human
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: OBJECTIVE : Emerging evidences implicate long noncoding RNAs ( lncRNAs ) are deregulated in cancer development . The purpose of the current study is to investigate the role of new lncRNA , named PlncRNA-1 , in prostate cancer ( CaP ) pathogenesis . MATERIALS AND METHODS : In this study , real-time q-PCR was used to demonstrate the expression of PlncRNA-1 in 16 pairs CaP tissues and matched normal tissues , 14 pairs CaP tissues and BPH tissues , 4 CaP cell lines , including LNCaP , LNCaP-AI , PC3 , and C4-2 , and 2 normal prostate epithelial cell lines RWPE-1 and PWR-1E . After PlncRNA-1 was suppressed by siRNA in LNCaP and LNCaP-AI cell lines , cell proliferation and apoptosis were assessed using CCK-8 and terminal deoxynucleotidyl transferase dUTP nick end labeling ( TUNEL ) . After PlncRNA-1 and AR was suppressed by siRNA in LNCaP and LNCaP-AI cell lines , real-time q-PCR and Western blotting were used to measure reciprocal regulation of PlncRNA-1 and AR . RESULTS : We showed that expression PlncRNA-1 , was significantly higher in CaP cells relative to normal prostate epithelial cells , as well as higher in human CaPs compared with normal tissues and benign prostatic hyperplasia ( BPH ) . Silencing of PlncRNA-1 significantly reduced cell proliferation and induced apoptosis in CaP cell lines LNCaP and LNCaP-AI . Mechanistically , PlncRNA-1 suppression by siRNA resulted in a decrease of androgen receptor ( AR ) mRNA , protein and AR downstream target . Of note , blockade of AR signaling with siRNA also resulted in a suppression of PlncRNA-1 expression in CaP cell lines . CONCLUSIONS : Our study suggests reciprocal regulation of PlncRNA-1 and androgen receptor contribute to CaP pathogenesis and that PlncRNA-1 is a potential therapy target .
    OUTPUT:

agent
resisting cell death;sustaining proliferative signaling
The task is to decide the Hallmarks of Cancer (HOC) taxonomy of the article based on its abstract. The input is an abstract text. There are 10 topics you will need to decide whether the article is related to. Topics: sustaining proliferative signaling, evading growth suppressors, resisting cell death, enabling replicative immortality, inducing angiogenesis, activating invasion and metastasis, genomic instability and mutation, tumor promoting inflammation, cellular energetics, avoiding immune destruction. The output should be topics from the above 10 topics, that are related to the input article. Please note one article can be related to multiple topics. Output format: provide a semicolon-separated list of relevant topics.
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    INPUT: OBJECTIVE : Emerging evidences implicate long noncoding RNAs ( lncRNAs ) are deregulated in cancer development . The purpose of the current study is to investigate the role of new lncRNA , named PlncRNA-1 , in prostate cancer ( CaP ) pathogenesis . MATERIALS AND METHODS : In this study , real-time q-PCR was used to demonstrate the expression of PlncRNA-1 in 16 pairs CaP tissues and matched normal tissues , 14 pairs CaP tissues and BPH tissues , 4 CaP cell lines , including LNCaP , LNCaP-AI , PC3 , and C4-2 , and 2 normal prostate epithelial cell lines RWPE-1 and PWR-1E . After PlncRNA-1 was suppressed by siRNA in LNCaP and LNCaP-AI cell lines , cell proliferation and apoptosis were assessed using CCK-8 and terminal deoxynucleotidyl transferase dUTP nick end labeling ( TUNEL ) . After PlncRNA-1 and AR was suppressed by siRNA in LNCaP and LNCaP-AI cell lines , real-time q-PCR and Western blotting were used to measure reciprocal regulation of PlncRNA-1 and AR . RESULTS : We showed that expression PlncRNA-1 , was significantly higher in CaP cells relative to normal prostate epithelial cells , as well as higher in human CaPs compared with normal tissues and benign prostatic hyperplasia ( BPH ) . Silencing of PlncRNA-1 significantly reduced cell proliferation and induced apoptosis in CaP cell lines LNCaP and LNCaP-AI . Mechanistically , PlncRNA-1 suppression by siRNA resulted in a decrease of androgen receptor ( AR ) mRNA , protein and AR downstream target . Of note , blockade of AR signaling with siRNA also resulted in a suppression of PlncRNA-1 expression in CaP cell lines . CONCLUSIONS : Our study suggests reciprocal regulation of PlncRNA-1 and androgen receptor contribute to CaP pathogenesis and that PlncRNA-1 is a potential therapy target .
    OUTPUT:
