Background: Hepatocellular carcinoma (HCC) is the most common tumor with severe morbidity and high mortality. The lncRNA ASAP1-IT1 [the intronic transcript 1 (IT-1) of ArfGAP with SH3 domain, ankyrin repeat and PH domain 1 (ASAP1)] have been shown to promote tumor formation in a variety of cancers. This study sought to investigate the effects of dysregulated ASAP1-IT1 on the biological processes of HCC.Methods: The expression levels of ASAP1-IT1 in 30 paired HCC and adjacent non-tumor tissues were measured by real-time-quantitative polymerase chain reaction (RT-qPCR). Several functional tests were performed to investigate the molecular mechanism of ASAP1-IT1 in HCC progression.Results: Our study showed that ASAP1-IT1 was highly expressed in the HCC tissues and cell lines. The knockdown of ASAP1-IT1 inhibited cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) progression and enhanced the sorafenib sensitivity of the HCC cells. Further investigations revealed that ASAP1-IT1 served as a sponge of microRNA-1294 (miR-1294) to promote transforming growth factor beta receptor 1 (TGFBR1) expression. In addition, the tumor-promoting effect of ASAP1-IT1 was blocked by inhibiting miR-1294/TGFBR1. Tumorigenic assays in nude mice demonstrated that the inhibition of ASAP1-IT1 inhibited the growth of HCC in vivo.Conclusions: These results suggest that lncASAP1-IT1 promotes HCC development by targeting TGFBR1 through miR-1294, which provides a potential target for HCC diagnosis and treatment.