AURKB as a Therapeutic Target and Key Driver of Liver Cancer Growth and Metastasis DOI
Chen Wang,

Jiang-wen Liu,

Y. Q. Wu

et al.

Apmis, Journal Year: 2025, Volume and Issue: 133(4)

Published: April 1, 2025

Hepatocellular carcinoma (HCC) is a major cause of cancer-related deaths worldwide. Aurora kinase B (AURKB), critical regulator mitosis, has been implicated in cancer progression, though its precise role HCC remains unclear. In this study, AURKB expression was found to be significantly elevated tissues and cell lines compared controls, as validated by GEPIA ENCORI databases. Functional assays revealed that knockdown reduced proliferation, invasion, migration, while increasing apoptosis. Furthermore, suppression affected epithelial-mesenchymal transition (EMT) markers, decreasing vimentin N-cadherin levels E-cadherin expression. vivo, xenograft mouse model demonstrated tumors derived from AURKB-silenced cells exhibited growth fewer lung metastases. Histological immunohistochemical analyses showed lower Ki-67, MMP-9, EMT markers these tumors, alongside increased E-cadherin. These findings highlight AURKB's promoting metastasis, regulation. Overexpression associated with poor prognosis, suggesting it could serve potential biomarker therapeutic target for liver cancer. Overall, targeting may provide novel approach inhibit improving patient outcomes.

Language: Английский

AURKB as a Therapeutic Target and Key Driver of Liver Cancer Growth and Metastasis DOI
Chen Wang,

Jiang-wen Liu,

Y. Q. Wu

et al.

Apmis, Journal Year: 2025, Volume and Issue: 133(4)

Published: April 1, 2025

Hepatocellular carcinoma (HCC) is a major cause of cancer-related deaths worldwide. Aurora kinase B (AURKB), critical regulator mitosis, has been implicated in cancer progression, though its precise role HCC remains unclear. In this study, AURKB expression was found to be significantly elevated tissues and cell lines compared controls, as validated by GEPIA ENCORI databases. Functional assays revealed that knockdown reduced proliferation, invasion, migration, while increasing apoptosis. Furthermore, suppression affected epithelial-mesenchymal transition (EMT) markers, decreasing vimentin N-cadherin levels E-cadherin expression. vivo, xenograft mouse model demonstrated tumors derived from AURKB-silenced cells exhibited growth fewer lung metastases. Histological immunohistochemical analyses showed lower Ki-67, MMP-9, EMT markers these tumors, alongside increased E-cadherin. These findings highlight AURKB's promoting metastasis, regulation. Overexpression associated with poor prognosis, suggesting it could serve potential biomarker therapeutic target for liver cancer. Overall, targeting may provide novel approach inhibit improving patient outcomes.

Language: Английский

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