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.