Linc00963: A novel, long non-coding RNA involved in the transition of prostate cancer from androgen-dependence to androgen-independence

Wang, Lijuan; Han, Suxia; Jin, Guihua; Zhou, Xia; Li, Meng; Xia, Ying; Wang, Le; Wu, Huili; Zhu, Qing

doi:10.3892/ijo.2014.2363

Cited by 74 publications

(74 citation statements)

References 31 publications

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“…LncRNAs also have significant biological functions in modulating gene at transcriptional, post-transcriptional and chromosomal levels [8]. LncRNAs participate in physiological processes of cell-type determination and tissue homeostasis, and it has been proved that LINC00963 was involved in the prostate cancer transition from androgen-dependent to androgen-independent and metastasis via the epidermal growth factor receptor (EGFR) signaling pathway [9]. Moreover, a previous study has demonstrated that overexpression of lncRNA MEG3 promotes hepatic insulin resistance by upregulating forkhead box O (FoxO) 1 expression [10].…”

Section: Introductionmentioning

confidence: 99%

Effects of Long Non-Coding RNA LINC00963 on Renal Interstitial Fibrosis and Oxidative Stress of Rats with Chronic Renal Failure via the Foxo Signaling Pathway

Chen

Zhang

Zhou

et al. 2018

Cell Physiol Biochem

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Background/Aims: Chronic renal failure (CRF) is usually associated with chronic diseases such as congestive heart failure and diabetes mellitus, the prevalence of which is increased with age. This study is designed to investigate the role of long intergenic non-coding RNA (lincRNA) LINC00963 in renal interstitial fibrosis (RIF) and oxidative stress (OS) of CRF via the forkhead box O (FoxO) signaling pathway. Methods: Microarray data and annotated probe files related to CRF were downloaded by retrieving Gene Expression Omnibus (GEO) database to screen differentially expressed lncRNA. Multi Experiment Matrix (MEM) website and dual-luciferase reporter gene assay were used to predict and verify the target gene of LINC00963, and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis to identify the major signaling pathways involved. A total of 60 Wistar male rats were randomly selected and divided into the sham (n = 10) and model (n = 50) groups. Five rats in the sham group and thirty rats in the model group were sub-categorized into the control, blank, negative control (NC), LINC00963 vector, si-LINC00963, si-FoxO3, and si-LINC00963 + si-FoxO3 groups (n = 5). Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blot analysis were performed to evaluate the expressions of LINC00963, FoxO3a, TGF-β1, FN, GSH-PX, Bax, and Bcl-2. Measurement of changes in OS indexes including BUN, MDA, GSH-Px, SOD, and Na⁺-K⁺-ATP were conducted. Enzyme-linked immunosorbent assay (ELISA) was used to determine the levels of inflammatory factors including TNF-α, IL-6, ICAM-1 and FN. TUNEL staining was performed to evaluate cell apoptosis. Results: LINC00963 was highly expressed in CRF rats and FoxO3 was predicted and then verified as a target gene of LINC00963. FoxO3 gene participated in the FOXO signaling pathway. Compared with the blank and NC groups, there were significantly decreased expressions of LINC00963, TGF-β1, FN, and Bax in the si-LINC00963 group, while increased expressions of GSH-PX, FoxO3a, and Bcl-2. The vitality values of BUN and MDA in the si-LINC00963 group declined, while enzymatic activities of GSH-Px, SOD and Na⁺-K⁺-ATP elevated in comparison to the blank and NC groups. The levels of TNF-α, IL-6, ICAM-1 and FN, and cell apoptosis rate in the si-LINC00963 group decreased in comparison to the blank and NC groups. All the results in the si-LINC00963 group were opposite in the LINC00963 vector and si-FoxO3 groups. Conclusion: Taken together, we conclude that down-regulation of LINC00963 suppresses RIF and OS of CRF by activating the FoxO signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Effects of Long Non-Coding RNA LINC00963 on Renal Interstitial Fibrosis and Oxidative Stress of Rats with Chronic Renal Failure via the Foxo Signaling Pathway

Chen

Zhang

Zhou

et al. 2018

Cell Physiol Biochem

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“…More importantly, these lncRNAs are reported to be associated with the development of prostate cancer. MALAT1 down-regulation by siRNA inhibits prostate cancer cell growth, invasion and migration49; NEAT1 drives prostate cancer growth by altering the epigenetic landscape of target gene promoters to favor transcription50; and LINC00963 is involved in the transition of prostate cancer from androgen dependent to androgen independent51. These results indicate that the core genes in this pathway may be influenced by the dysregulated lncRNAs in the development of prostate cancer.…”

