In conclusion, PTK2 and EIF3S3, which, respectively, encode focal adhesion kinase and the p40 subunit of the eukaryotic initiation factor 3, were probable targets within the amplification at 8q23-q24 and may be involved in progression of HCC.
In conclusion, Rab5a is overexpressed in human HCC and contributes to cancer cell proliferation and invasion through regulation of FAK and AKT signaling.
Circ_0015756 knockdown was shown to increase the expression of miR-7, reduce the proliferation, invasion, migration and resistance to apoptosis, and down-regulate the expression of FAK in HCC.
Integrin alpha 7 correlates with poor clinical outcomes, and it regulates cell proliferation, apoptosis and stemness via PTK2-PI3K-Akt signaling pathway in hepatocellular carcinoma.
Inhibition of SRC/FAK cue: A novel pathway for the synergistic effect of rosuvastatin on the anti-cancer effect of dasatinib in hepatocellular carcinoma.
DBH-AS1 facilitated the development of HCC via miR-138/FAK/Src/ERK pathway, establishing the molecular basis of DBH-AS1 in clinical application for HCC.
Taken together, our data demonstrate a novel function of LOXL4 in tumor metastasis mediated by exosomes through regulation of the FAK/Src pathway and angiogenesis in HCC.
Moreover, the expression levels of beta-catenin, cyclin D1, c-Myc, MMP-2, and FAK detected by western blotting were downregulated in SLC5A8-transfected HCC cells compared with control-transfected cells, indicating that SLC5A8 has a tumor-suppressive function that acts by interfering with Wnt/β-catenin signaling in HCC.
Interestingly, western blot analysis showed that treatment with oxaliplatin increased GAS7C and N-WASP protein levels and decreased the levels of proteins involved in the fibronectin/integrin/FAK pathway, such as FAK, in both HCC cell lines.
The focal adhesion kinase (FAK) gene protein tyrosine kinase 2 is amplified in 16.4% of The Cancer Genome Atlas HCC specimens, and its amplification leads to increased FAK mRNA expression.