Document Type : Original Article
Department of Hepatobiliary Surgery, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, China
Objective: This study aimed to investigate functional role of long ncRNA (lncRNA) 91H in liver cancer tumorigenesis,
focusing on its effect on cell proliferation, apoptosis, cell cycle progression, migration, invasion, epithelial-mesenchymal
transition (EMT) and in vivo tumor growth.
Materials and Methods: In this experimental study, liver cancer tissues and cell lines were analyzed for lncRNA 91H
expression using quantitative reverse transcription polymerase chain reaction (qRT-PCR). By employing si-RNA to
silence 91H, we aimed to gain a more in-depth understanding of its specific contributions and effects within these cells.
Cell proliferation was assessed through the CCK-8 assay, while apoptosis and cell cycle progression were quantified
using Annexin V-FITC staining and flow cytometry, respectively. Migration and invasion capabilities of liver cancer cells
were assessed through transwell assay. EMT was assessed by analyzing protein expression levels of EMT-associated
markers through western blotting. In vivo effect of 91H was assessed through xenograft experiments.
Results: Significantly higher levels of lncRNA 91H were observed in the liver cancer tissues and cell lines, than the
normal cells. Silencing 91H in liver cancer cells led to a notable reduction of cell proliferation by inducing apoptosis
and arresting the cell cycle. Liver cancer cells with decreased 91H expression exhibited diminished migration and
invasion abilities, suggesting a role for 91H in promoting these processes. Furthermore, 91H knockdown weakened
EMT in liver cancer cells, indicating its involvement in modulating this critical cellular transition. Furthermore, growth of
subcutaneous xenograft tumors and weight was effectively suppressed by sh-lncRNA 91H.
Conclusion: Our study strongly supports lncRNA 91H's role in liver cancer progression by enhancing proliferation, migration,
invasion, and EMT. Targeting 91H reduced in vivo tumor growth, highlighting its potential as a therapeutic liver cancer target.
These findings suggest 91H's pivotal role in liver cancer aggressiveness, opening doors for future therapeutic approaches.