Mechanistic study of LINC00839-mediated suppression of anoikis in hepatocellular carcinoma via regulation of FOXM1

This study investigated the role of LINC00839 in regulating anoikis in hepatocellular carcinoma (HCC) cells. Bioinformatic analysis using UALCAN and Sparkle databases revealed that LINC00839 is highly expressed in HCC tissues and is associated with poor patient prognosis. Functional experiments demonstrated that LINC00839 expression was significantly upregulated in an anoikis model, and its overexpression inhibited apoptosis in HCC cells. This was evidenced by decreased levels of pro-apoptotic proteins Caspase-3 and Bax and increased levels of the anti-apoptotic protein Bcl-2. Transcriptome sequencing and database predictions identified the transcription factor FOXM1 as a key downstream effector. Crucially, siRNA-mediated knockdown of FOXM1 reversed the anti-anoikis effect of LINC00839, confirming its essential role in this pathway. Furthermore, LINC00839 overexpression promoted HCC cell proliferation, migration, and invasion. The study concludes that LINC00839 promotes hepatocellular carcinoma progression by inhibiting anoikis through the upregulation of FOXM1, highlighting its potential as a novel therapeutic target.