Focal loss of long non-coding RNA-PRAL, as determinant of cell function and phenotype of hepatocellular carcinoma

Hepatocarcinogenesis is a long process characterized by the progressive development of preneoplastic and neoplastic lesions, and the acquisition of multiple genetic and epigenetic events contributing to the biochemical and molecular heterogeneity of the disease (1,2). Hepatocellular carcinoma (HCC) constitutes the second/third cause of cancer-related deaths in the world (3). Curative strategies of HCC, such as liver transplantation, radiofrequency ablation, alcoholization, or sorafenib (a multikinase inhibitor) are available (4). Unfortunately, the majority of patients are not candidates for these therapies, due to the delay of HCC diagnosis. In addition, the survival benefit of sorafenib is still modest. Therefore, there is an urgent need to develop molecular tools and guarantee patients stratification on the basis of the molecular and clinical features, and to identify new strategies to prevent relapse and prolong patient survival (5). Although significant progress has been made in the knowledge of HCC pathogenesis, the information on molecular mechanisms underlying HCC development and progression is still incomplete (1,2).