Section: Resultsmentioning

confidence: 99%

LncRNAs2Pathways: Identifying the pathways influenced by a set of lncRNAs of interest based on a global network propagation method

Han

Liu

Sun

et al. 2017

Sci Rep

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Long non-coding RNAs (lncRNAs) have been demonstrated to play essential roles in diverse cellular processes and biological functions. Exploring the functions associated with lncRNAs may help provide insight into their underlying biological mechanisms. The current methods primarily focus on investigating the functions of individual lncRNAs; however, essential biological functions may be affected by the combinatorial effects of multiple lncRNAs. Here, we have developed a novel computational method, LncRNAs2Pathways, to identify the functional pathways influenced by the combinatorial effects of a set of lncRNAs of interest based on a global network propagation algorithm. A new Kolmogorov–Smirnov-like statistical measure weighted by the network propagation score, which considers the expression correlation among lncRNAs and coding genes, was used to evaluate the biological pathways influenced by the lncRNAs of interest. We have described the LncRNAs2Pathways methodology and illustrated its effectiveness by analyzing three lncRNA sets associated with glioma, prostate and pancreatic cancers. We further analyzed the reproducibility and robustness and compared our results with those of two other methods. Based on these analyses, we showed that LncRNAs2Pathways can effectively identify the functional pathways associated with lncRNA sets. Finally, we implemented this method as a freely available R-based tool.

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“…Epigenetic alterations, including DNA methylation in tumor suppresser genes promoters and modification in histone modifying enzymes also contribute to PCa carcinogenesis [20]. Recent studies have showed that alteration in different lncRNAs, such as PTENP1 [21,22], Linc00963 [23], PCGIM1 [24], PRNCR1 [25], CBR-3AS1 [26], CTP1 AS [27], GAS5 [28], ANRIL [29], ANRASSF1 [30] and PCAT1 [8, 31] are associated with PCa. LncRNAs, such as prostate cancer associated transcript ( PCAT1 and PCAT3) , increase cancer cells proliferation [8,31].…”

Section: Introductionmentioning

confidence: 99%

Tonic suppression of PCAT29 by the IL-6 signaling pathway in prostate cancer: Reversal by resveratrol

et al. 2017

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Prostate cancer (PCa) is the second leading cause of cancer deaths in men. A better understanding of the molecular basis of prostate cancer proliferation and metastasis should enable development of more effective treatments. In this study we focused on the lncRNA, prostate cancer associated transcript 29 (PCAT29), a putative tumor suppressive gene. Our data show that the expression of PCAT29 was reduced in prostate cancer tumors compared to paired perinormal prostate tissues. We also observed substantially lower levels of PCAT29 in DU145 and LNCaP cells compared to normal prostate (RWPE-1) cells. IL-6, a cytokine which is elevated in prostate tumors, reduced the expression of PCAT29 in both DU145 and LNCaP cells by activating signal transducer and activator of transcription 3 (STAT3). One downstream target of STAT3 is microRNA (miR)-21, inhibition of which enhanced basal PCAT29 expression. In addition, we show that resveratrol is a potent stimulator of PCAT29 expression under basal condition and reversed the down regulation of this lncRNA by IL-6. Furthermore, we show that knock down of PCAT29 expression by siRNA in DU145 and LNCaP cells increased cell viability while increasing PCAT29 expression with resveratrol decreased cell viability. Immunohistochemistry studies showed increased levels of STAT3 and IL-6, but low levels of programmed cell death protein 4 (PDCD4), in prostate tumor epithelial cells compared to adjacent perinormal prostate epithelial cells. These data show that the IL-6/STAT3/miR-21 pathway mediates tonic suppression of PCAT29 expression and function. Inhibition of this signaling pathway by resveratrol induces PCAT29 expression and tumor suppressor function.

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Linc00963: A novel, long non-coding RNA involved in the transition of prostate cancer from androgen-dependence to androgen-independence

Cited by 74 publications

References 31 publications

Effects of Long Non-Coding RNA LINC00963 on Renal Interstitial Fibrosis and Oxidative Stress of Rats with Chronic Renal Failure via the Foxo Signaling Pathway

Effects of Long Non-Coding RNA LINC00963 on Renal Interstitial Fibrosis and Oxidative Stress of Rats with Chronic Renal Failure via the Foxo Signaling Pathway

LncRNAs2Pathways: Identifying the pathways influenced by a set of lncRNAs of interest based on a global network propagation method

Tonic suppression of PCAT29 by the IL-6 signaling pathway in prostate cancer: Reversal by resveratrol

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