaldo Cruz, Bio-Manguinhos, Rio de Janeiro, Brazil | pt_BR |
Affilliation | Instituto de Patologia Molecular e Imunologia da Universidade do Porto, Porto, Portugal | pt_BR |
Affilliation | Fundação Centro Universitário Estadual da Zona Oeste, Rio de Janeiro, Brazil | pt_BR |
Affilliation | Instituto Nacional de Câncer José Alencar Gomes da Silva, Coordenação de Pesquisa, Rio de Janeiro, Brazil | pt_BR |
Affilliation | Fundação Oswaldo Cruz, Vice-presidência de Pesquisa e Laboratórios de Referência, Rio de Janeiro, Brazil | pt_BR |
Affilliation | Universidade Federal Fluminense, Instituto de Humanidades e Sáude, Departamento de Ciências da Natureza, Rio de Janeiro, Brazil | pt_BR |
Subject | PCA3 | pt_BR |
Subject | Long noncoding RNA | pt_BR |
Subject | Gene expression | pt_BR |
Subject | Cancer-related genes | pt_BR |
Subject | Prostatic Neoplasms | pt_BR |
DeCS | Expressão Gênica | pt_BR |
DeCS | Prostatic Neoplasms | pt_BR |
e-ISSN | 1423-0380 | |