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Hepatitis B virus (HBV) infection is closely related to hepatocellular carcinoma (HCC) development. To investigate the mechanism of HBV causing HCC, we previously analyzed the transcription of the HBV-transgenic cell line HepG2-4D14 and parental HepG2 cells and identified a subset of long noncoding RNAs (lncRNAs) differentially expressed between them. In this study, we focus on lncRNA  LINC01010 , as it is significantly downregulated in HepG2-4D14 cells and in liver tissues of HCC patients, and positively correlated with survival. We found that HBV-encoded HBx can reduce the transcription of  LINC01010 . Functional analysis showed that the overexpression of  LINC01010  inhibits proliferation, migration and invasion of HepG2 cells while the knockdown of  LINC01010  promotes these processes. By taking the approach of RNA immunoprecipitation (RIP) and mass spectrometry, we identified that  LINC01010  can interact with vimentin. Further studies demonstrated that  LINC01010  negatively affects the vimentin network extension and causes more rapid subunit exchange and lower stability of vimentin filaments. In addition,  LINC01010  can reduce the amount of insoluble vimentin within cells, which suggests that  LINC01010  interfers with vimentin polymerization. These data indicate that  LINC01010  can inhibit the assembly of vimentin filament. Thus, we revealed that HBV HBx-downregulated  LINC01010 , which suppresses cell proliferation and migration by negatively regulating the formation of vimentin filament. Taken together,  LINC01010  is a potential tumor suppressor that may restrain HBV-related HCC development.

HBV HBx-Downregulated lncRNA LINC01010 Attenuates Cell Proliferation by Interacting with Vimentin