Abstract

Phospholipid scramblase 1 (PLSCR1) serves a function in the pathogenesis and progression of various types of cancer. However, the role of PLSCR1 in human primary liver cancer remains unknown. The aim of the present study was to evaluate the expression of PLSCR1 in primary liver cancer and analyse the clinical significance. In addition, the present study detected and compared the biological behaviours of HepG2 cells with different levels of activated PLSCR1 or silenced PLSCR1. PLSCR1 expression in primary liver cancer tissue samples was examined using immunohistochemistry. Cultured HepG2 cells were infected with lentiviruses to suppress or activate PLSCR1 expression. Reverse transcription-quantitative PCR and western blotting were performed to analyse the effects of silencing or activating PLSCR1 in cell lines at the mRNA and protein levels, respectively. The effects of PLSCR1 expression on cell proliferation, adhesion, migration and invasion were subsequently determined using Cell Counting Kit 8, adhesion, and Transwell migration and invasion assays. PLSCR1 expression in primary liver cancer tissue samples was higher compared with that in adjacent non-cancerous liver tissue samples and normal tissue samples, and positively correlated with the clinical stage. PLSCR1 was effectively downregulated or overexpressed in HepG2 cells using small interfering RNA and lentivirus techniques, respectively. PLSCR1 upregulation promoted cell proliferation, invasion and migration, while PLSCR1 downregulation inhibited these effects. PLSCR1 is highly expressed in primary liver cancer and associated with the clinical stage. Downregulating the expression of PLSCR1 significantly inhibited the proliferation, adhesion, migration and invasion of cancer cells, suggesting that PLSCR1 may be a potential therapeutic target for preventing the progression of primary liver cancer.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.