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.
    ###
    INPUT: The metastasis-associated lung adenocarcinoma transcript 1 , MALAT1 , is a long non-coding RNA ( lncRNA ) that has been discovered as a marker for lung cancer metastasis . It is highly abundant , its expression is strongly regulated in many tumor entities including lung adenocarcinoma and hepatocellular carcinoma as well as physiological processes , and it is associated with many RNA binding proteins and highly conserved throughout evolution . The nuclear transcript MALAT-1 has been functionally associated with gene regulation and alternative splicing and its regulation has been shown to impact proliferation , apoptosis , migration and invasion . Here , we have developed a human and a mouse knockout system to study the loss-of-function phenotypes of this important ncRNA . In human tumor cells , MALAT1 expression was abrogated using Zinc Finger Nucleases . Unexpectedly , the quantitative loss of MALAT1 did neither affect proliferation nor cell cycle progression nor nuclear architecture in human lung or liver cancer cells . Moreover , genetic loss of Malat1 in a knockout mouse model did not give rise to any obvious phenotype or histological abnormalities in Malat1-null compared with wild-type animals . Thus , loss of the abundant nuclear long ncRNA MALAT1 is compatible with cell viability and normal development .
    OUTPUT:

agent
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.
    ###
    INPUT: The metastasis-associated lung adenocarcinoma transcript 1 , MALAT1 , is a long non-coding RNA ( lncRNA ) that has been discovered as a marker for lung cancer metastasis . It is highly abundant , its expression is strongly regulated in many tumor entities including lung adenocarcinoma and hepatocellular carcinoma as well as physiological processes , and it is associated with many RNA binding proteins and highly conserved throughout evolution . The nuclear transcript MALAT-1 has been functionally associated with gene regulation and alternative splicing and its regulation has been shown to impact proliferation , apoptosis , migration and invasion . Here , we have developed a human and a mouse knockout system to study the loss-of-function phenotypes of this important ncRNA . In human tumor cells , MALAT1 expression was abrogated using Zinc Finger Nucleases . Unexpectedly , the quantitative loss of MALAT1 did neither affect proliferation nor cell cycle progression nor nuclear architecture in human lung or liver cancer cells . Moreover , genetic loss of Malat1 in a knockout mouse model did not give rise to any obvious phenotype or histological abnormalities in Malat1-null compared with wild-type animals . Thus , loss of the abundant nuclear long ncRNA MALAT1 is compatible with cell viability and normal development .
    OUTPUT:
