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 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. 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.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10777316 | PMC |
| http://dx.doi.org/10.22074/cellj.2023.2010456.1395 | DOI Listing |
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