Aims
Worldwide, hepatocellular carcinoma (HCC) is one of the most common causes of death in people. Albumin (ALB) is considered as an important indicator for HCC prognosis, and evidence has shown HCC cell growth can be regulated by ALB. However, the role of ALB in hepatocarcinogenesis and the mechanism of action is still unknown.
Background & aims
Worldwide, hepatocellular carcinoma (HCC) is one of the most common causes of death in people. Albumin (ALB) is considered as an important indicator for HCC prognosis, and evidence has shown HCC cell growth can be regulated by ALB. However, the role of ALB in hepatocarcinogenesis and the mechanism of action is still unknown.
Conclusions
ALB acts as a tumour suppressor and plays a key role in HCC progression, particularly in invasion and metastasis. Suppression of ALB promoted migration and invasion of HCC cells by increasing uPAR, matrix metalloproteinase (MMP2), and MMP9.
Methods
The expression of ALB was determined by clinical profiles, immunohistochemistry, and western blot. Wound healing and Transwell assays were conducted to evaluate the effects of ALB during migration and invasion in HCC. We used mass spectrometry coupled isobaric tags for relative and absolute quantitation (iTRAQ)-technology to identify secretory differentially expressed proteins (DEPs) in ALB knockdown HepG2 cells. Western blot, reverse transcription-quantitative polymerase chain reaction and enzyme-linked immunosorbent assay techniques were used for verification.
Results
We suggested that ALB was associated with aggressive metastasis and depleting ALB significantly promoted invasion and migration of HCC. A total of 210 DEPs were identified after silencing of ALB. We observed that a negative correlation between ALB and urokinase plasminogen activator surface receptor (uPAR) expression levels. Conclusions: ALB acts as a tumour suppressor and plays a key role in HCC progression, particularly in invasion and metastasis. Suppression of ALB promoted migration and invasion of HCC cells by increasing uPAR, matrix metalloproteinase (MMP2), and MMP9.