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Article Abstract
Background: The role of estrogen in liver cancer cells has attracted attention, but its specific actions and underlying mechanisms remain unclear.
Methods: Flow CytoMetry and Western blotting were used to investigate the mechanism of HOXA11-AS and estrogen in promoting apoptosis of hepatocellular carcinoma (HCC). In vivo subcutaneous tumorigenesis assays were uesd to confirm the regulatory role of HOXA11-AS in HCC progression. Through immunohistochemistry, the correlation between HOXA11 expression and the prognosis of patients with HCC was explored.
Results: Estrogen was found to promote apoptosis in HCC cells, dependent on HOXA11-AS. HOXA11 and HOXA11-AS are upregulated in HCC tissues. Downregulation of HOXA11-AS and HOXA11 significantly inhibited cell proliferation, migration, and invasion in HCC. HOXA11-AS forms an RNA duplex with HOXA11, preventing RNase degradation. In HCC patients, high HOXA11 expression was significantly associated with lower overall survival (OS) (p=0.001) and disease-free survival (DFS) (p=0.002). High HOXA11 expression was also significantly correlated with recurrence (p<0.001), major vascular invasion (p=0.002) and increased tumor volume (p=0.007). Estrogen activated the c-met/AKT/mTOR pathway in the HCC cell line.
Conclusion: Estrogen and its related proteins have therapeutic effects in HCC and may be new potential therapeutic targets.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12138468 | PMC |
| http://dx.doi.org/10.1016/j.tranon.2025.102404 | DOI Listing |
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