AI Article Synopsis
- The study investigates the role of HtrA1 in epithelial-mesenchymal transition (EMT) and its impact on metastasis in hepatocellular carcinoma (HCC).
- Researchers found that lower HtrA1 expression in tumor tissues correlated with increased lymph node metastasis and enhanced cell migration, characterized by higher Vimentin and lower E-cadherin levels.
- Overall, the findings suggest that HtrA1 might influence EMT mechanisms, implying it could be a potential target for combating metastasis in HCC patients.
Article Abstract
Background And Aims: Epithelial-mesenchymal transition (EMT) is involved in the development and progression of cancer. HtrA1 had been showed to play a modulatory role in metastasis of hepatocellular carcinoma (HCC). The relationship between HtrA1 and EMT in HCC was investigated in the present study.
Methods: The HtrA1 expression in human HCC tumor tissues and cells was determined by real-time PCR. SiRNA-HtrA1 and pcDNA-HtrA1 were respectively transfected into HepG2 and MHCC97H cells to observe their effects on cell migration and expression of EMT-associated markers Vimentin and E-cadherin. The relationship between HtrA1 and EMT in 60 HCC patients was also investigated.
Results: HtrA1 expression of tumor tissues was down-regulated with the increasing of number in lymph nodes metastasis in HCC patients. HtrA1 down-regulation led to the significant increase of cell migration, Vimentin expression and decrease of E-cadherin expression, while HtrA1 overexpression resulted in an opposite function. The HtrA1 expression was positively related to the E-cadherin level (R(2) = 0.5903, P < 0.001) and negatively correlated with Vimentin level (R(2) = 0.6067, P < 0.001) in tumor tissues of HCC, respectively.
Conclusion: HtrA1 expression was closely related to EMT, which might be a potential mechanism underlying metastasis of HCC.
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| http://dx.doi.org/10.1016/j.bbrc.2015.09.105 | DOI Listing |
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